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30 November 2024, Volume 21 Issue 6
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ERK Pathway Activation by Fam172a Gene Knockdown Aggravates Lipotoxic Hepatocyte Injury #br#
LI Mengqi, WEI Herui, LOU Jing, AN Wen, SONG Aqian, HE Lingling, YANG Junru, WEI Hongshan, #, XIAO Fan, #
2024, 21(6):  501-507.  doi:10.3870/j.issn.1672-8009.2024.06.001
Abstract ( 128 )   PDF (2261KB) ( 28 )  
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Objective To preliminarily explore the mechanism of Fam172a gene knockout in lipid toxic liver cell injury. Methods Fam172a gene knockout (Fam172a - / - ) mice was used to assess liver function, liver tissue lipid accumulation, and inflammatory cytokine levels. Fam172a geneknockdown HepG2 cell lines were performed to assess intracellular lipid accumulation and inflammato
ry cytokine levels. Protein levels were analyzed via Western blotting. Results Compared to the controlgroup, Fam172a - / - mice exhibited significantly elevated serum ALT and AST levels, aggravated hepatic structural damage, lipid accumulation, and inflammation. Moreover, there was a significant upregulation in hepatic pERK/ ERK relative expression levels. Fam172a gene knockdown led to increased triglyceride content and inflammatory cytokine levels in HepG2 cells, along with a significant elevation in the relative expression level of pERK/ ERK. However, the administration of the ERK inhibitor U0126 notably mitigated the lipotoxic hepatocyte injury induced by Fam172a gene knockdown. Conclusion Fam172a gene knockdown exacerbates hepatocyte lipotoxicity through the activation of the ERK pathway.
Inhibitory Effect of FOXO4 on Lipopolysaccharide-induced Apoptosis in Cardiomyocytes #br#
LI Hongjian, WANG Siyue
2024, 21(6):  508-514.  doi:10.3870/j.issn.1672-8009.2024.06.002
Abstract ( 52 )   PDF (3411KB) ( 15 )  
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Objective This study was to investigate the effects of FOXO4 on lipopolysaccharide(LPS) -induced inflammation and apoptosis of cardiomyocytes, and to explore the potential molecular mechanism. Methods LPS treated H9C2 cells were treated with FOXO4 recombinant lentiviralvector (LPS + Lv-FOXO4), control vector ( LPS + Lv-NC group) and / or nigericin ( LPS + LvFOXO4 + N group) respectively. Real-time quantitative polymerase chain reaction ( RT-qPCR) was used to detect the expression level of FOXO4 mRNA. The levels of TNF-α and IL-1β in cell supernatant were detected by enzyme-linked immunosorbent assay. The apoptosis was detected by flow cytometry. The expression levels of FOXO4 and NF-κB / NLRP3 pathway-related proteins was analyzed by Western blotting. Results LPS treatment could inhibit the expression of FOXO4 in myocytes (P < 0. 05), while overexpression of FOXO4 could decrease the levels of TNF-α and IL-1β,inhibit the apoptosis of myocytes, decrease the expression level of pro-apoptotic protein Bax and increase the expression level of anti-apoptotic protein Bcl-2 in myocytes treated with LPS (P < 0. 05).In addition, overexpression of FOXO4 could inhibit the activation of NF-κB signaling pathway by inhibiting P65, IκBα phosphorylation and P65 nuclear shift ( P < 0. 05). Overexpression of FOXO4inhibited NLRP3 inflammasome activation and pyroptosis by inhibiting NLRP3, ASC, cleavedcaspase-1, and N-GSDMD protein expression ( P < 0. 05 ). The NLRP3 inflammasome activator Nigeritin could reverse the protective effect of FOXO4 overexpression on LPS-induced myocardialcell injury ( P < 0. 05). Conclusion Overexpression of FOXO4 can protect cardiomyocytes fromLPS-induced inflammation and apoptosis, possibly by inhibiting pyroptosis mediated by NF-κB / NLRP3 inflammasome signaling pathway.

Anti-tumor Effect of Pterostilbene on Tongue Squamous Cell Carcinoma CAL-27 Cells #br#
DAI Xiaoyan, WANG Yansong, DAI Juan, ZHAI Yan
2024, 21(6):  515-520.  doi:10.3870/j.issn.1672-8009.2024.06.003
Abstract ( 51 )   PDF (4441KB) ( 14 )  
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Objective Explore the effect of Pterostilbene on the biological behavior of humantongue squamous cell carcinoma CAL-27 cells. Methods CAL-27 cells were divided into 2 groups:control group and experimental group. Cells in the experimental group were treated with Pterostilbene(10, 20, 40 μmol / L). CCK-8 assay, colony formation assay and EdU staining were used to measure the proliferation of CAL-27 cells. Flow cytometry was used to determine the apoptosis of CAL-27cells. Wound-healing and Transwell assay were used to detect the migration and invasion ability of CAL-27 cells. Western blotting was used to detect the expression levels of epithelial-mesenchymaltransition (EMT) -related proteins in CAL-27 cells. Xenograft model was used to verify the effect ofpterostilbene on tumor in vivo. Results The proliferation, migration and invasion abilities of CAL-27 cells were weakened, the apoptosis rate was increased, the expression levels of Bax, E-cadherin and Claudin1 proteins in the cells were increased, and the expression levels of Bcl-2, N-cadherin, Vimentin and Snail proteins were decreased after 24 h treatment with 20 and 40 μmol / Lpterostilbene when compared with those in the control group ( P < 0. 05). After treatment with 30mg / kg pterostilbene, the weight and volume of transplanted tumors in nude mice decreased significantly, the number of Ki67 and Vimentin positive cells decreased significantly, and the number of TUNEL positive cells increased significantly ( P < 0. 05). Conclusion Pterostilbene can inhibitCAL-27 cells proliferation, migration, invasion and EMT and induce its apoptosis.

Effect of Tanshinone Ⅱ-A on Th17 / Treg Balance and TLR4 Related Pathways in Osteoarticular Cartilage Degeneration Rats #br#
SUN Mengdi, SHANG Xiaolin, WANG Xiaojing
2024, 21(6):  521-529.  doi:10.3870/j.issn.1672-8009.2024.06.004
Abstract ( 41 )   PDF (5685KB) ( 11 )  
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Objective To investigate the effect of tanshinone Ⅱ -A (TSⅡ -A) on regulatory T(Treg) / helper T cell 17 (Th17) in osteoarthritis (OA) cartilage degeneration rats, and its regulation on the expression of Toll like receptor 4 (TLR4) signaling pathway related genes. Methods The rat OA model was constructed by injecting papain into the joint cavity, rats then were dividedinto 3 groups for drug intervention: TS Ⅱ -A low-dose group ( TS Ⅱ -A-L), TS Ⅱ -A high-dosegroup (TSⅡ -A-H), and glucosamine sulfate (DGS) group as positive control. Enzyme linked immunosorbent assay was used to detect the levels of tumor crossing factor-α (TNF-α) and interleukin-6 ( IL-6) in serum. TUNEL assay was used to detect the cell apoptosis in rat cartilage tissues. Flow cytometry was used to detect the proportion of Treg and Th17 in spleen tissues. qRT-PCRwas used to detect the mRNA expression levels of TLR4, myeloid differentiation factor 88(MyD88), nuclear factor κB ( NF-κB), aggrecan, Collagen Ⅱ , forkhead / winged helix transcription factor 3 (Foxp3), IL-17, B cell lymphoma-2 (Bcl-2), and Bcl-2 associated x protein(Bax) in rat knee joint cartilage tissues. Western blotting assay was used to detect the expressionlevels of TLR4, MyD88, p-NF-κB, Bcl-2 and Bax in the cartilage tissues. Results The proportion of Treg cells, and the expression levels of aggrecan, Collagen Ⅱ , Foxp3, and Bcl-2 in theOA group were significantly decreased, and the levels of TNF-α and IL-6, the cell apoptosis rate,the proportion of Th17 cells, and the expression levels of IL-17, TLR4, MyD88, p-NF-κB andBax were significantly increased when compared with those in the Sham group. The proportion of Tregcells, and the expression levels of aggrecan, Collagen Ⅱ , Foxp3, and Bcl-2 in the TSⅡ -A-Lgroup, TSⅡ -A-H group, and DGS group were significantly increased, and the levels of TNF-αand IL-6, the cell apoptosis rate, the proportion of Th17 cells, and the expression levels of IL-17,TLR4, MyD88, p-NF-κB and Bax were significantly decreased when compared with those in theOA group. The proportion of Treg cells and the expression levels of aggrecan, Collagen Ⅱ , Foxp3,and Bcl-2 in the TSⅡ -A-H group and the DGS group were significantly increased, and the levels ofTNF-α and IL-6, the cell apoptosis rate, the proportion of Th17 cells, and the expression levels ofIL-17, TLR4, MyD88, p-NF-κB and Bax were significantly decreased when compared with thosein the TSⅡ -A-L group ( all P < 0. 05). No statistically significance in those above indexes werefound between the TSⅡ -A-H group and the DGS group (P> 0. 05). Conclusion Tanshinone Ⅱ -A(TSⅡ -A) could significantly inhibit the expression of TLR4, MyD88, p-NF-κB and reduce thecell apoptosis rate in the articular cartilage tissues of OA rats, which may be related to the improvement of Treg / Th17 imbalance in rats.

Cordycepin Relieves Brain Tissue Damage in Rats with Cerebral Ischemia and Reperfusion by Activating Nrf2 / HO-1 / NQO1 Pathway#br#
WU Shuang, DAI Xubo, CUI Zhen, JIANG Fengying, PANG Suqiu
2024, 21(6):  530-536.  doi:10.3870/j.issn.1672-8009.2024.06.005
Abstract ( 26 )   PDF (3110KB) ( 15 )  
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Objective To investigate the protective effect of cordycepin (COR) on brain tissue damage in rats with cerebral ischemia-reperfusion, and to preliminarily clarify the protectivemechanism. Methods Sixty Wistar rats were divided into 3 groups: Normal control group, modelgroup, and model plus drug group. Detection of learning and memory capacities in rats by step-down test and Y maze test. HE staining was employed to observe the pathological changes of brain tissues. Dry and wet weight ratio was used to calculate brain water content and brain index. TUNEL was used to observe cell apoptosis in brain tissues. The levels of serum SOD, MDA and LDH of rats were determined by ELISA. Western blotting was used to detect the expression levels of Bax / Bcl-2,cleaved cas9 / cas9, cleaved cas3 / cas3, Nrf2, HO-1 and NQO1 proteins. Results Compared withthe model group, COR can dose dependently improve brain tissue damage, inhibit oxidative stress,and promote activation of the Nrf2 / HO-1 / NQO1 pathway. Conclusion Cordycepin can improve brain tissue damage by upregulating the Nrf2 pathway.

Effect of M2-type Macrophage-derived Exosomes on Multiple Myeloma Cell Metastasis by Regulation of HGF / c-Met Pathway #br#
Mukeremu Aikepaer, Vinila Tuerhong, Bahaguli Yusufu, Aikebaier Abudureyimu
2024, 21(6):  537-543.  doi:10.3870/j.issn.1672-8009.2024.06.006
Abstract ( 20 )   PDF (1295KB) ( 13 )  
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Objective To investigate the effect of M2-type macrophage-derived exosomes on human multiple myeloma cell metastasis and its mechanism. Methods THP-1 cells were induced to differentiate into M0 and M2 macrophages in vitro. Real-time fluorescent quantitative polymerase reaction ( RT-qPCR) was used to detect the expression levels of hemoglobin scavenger receptor ( CD163 ), interleukin-10 ( IL-10 ), arginase-1 ( Arg-1 ) and transforming growth factor-β1 ( TGF-β1 ) in induced M2 macrophages. Exosomes derived from M2 macrophages were isolated. RPMI-8226 cells were divided into 3 groups: control group, M0-Exos group and M2-Exos group. Then the cell migration and invasion were detected by Transwell. The expression levels of Ncadherin, Vimentin, E-cadherin and the transcription factor Snail, and hepatocyte growth factor (HGF) / c-Met related proteins were detected by Western blotting. Moreover, RPMI-8226 cells were then divided into 4 groups: control group, M2-Exos group, SU11274 group and SU11274 + M2-Exos group, and cell migration and invasion were detected by Transwell, and the expressionlevels of N-cadherin, Vimentin, E-cadherin and Snail were detected by Western blotting. Results The mRNA expression levels of CD163, IL-10, Arg-1 and TGF-β1 in the M2 macrophages weresignificantly up-regulated when compared with those in the M0 macrophages (P< 0. 05). The particles isolated from the M2 macrophages showed protein expressions of CD9, CD63, TSG101 and ALIX, and were identified as exosomes. The numbers of cell migration and invasion in the M2-Exosgroup were significantly increased when compared with those in the control group (P < 0. 05), theprotein expression levels of N-cadherin, Vimentin and Snail, and the HGF protein expression andp-c-Met / c-Met ratio were significantly increased (P< 0. 05), and the protein expression level of Ecadherin was significantly decreased (P< 0. 05). The numbers of cell migration and invasion in theSU11274 + M2-Exos group were significantly decreased when compared with those in the M2-Exosgroup (P< 0. 05), the protein expression levels of N-cadherin, Vimentin and Snail were significantly decreased (P< 0. 05), and the protein expression level of E-cadherin was significantly increased (P< 0. 05). Conclusion M2-type macrophage-derived exosomes can promote the migration, invasion and EMT of human multiple myeloma cells, which exacerbate tumor cell metastasis, the mechanism may relate to the regulation of HGF / c-Met pathway.

Mechanism of Upregulation of Numb to Increase Chemotherapy Sensitivity of Gastric Cancer Cells by Regulating Iron Death Pathway #br#
WANG Yongqi, LI Qiang, HE Donglei, CHEN Yong, LIU Lijie
2024, 21(6):  544-550.  doi:10.3870/j.issn.1672-8009.2024.06.007
Abstract ( 26 )   PDF (961KB) ( 14 )  
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Objective To investigate the effect of up-regulated cell fate determinant Numb on chemotherapy sensitivity of gastric cancer cells and its mechanism. Methods pcDNA3. 1 plasmidvector and PCDNA3. 1-Numb plasmid were transfected into gastric cancer cell line BGC-823 by liposome transfection technique. The transfected BGC-823 cells were treated with different concentrations of doxorubicin ( ADM ), and the cell proliferation inhibition rate was determined by MTT assay. BGC-823 cells were divided into 4 groups: control group, NC group, Numb group, and Numb + Ferrostatin-1 ( Fer-1) group, and the cell proliferation inhibition rate of each group was determined, and the level of reactive oxygen species (ROS) in each group was detected by DCFH-DA fluorescent probe method. The levels of glutathione (GSH), malondialdehyde (MDA) and theactivity of superoxide dismutase (SOD) were measured by kits, and the concentration of iron ionin cells was determined by the iron ion detection kit. The expression levels of Numb, iron death related pathway factor P53, glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11(SLC7A11) were detected by qRT-PCR and Western blotting. Results The mRNA and protein relative expression levels of Numb in the Numb group were significantly up-regulated (P < 0. 05), and the cell proliferation inhibition rate was significantly increased after ADM treatment (P< 0. 05)when compared with those in the control and NC groups. In comparison of those in the control group and NC group, the cell proliferation inhibition rate in the Numb group was significantly increased( P< 0. 05), the levels of ROS and MDA in cells were significantly increased (P< 0. 05), the level of GSH content and the activity of SOD was significantly decreased (P < 0. 05), the Fe2 + concentration was significantly increased (P< 0. 05), the expression level of P53 was significantly increased (P< 0. 05), and the expression levels of GPX4 and SLC7A11 were significantly decreased (P < 0. 05). After the intervention by Fer-1 treatment, the proliferation inhibition rate of BGC-823 cells in the Numb + Fer-1 group was significantly decreased (P<0. 05), the levels of ROS and MDA were significantly decreased (P<0. 05), the GSH level and SOD activity were significantly increased (P<0. 05), the Fe2 + concentration was significantly decreased (P < 0. 05), the expression level of P53 were significantly decreased (P<0. 05), and the expression levels of GPX4 and SLC7A11 were significantly up-regulated (P< 0. 05) when compared with those in the Numb group. Conclusion Up-regulation of Numb can enhance the sensitivity of gastric cancer cells to ADM, which may be related to the regulation of P53 / SLC7A11 / GPX4 pathway to induce ferroptosis.

Effect of Interaction Between miR-146a-5p and miR-21 on Risk and Severity of Primary Nephrotic Syndrome #br#
CHEN Jinghe, ZHANG Yanqin, LI Wendong
2024, 21(6):  551-556.  doi:10.3870/j.issn.1672-8009.2024.06.008
Abstract ( 21 )   PDF (1000KB) ( 11 )  
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Objective To investigate the relationship between the interaction of microRNA-146a-5p (miR-146a-5p) and microRNA-21 ( miR-21) and its effect on the risk and severity ofprimary nephrotic syndrome (NS). Methods A total of 103 patients with NS from August 2021 toAugust 2023 were selected as the study group, and another 103 healthy volunteers who underwent physical examination during the same period were selected as the control group. Compare the different pathological types [minimal change disease (MCD), membranous nephropathy (MN), focal segmental glomerulosclerosis (FSGS)] and the degree of renal injury in the two groups, and study the relative expression levels of serum miR-146a-5p and miR-21 in patients. Analyze the diagnostic value and interactive effects of miR-146a-5p and miR-21 on NS, and further analyze the correlationbetween miR-146a-5p, miR-21, and disease severity. Results The relative expression level ofmiR-146a-5p in the study group was lower than that in the control group, and the relative expressionlevel of miR-21 was higher than that in the control group (P < 0. 05). The relative expression levels of serum miR-146a-5p and miR-21 in patients with different pathological types or different degrees ofrenal injury in the study group showed significant differences (both P< 0. 05). The AUC of the combined diagnosis of NS by miR-146a-5p and miR-21 was 0. 923 (95 % CI: 0. 877 - 0. 955), thesensitivity was 78. 64 % , and the specificity was 90. 29 % , which were significantly better than those of miR-146a-5p and miR-21 alone. The optimal cut-off value was used to divide miR-146a-5p and miR-21 into high expression group and low expression group. The low expression of miR-146a-5p and high expression of miR-21 had a positive interaction on the risk of NS development, which was a sub-multiplication model. miR-146a-5p was negatively correlated with NS pathological types andthe degree of kidney injury (r = - 0. 613, - 0. 657, P< 0. 05), while miR-21 was positively correlated with NS pathological types and the degree of kidney injury (r = 0. 664, 0. 702, P< 0. 05). Conclusion The abnormal expression of miR-146a-5p and miR-21 in the serum of NS patients isassociated with the degree of kidney injury in patients. In addition, miR-146a-5p and miR-21 have a positive interactive effect on the risk of NS, and their simultaneous exposure can increase the risk of NS.

Effect of miR-660-5p on High Glucose-induced Glomerular Mesangial Cell Injury by Regulation of P53 #br#
GU Liang, MA Xiaoxi, JIN Zhimin
2024, 21(6):  557-561.  doi:10.3870/j.issn.1672-8009.2024.06.009
Abstract ( 28 )   PDF (2601KB) ( 8 )  
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Objective To investigate the effect of miR-660-5p on high glucose-induced glomerular mesangial cell injury by regulating P53. Methods SV40-MES-13 cells were divided into two groups: control group and high glucose group, to analyze the effect of high glucose on cell viability and expression of miR-660-5p / P53. Then SV40-MES-13 cells treated with high glucose were divided into four groups: miR NC group, miR-660-5p mimic group, siNC group and siP53 group. The expression levels of miR-660-5p and P53 in SV40-MES-13 cells were detected by real-time fluorescence quantitative PCR. The growth ability of SV40-MES-13 cells was analyzed by methyl thiazolyl tetrazolium (MTT) assay. The apoptosis rate of SV40-MES-13 cells was analyzed by TUNEL and flow cytometry. Targetscan and luciferase reporter assay were used to analyze the targeting relationship between miR-660-5p and P53 in SV40-MES-13 cells. The expression level of P53 protein wasanalyzed by Western blotting. Results Compared with cells in the control group, SV40-MES-13cells treated with high glucose showed decreased proliferation activity, increased apoptosis rate, decreased expression level of miR-660-5p and increased expression level of P53. The proliferation activity of SV40-MES-13 cells treated with miR-660-5p mimic was increased, and the apoptosis rate was decreased when compared with those in the miR-660-5p NC group. The proliferation activity of SV40-MES-13 cells treated with siP53 was increased, and the apoptosis rate was decreased when compared with those in the siNC group. miR-660-5p could bind with P53 and inhibit the expressionof P53. Conclusion The expression level of miR-660-5p is decreased and the expression level ofP53 is increased in high glucose-treated mesangial cells. Up-regulation of miR-660-5p expression in high glucose-treated mesangial cells increases the proliferation activity and decreases the apoptosis rate, and the effect of miR-660-5p is related to the inhibition of P53 expression.

The Role and Mechanism of miR-499a-3p/ GAB1 Axis in Heart Failure #br#
GUO Mei, XIA Li, XIE Zhiwen
2024, 21(6):  562-567.  doi:10.3870/j.issn.1672-8009.2024.06.010
Abstract ( 25 )   PDF (3596KB) ( 9 )  
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Objective To explore the expression level of miR-499a-3p in the plasma of patients with heart failure (HF) and its potential mechanism. Methods The plasma from HF patients andhealthy controls was collected, and the expression level of miR-499a-3p was detected by RTqPCR. After transfecting miR-499a-3p mimics into human cardiomyoblast cells, CCK-8 was used to detect the effect of miR-499a-3p on cell proliferation. Flow cytometry and TUNEL were used to detect apoptosis, and Western blotting was used to detect the expression levels of apoptosis-related proteins. The heart failure cell model was established, and miR-499a-3p inhibitor was transfected, CCK-8 and flow cytometry were used to detect cell viability and apoptosis. Dual luciferase reporter gene assay was used to investigate the targeted binding of miR-499a-3p to GAB1. The effect of miR- 499a-3p on GAB1 expression were detected. Finally, miR-499a-3p mimics and GAB1 plasmid wereco-transfected into human cardiomyoblast cells to detect the functional changes. Results Compared with the healthy volunteers, the expression level of miR-499a-3p in the plasma of patients with HFwas significantly higher ( t = 77. 47, P < 0. 01). miR-499a-3p mimics significantly decreased theproliferation rate of human cardiomyoblast cells and increased the proportion of apoptotic cells andTUNEL-positive cells (P < 0. 05). After transfection of miR-499a-3p mimics, the expression levelof apoptosis-inhibiting protein Bcl-2 was decreased, while the expression levels of apoptosis-promoting proteins Caspase-3 and Bax were up-regulated. Further studies showed that miR-499a-3p was significantly overexpressed in heart failure cells, and after inhibiting the expression of miR-499a- 3p, the proliferation rate of heart failure cells was significantly increased, and the apoptosis ratiowas significantly decreased (P< 0. 05). miR-499a-3p could bind to the 3′-untranslated region (3′-UTR) of GAB1, and targetly inhibit GAB1 mRNA and protein expression. Moreover, overexpression of GAB1 reversed the effect of miR-499a-3p on proliferation and apoptosis of human cardiomyoblast cells. Conclusion miR-499a-3p is upregulated in patients with HF, which can affect the proliferation and apoptosis of human cardiomyoblast cells through targeted inhibition of GAB1 protein expression, thus participating in the progression of HF.
Reparative Effect of Mesenchymal Stem Cells Overexpressing LincRNA-p21 on Acute Lung Injury in Mice #br#
YAO Lidan, TANG Yongjun, ZHANG Yuhua, Yushanjiang ZHU MAHE, ZHANG Hongyu
2024, 21(6):  568-575.  doi:10.3870/j.issn.1672-8009.2024.06.011
Abstract ( 24 )   PDF (974KB) ( 6 )  
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Objective To investigate the reparative effect of mesenchymal stem cells (MSCs)overexpressing long intergenic non-coding RNA ( lincRNA) -p21 on acute lung injury ( ALI) inmice. Methods Seventy male C57BL / 6 mice were randomly divided into 7 groups, with n = 10 ineach group. The 7 groups were as follows: sham group, ALI group, MSC + ALI group, p21-MSC + ALI group, empty vector-MSC + ALI group, p21 + ALI group, and empty vector + ALI group. Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect the expression level of lincRNA-p21 in lung tissues of each group. ELISA was used to detect the levels of TNF-α, IL- 1β, IL-8, IL-6, IL-10, IL-13, IL-1Ra, and caspase3 in bronchoalveolar lavage fluid. The effects on arterial blood oxygen pressure ( PaO2 ), lung index ( LI), lung permeability index (LPI), and oxygenation index (OI) were evaluated. Flow cytometry was used to detect and ana
lyze the proportion of apoptotic cells in lung tissues. Western blotting was used to detect the expression levels of Bcl-2, Bax, caspase3, and cleaved-caspase3 in lung tissues. Results The levels of lincRNA-p21, IL-10, IL-13, IL-1Ra, Bcl-2, and the values of PaO2 and OI in the ALI group were decreased, while LI, LPI, TNF-α, IL-1β, IL-8, IL-6, Bax, caspase3, cleaved-caspase3 were upregulated, and the proportion of apoptotic cells was increased when compared with those inthe sham group ( all P < 0. 05). The levels of IL-10, IL-13, IL-1Ra, Bcl-2, and the values ofPaO 2and OI were all increased in the MSC + ALI group, and the levels of TNF-α, IL-1β, IL-8, IL-6, Bax, caspase3 and cleaved caspase3, and the values of LI were all decreased when compared with those in the ALI group, the proportion of apoptotic cells was decreased (all P< 0. 05).The expression level of lincRNA-p21 and the value of LPI had no significant change between abovegroups (P > 0. 05). The levels of lincRNA-p21, IL-10, IL-13, IL-1Ra, Bcl-2, and the valuesof PaO 2and OI were increased, while values of LI, LPI, and levels of TNF-α, IL-1β, IL-8, IL- 6, Bax, caspase3, cleaved-caspase3 were decreased, and the proportion of apoptotic cells was decreased in the p21-MSC + ALI group when compared with those in the empty vector-MSC + ALIgroup (all P< 0. 05). The levels of lincRNA-p21, IL-10, IL-13, IL-1Ra, Bcl-2, and the values of PaO 2and OI in the p21 + ALI group were increased (all P < 0. 05), and the levels of TNF-α,IL-1β, IL-8, IL-6, Bax, caspase3, and cleaved caspase3, and the values of LI, LPI were decreased, and the proportion of apoptotic cells was decreased when compared with those in the emptyvector + ALI group (all P< 0. 05). Conclusion MSCs overexpressing lincRNA-p21 have an inhibitory effect on inflammatory injury and lung cell apoptosis in ALI mice.
Effect of P38 MAPK on Osteogenic Differentiation of Periodontal Ligament Stem Cells by Regulating Wnt / Ca2 + Signaling Pathways under Inflammatory Microenvironment #br#
CHEN Qi, ZHOU Chun, QI Xue, XIA Jingping
2024, 21(6):  576-580.  doi:10.3870/j.issn.1672-8009.2024.06.012
Abstract ( 33 )   PDF (1578KB) ( 6 )  
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Objective To explore the effect of P38 mitogen-activated protein kinase (MAPK)on osteogenic differentiation and Wnt / Ca2 + signaling pathways in periodontal ligament stem cells(PDLSC) under microinflammatory environment. Methods Human PDLSC were divided into 4groups: control group, TNF-α group, TNF-α + SB203580 group ( 20 μmol / L SB20358 ) and TNF-α + SB203580 + XAV939 group (20 μmol / L SB20358 + 10 μmol / L XAV939). Except for cells in the control group, cells in the other groups were given 10 ng / mL TNF-α to simulate inflammatory microenvironment. The osteogenic differentiation ability was detected by alizarin red staining. The activity of alkaline phosphatase (ALP) in each group was compared. The expression levels of RUNt-related transcription factor 2 (Runx2), osteocalcin (OCN), Osterix (OSX) and osteopontin (OPN) were detected by qRT-PCR, and the expression levels of P38 MAPK, β-catenin, calmodulin dependent protein kinase Ⅱ (CaMKⅡ ) and Nemo-like (NLK) were detected byWestern blotting. Results The staining intensity and number of calcification nodules in the TNF-αgroup were significantly decreased, and in comparison of those in the TNF-α group, the staining intensity and number of calcification nodules were significantly improved in the TNF-α + SB203580 group, but there was no significant difference in staining intensity or number of calcification nodules between the TNF-α + SB203580 + XAV939 group and the TNF-α + SB203580 group. Compared with those in the control group, the activity of ALP and mRNA expression levels of Runx2, OCN, OSXand OPN were decreased in the TNF-α group (P< 0. 05), the expression level of P38 MAPK protein was increased (P< 0. 05), and the expression levels of β-catenin, CaMKⅡ and NLK proteins were decreased (P< 0. 05). Compared with those in the TNF-α group, the activity of ALP and mRNA expression levels of Runx2, OCN, OSX and OPN were increased in the TNF-α + SB203580group (P< 0. 05), the expression level of P38 MAPK protein was decreased (P< 0. 05), and the expression levels of β-catenin, CaMKⅡ and NLK proteins were increased (P < 0. 05). Comparedwith those in the TNF-α + SB203580 group, the expression level of β-catenin protein was decreasedin the TNF-α + SB203580 + XAV939 group (P< 0. 05), but there was no significant difference inALP activity, mRNA expression levels of Runx2, OCN, OSX and OPN or expression levels of P38MAPK, CaMKⅡ and NLK proteins between the two groups (P> 0. 05). Conclusion P38 MAPKinhibitor can improve osteogenic differentiation of PDLSC under inflammatory microenvironment, which may be related to activating Wnt / Ca2 + signaling pathways.
Non Coding RNA TUG1 Affects the in vitro Metastatic Activity of Bladder Cancer Cells by Regulating P38 MAPK Signaling Pathway #br#
GAO Bo, FAN Xiaomeng, CUI Jun, LI Wenhua, SHI Jiabao
2024, 21(6):  581-585.  doi:10.3870/j.issn.1672-8009.2024.06.013
Abstract ( 32 )   PDF (2530KB) ( 12 )  
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Objective To investigate the effect of Long non-coding RNA taurine-upregulatedgene 1 (lnc TUG1) on the metastasis of bladder cancer cells and the related mechanism. Methods Tissue samples were collected from patients with bladder urothelial carcinoma treated in BaodingSecond Hospital, and the expression levels of lnc TUG1 and P38 mitogen-activated protein kinases(P38 MAPK) in tissues were detected by real-time fluorescence quantitative PCR. Human bladdercancer cell line 5637 cells were divided into three groups: siNC group, si TUG1 group and si P38 group. The siNC, si TUG1 and si P38 plasmids were transfected into the corresponding experimentalgroups, and the cell growth ability, invasion ability, apoptosis rate and the expression level of P38 MAPK were detected by cell colony formation assay, Transwell assay, flow cytometry and Westernblotting. Results The expression level of TUG1 was increased, while the expression level of P38MAPK was decreased in the cancer tissues when compared with those in the cancer tissues. The number of colony formation and invasion of bladder cancer cells in the si TUG1 group was significantly decreased, the apoptosis rate was significantly increased, and the expression level of P38MAPK protein in the si TUG1 group was significantly up-regulated when compared with those in thesi NC group. However, the number of colony formation and invasion of bladder cancer cells in the si P38 group were significantly increased, and the apoptosis rate was significantly decreased whencompared with those in the siNC group. Conclusion Inhibition of lnc TUG1expression can inhibit the colony formation ability and invasion ability of bladder cancer cells, and promote the apoptosis of bladder cancer cells, and the potential mechanism might be associated with the inhibition of P38 MAPK.

Influence of Ischemic Postconditioning on Cardiac Function, Myocardial Apoptosis and Expressions of Myocardial Tissue Mitochondrial Apoptosis-related Molecules in Rats with Myocardial Ischemia-reperfusion #br#
WANG Tao, HAO Engang
2024, 21(6):  586-590.  doi:10.3870/j.issn.1672-8009.2024.06.014
Abstract ( 19 )   PDF (858KB) ( 8 )  
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Objective To analyze the influence of ischemic postconditioning (IP) on cardiacfunction, myocardial apoptosis and expressions of myocardial tissue mitochondrial apoptosis-relatedmolecules in rats with myocardial ischemia-reperfusion (IR). Methods Forty 8-week-old male SDrats were fed in separate cages with 5 rats in each cage for 7 days of adaptive feeding, and were randomly divided into 4 groups: blank control group ( control group), sham operation group ( S group), myocardial IR model group ( IR group) and myocardial IR model + IP treatment group (IP group), with 10 rats in each group. At 4 hours after surgery, the cardiac function indicators [left ventricular systolic pressure ( LVSP), left ventricular end-diastolic pressure ( LVEDP), maximum rate of left ventricular pressure change ( ± dp / dtmax)] were recorded by biological functional system, and the apoptosis of myocardial cells was detected by TUNEL method. RT-PCR was used to detect the relative expression levels of myocardial apoptosis-related proteins BCL-2, BAX, cysteinyl aspartate specific protease-3 ( Caspase-3), farnesoid X receptor ( FXR) and small heterodimer partner (SHP). Western blotting was applied to detect the release of myocardial mitochondrial apoptosis pathway marker cytochrome C ( Cyt-C). Results The LVEDP, apoptosis index ofmyocardial cells, and the expression levels of BAX, CASPASE-3, FXR and SHP in myocardial tissues and the expression level of Cyt-C protein in myocardial cytoplasm were higher in the IP andIR groups than those in the S and control groups ( P < 0. 05), moreover, the above indicators in the IR group were higher than those in the IP group (P < 0. 05). The LVSP, ± dp / dtmax and theexpression level of BCL-2 in myocardial tissues in the IP group and IR group were lower than thosein the S group and control group (P< 0. 05), and the above indicators were lower in the IR group than those in the IP group (P < 0. 05). Conclusion IP treatment can alleviate the myocardial IRinjury and improve the cardiac function in rats, which may be related to the regulations of apoptosisrelated signal proteins such as BCL-2 / BAX and FXR / SHP.
Expression of GATA3 Protein in Thyroid Carcinoma and Its Relationship with Clinicopathologic Features and Surgical Prognosis #br#
XUE Cui’e, WANG Xinlei, WANG Yahong
2024, 21(6):  591-596.  doi:10.3870/j.issn.1672-8009.2024.06.015
Abstract ( 29 )   PDF (1425KB) ( 7 )  
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Objective To analyze the expression of GATA binding protein 3 ( GATA3) inthyroid carcinoma and its relationship with clinicopathological features and surgical prognosis. Methods A total of 150 patients with thyroid carcinoma treated by surgery in Xilingol LeagueCentral Hospital, Inner Mongolia from August 2016 to December 2017 were selected, and the expression level of GATA3 protein was detected by immunohistochemistry between the cancer tissues and the normal tissues at the cutting edge. The expression level of GATA3 protein was compared between the cancer tissues and the normal tissues at the cutting edge, and the expression level of GATA3 protein in the thyroid carcinoma tissues of patients with different clinical and pathological characteristics was also compared. The relationship between the expression level of GATA3 protein incancer tissues and the surgical prognosis was analyzed after 5 years follow-up. Results The expression level of GATA3 protein in the thyroid carcinoma tissues was lower than that in the normal tissues (P < 0. 05). The expression level of GATA3 protein was lower in the thyroid carcinoma tissuesof undifferentiated and medullary carcinoma, TNM stage Ⅲ -Ⅳ, multiple lesions, maximum tumor diameter ≥ 2 cm, and patients with lymph node metastasis than in the thyroid carcinoma tissues of papillary adenocarcinoma and follicular adenocarcinoma, TNM stage Ⅰ -Ⅱ , single lesion, maximum tumor diameter < 2 cm, and patients without lymph node metastasis (P < 0. 05). During thefollow-up period, the survival rate of thyroid cancer patients was 83. 45 % , and the mortality ratewas 16. 55 % . Undifferentiated carcinoma ( RR = 1. 772, 95 % CI: 1. 221-2. 571 ), medullary carcinoma (RR = 2. 423, 95 % CI: 1. 609-3. 650), TNM stage Ⅲ -Ⅳ ( RR = 2. 020, 95 % CI:1. 447-2. 818), multiple lesions (RR = 1. 914, 95 % CI: 1. 421-2. 578), maximum tumor diameter ≥ 2 cm (RR = 1. 818, 95 % CI: 1. 129-2. 928), lymph node metastasis (RR = 1. 937, 95 %CI: 1. 241-3. 022), GATA3 protein expression (RR = 0. 488, 95 % CI: 0. 333-0. 715) were allfactors affecting the death of thyroid carcinoma patients ( P < 0. 05). The survival rate of patientswith high expression of GATA3 protein was higher than that of patients with low expression of GATA3 protein (P< 0. 05). Conclusion The expression of GATA3 protein is low in thyroid cancertissues, and the expression of GATA3 protein is related to pathological type, TNM stage, numberof lesions, tumor size and lymph node metastasis. The above indicators are all factors affecting theprognosis of patients after surgery.