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31 July 2024, Volume 21 Issue 4
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GATA3 Inhibits Migration of Human Breast Cancer Cells by Regulating LIFR #br#
ZHANG Lu, ZHANG Rui, LIU Jun, YANG Angang
2024, 21(4):  293-299.  doi:10.3870/j.issn.1672-8009.2024.04.001
Abstract ( 108 )   PDF (2983KB) ( 68 )  
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Objective To explore the effect of GATA binding protein 3 on the migration abilityof breast cancer cells. Methods Lentivirus-mediated GATA3-knockdown cell line was establishedto study the expression levels and function of GATA3 by performing real-time quantitative fluorescentPCR, Western blotting and Transwell assay in vitro. The binding sites of GATA3 in LIFR promoterregion was detected by Chromatin immunoprecipitation assay ( ChIP-qPCR) assay in MCF7 andT47D cells. LIFR was overexpressed in MCF7 cells with reduced GATA3 expression, and the migration capacity of MCF7 cells was measured by Wound healing assay and Transwell assay. Results Compared with the control group, the group of MCF7 cells that knocked down GATA3 had enhancedmigration ability (all P< 0. 05), and decreased expression of LIFR ( all P < 0. 05). ChIP-qPCRdata showed a physical binding of GATA3 on the promoter region of LIFR in MCF7 and T47D cells(all P< 0. 05). Overexpression of LIFR rescued the enhanced cell migration induced by depletion of GATA3 in MCF7 cells (all P< 0. 05). Conclusion GATA3 inhibits the migration of breast cancercells MCF7 through transcriptional activation of LIFR.
Effect of miR-155 Target Gene CEBPβ on Apoptosis and Inflammatory Response of Intervertebral Disc Chondrocytes in Rat with Cervical Spondylosis through Regulation of NF-κB Signaling Pathway #br#
NA Qing, Tuersunayi Abudureyimu, WU Gang
2024, 21(4):  300-308.  doi:10.3870/j.issn.1672-8009.2024.04.002
Abstract ( 100 )   PDF (2923KB) ( 104 )  
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Objective To explore the role and potential mechanisms of CCAAT-enhancerbinding protein β (C / EBPβtargeted by microRNA (miR) -155 in apoptosis and inflammatory response of rat intervertebral disc chondrocytes with cervical spondylosis. Methods Forty adult maleSD rats were randomly divided into 4 groups with 10 rats in each group: Sham group, CervicalSpondylosis group, Cervical Spondylosis + C / EBPβ overexpression group, and Cervical Spondylosis + empty vector group. Rat chondrocyte cell line, atdc5 cells, were divided into 6 groups: control group, tumor necrosis factor α ( TNF-α) stimulation group, empty vector + TNF-α group, C / EBPβ overexpression + TNF-α group, mimic-NC + C / EBPβ overexpression + TNF-α group, and miR-155 mimic + C / EBPβ overexpression + TNF-α group. The expression of miR-155, apoptosis-related proteins (cleaved-caspase3, Bax, Bcl-2, PPARγ), NF-κB signaling pathway proteins (pNF-κB P65, NF-κB P65, IκB), pro-inflammatory cytokines ( TNF-α, IL-6, IL-1β), and C / EBPβ in rat cartilage tissues and atdc5 cells were detected using qRT-PCR and Western blotting experiments. Dual-luciferase reporter gene assay was conducted to determine the targeted regulatoryeffect of miR-155 on C / EBPβ expression. Results miR-155, cleaved-caspase3, Bax, PPARγ,p-NF-κB P65, TNF-α, IL-6, and IL-1β were upregulated in the Cervical Spondylosis group when compared with those in the Sham group, while Bcl-2, IκB, and C / EBPβ were downregulated inthe Cervical Spondylosis group (P< 0. 05)Ceaved-caspase3, Bax, PPARγ, p-NF-κB P65, TNF-α, IL-6, and IL-1β were downregulated in the Cervical Spondylosis + C / EBPβ overexpression group when compared with those in the Cervical Spondylosis + empty vector group, while Bcl-2, IκB, and C / EBPβ were upregulated in the Cervical Spondylosis + C / EBPβ overexpression group(P< 0. 05), but there were no significant change in miR-155 expression level (P > 0. 05). There was a significant negative correlation between the expression levels of miR-155 and C / EBPβ in thecartilage of rats with cervical spondylosis (r = - 0. 721, P < 0. 05). The TNF-α group showed upregulations of miR-155, cleaved-caspase3, Bax, PPARγ, p-NF-κB P65, IL-6, and IL-1β expression (P< 0. 05), and downregulations of Bcl-2, IκB, and C / EBPβ expression when compared with the control group (P< 0. 05). The C / EBPβ overexpression + TNF-α group showed downregulations of cleaved-caspase3, Bax, PPARγ, p-NF-κB P65, IL-6, and IL-1β expression, and upregulations of Bcl-2, IκB, and C / EBPβ expression when compared with the empty vector + TNF-α group (P < 0. 05), but no significant change was observed in miR-155 expression level ( P >0. 05). The mimic + C / EBPβ overexpression + TNF-α group showed upregulations of miR-155,cleaved-caspase3, Bax, PPARγ, p-NF-κB P65, IL-6, and IL-1β expression ( P < 0. 05), anddownregulations of Bcl-2, IκB, and C / EBPβ expression when compared with the mimic-NC + C /EBPβ overexpression + TNF-α group ( P < 0. 05). Dual-luciferase reporter gene assay confirmedCEBPβ as a target gene of miR-155 in chondrocytes. Conclusion miR-155 promotes the activationof the NF-κB signaling pathway in intervertebral disc cartilage tissues and chondrocytes in rat withcervical spondylosis by inhibiting the target gene CEBPβ, which leads to enhanced apoptosis and inflammatory response.

Effect of Extracellular Histone on Epithelial Mesenchymal Transformation and Invasion of Bladder Cancer Cells by Regulation of TLR4 / NF-κB Pathway #br#
HAN Zhijun, SHU Linfei, YI Xiangmeng, TAN Huajun, ZHENG Guoqiu, YANG Fan
2024, 21(4):  309-314.  doi:10.3870/j.issn.1672-8009.2024.04.003
Abstract ( 104 )   PDF (4549KB) ( 61 )  
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Objective To investigate the effect of extracellular histone on epithelial mesenchymal transformation (EMT) and invasion of bladder cancer cells by regulating toll-like receptor 4(TLR4) / nuclear factor-κB (NF-κB) pathway. Methods T24 bladder cancer cells were culturedand divided into 7 groups: control group, histone H3 groups with different concentrations (50, 100, 200 μg / mL), solvent control (0. 1 % DMSO) group, histone H3 (200 μg / mL) + solvent control (0. 1 % DMSO) group, and histone H3 (200 μg / mL) + NF-κB inhibitor Bay11-7082 (10 μmol / L) group. The number of invasion cells and the protein expression levels of E-cadherin, N-cadherin, Vimentin, TLR4 and phosphorylated P65 NF-κB ( p-P65 NF-κB) were detected 24 h after administration. Results The number of invasion cells and the expression levels ofN-cadherin, Vimentin, TLR4 and p-P65 NF-κB in the histone H3 groups were higher than those inthe control group, and the protein expression level of E-cadherin was lower than that in the controlgroup (P < 0. 05), the number of invasion cells and the expression levels of those proteins werechanged with the concentration of histone H3 treatment in a dose-dependent manner. The number ofcell invasion and the protein expression levels of N-cadherin, Vimentin and p-P65 NF-κB in thehistone H3 + Bay11-7082 group were lower than those in the histone H3 + solvent control group,and the expression level of E-cadherin was higher than that in the histone H3 + solvent control group(P< 0. 05). Conclusion Extracellular histone promotes EMT and invasion of bladder cancer cells,which is related to the activation of TLR4 / NF-κB pathway.

Effect of TLR2-mediated Microglia Activation and Neuroinflammation on Vascular Dementia Progression #br#
SUN Yangzi, WU Zhenyu, ZENG Chaosheng, YOU Yong
2024, 21(4):  315-322.  doi:10.3870/j.issn.1672-8009.2024.04.004
Abstract ( 111 )   PDF (2129KB) ( 41 )  
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Objective To investigate the effect of TLR2 in mediating the pathological activation of microglia and neuronal injury in vascular dementia ( VaD) rat model and its molecularmechanisms. Methods In vitro experiments were carried out by using LPS-induced activation of human microglia cell line HMC3 cells. The proliferation ability of HMC3 cells was determined by CCK- 8 assay. Systemic TLR2 knockdown was performed by using Adv-TLR2 shRNA or Adv-shRNA NT. The VaD rat model was established by permanent bilateral common carotid artery occlusion (2VO) . The expression levels of TLR2, NF-κB, Iba-1, Claudin-5 and ZO-1 in HMC3 cells and rats’white matter tissues were determined by Western blotting. The levels of inflammatory cytokines IL-6, IL-1β and TNF-α, and the ferroptosis-related indicators of Fe2 + , malondialdehyde (MDA) and glutathione (GSH) in rats’white matter tissues were determined by ELISA. Morris water maze (MWM) test was used to determine rats’brain neuronal injury. Results The expression levels ofTLR2, NF-κB and Iba-1 in the LPS group were enhanced when compared with those in the Controlgroup (P< 0. 05). The expression levels of the above proteins in the Adv-TLR2 shRNA group were decreases when compared with those in the LPS groups ( P < 0. 05). The expression levels ofTLR2 / NF-κB and Iba-1 were up-regulated, and those of Claudin-5 and ZO-1 were down-regulatedin the white matter tissues of Model group rats, when compared with those of the Sham group, (P<0. 05). In addition, the levels of inflammatory cytokines IL-6, IL-1β and TNF-α were up-regulated(P< 0. 05), the Fe2 + and MDA levels were increased, and the GSH levels were decreased (P <0. 05). TLR2 knockdown had reversed the values of above indicators in the Model + Adv-TLR2 shRNA group when compared with those in the Model group (P< 0. 05). Morris water maze test showedthat rats in the Model group and Model + Adv-TLR2 shRNA group took longer time to find the targetquadrant (upper left quadrant) ( P < 0. 05), stayed shorter time in the target quadrant ( P <0. 05) when compared with those in the Sham group, the swimming routes of rats in the four quadrants of MWM were evenly distributed. Compared with Model group, the Model + Adv-TLR2 shRNAgroup showed a reversion in the values of above indicators and had a denser distribution of swimroutes in the target quadrant. Conclusion Knock-down of TLR2 could inhibit the activation of microglia and its mediated tight junction protein degradation and cerebrovascular barrier network leakage, and reduce nerve damage in the vascular dementia rat model.

Effect of Knocking down Astrocyte Elevated Gene-1 on Diethylnitrosamine-induced Primary Hepatocellular Carcinoma in Rats #br#
CHEN Jianxiong, JI Ru, CAI Qing, ZHANG Qian
2024, 21(4):  323-328.  doi:10.3870/j.issn.1672-8009.2024.04.005
Abstract ( 89 )   PDF (3830KB) ( 46 )  
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Objective To explore the effect of knocking down astrocyte elevated gene-1 (AEG-1 ) on diethylnitrosamine ( DEN ) -induced primary hepatocellular carcinoma ( PHC ). Methods A total of 60 rats were randomly divided into 4 groups: Control group, DEN group,AEG-1 NC KO DEN group and AEG-1 KO DEN group, 15 rats in each group. Rats were given intragastric administration of DEN to construct PHC models in each group except in the Control group, while rats in the Control group were given the same volume of normal saline. The rats in AEG-1 KO DEN group and AEG-1 NC KO DEN group were given intraperitoneal injection of HCCLM6 withstably transfected AEG-1 shRNA or shRNA-NC lentivirus expression vector, respectively. The liver cell damage, apoptosis, levels of superoxide dismutase ( SOD), malondialdehyde ( MDA) and glutathione peroxidase (GSH), liver function, levels of serum IL-6 and TNF-α, expressions of caspase-3 (Cas-3), caspase-9 ( Cas-9 ) and P65 in liver tissues were compared among eachgroup. Results The expression level of AEG-1 in the DEN group was significantly higher than that in the Control group ( P < 0. 05). The mortality of rats and incidence of ascites in the AEG-1 KO DEN group were lower than those in the DEN group ( P < 0. 05), and the levels of serum AST, ALT, IL-6 and TNF-α were lower than those in the DEN group ( P < 0. 05), SOD activity was higher than that in the DEN group (P< 0. 05), levels of GSH and MDA were lower than those in the DEN group (P< 0. 05), and expressions levels of cleaved cas9 / cas9, cleaved cas3 / cas3 and p-P65 / P65 were lower than those in the DEN group (P< 0. 05). Conclusion Knocking out AEG-1can reduce the levels of oxidative stress and inflammatory factors induced by DEN, relieve liver tissue damage and improve liver function in rats.

Effect of MRPL21 on Activity of Non-small Cell Lung Cancer A549 Cells by Regulating YAP1 / TAZ Pathway #br#
FANG Hanlin, PAN Huaguang, CHEN Yu, ZHANG Renquan
2024, 21(4):  329-333.  doi:10.3870/j.issn.1672-8009.2024.04.006
Abstract ( 107 )   PDF (3267KB) ( 37 )  
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Objective To investigate the effect of MRPL21 and YAP1 / TAZ pathway on theactivity of non-small cell lung cancer A549 cells, so as to provide new ideas for the treatment ofnon-small cell lung cancer. Methods Non-small cell lung cancer tissues and adjacent tissues were obtained from 9 patients with non-small cell lung cancer who underwent surgical treatment in the First Affiliated Hospital of Anhui Medical University between June, 2021 and September, 2023. Theexpression of MRPL21 in the tissues was analyzed by immunohistochemistry. A549 cells were randomly divided into three groups: siNC group, siMRPL21 group and BPD-MA group. CCK-8 assay and Hoechst staining were used to detect the proliferation of A549 cells. Transwell assay was used to analyze the invasion ability of A549 cells. TUNEL staining was used to detect the apoptosis of A549 cells. Western blotting assay was used to detect the expression levels of MRPL21, YAP1 and TAZproteins in A549 cells. Results The results of immunohistochemistry showed that the expression ofMRPL21 was up-regulated in the non-small cell lung cancer tissues compared with that in the adjacent tissues (P < 0. 05). Compared with the A549 cells in the siNC group, cells in the siMRPL21group and the BPD-MA group showed decreased proliferation ability as detected by CCK8 assay and Hoechst staining assay (P< 0. 05). Transwell assay showed that the invasion abilities of A549 cells in the siMRPL21 group and the BPD-MA group were decreased ( P < 0. 05 ). TUNEL stainingshowed that the apoptosis rates of A549 cells were increased in the siMRPL21 group and the BPDMA group (P< 0. 05). Western blotting results showed that the siMRPL21 group and the BPD-MA group had significant reduced protein levels of YAP1 and TAZ in A549 cells (P< 0. 05). Conclusion MRPL21 is highly expressed in non-small cell lung cancer tissues. After inhibiting the expression of MRPL21, the proliferation activity and invasion ability of A549 cells are weakened, and the apoptosis rate is increased, which is related to the regulation of YAP1 / TAZ signaling pathway. MRPL21 is expected to be a new target for the treatment of non-small cell lung cancer.

Effect of miR-424 on Proliferation and Apoptosis of Multiple Myeloma Cells by Targeting FBXW7 #br#
DUAN Xiaojuan, XI Zhenfang, HOU Ruihong
2024, 21(4):  334-340.  doi:10.3870/j.issn.1672-8009.2024.04.007
Abstract ( 67 )   PDF (3220KB) ( 42 )  
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Objective To investigate the effect of miR-424 on the proliferation and apoptosisof multiple myeloma ( MM) cells by targeting the F-box and WD repeat domain containing 7(FBXW7). Methods Real-time fluorescence quantitative PCR ( RT-qPCR) experiment was applied to detect the expression levels of miR-424 and FBXW7 in human normal bone marrow plasma cells and MM cell lines MM. 1S, RPMI 8226, U266. U266 cells were cultured in vitro and randomly separated into 5 groups: control group, miR-424 inhibitor group, FBXW7 overexpression group, negative control group, miR-424 inhibitor + FBXW7 knockdown group. Edu staining and TUNELstaining were applied to detect the cell proliferation and apoptosis, respectively. Western blotting assay was applied to detect the expression levels of proliferation related proteins ( Cyclin D1, PCNA), apoptosis related proteins (Bax, Bcl-2), and FBXW7 protein. A nude mouse model of multiple myeloma transplantation was constructed by subcutaneous inoculation of transfected U266 cells in the right axilla of nude mice, the growth of the transplanted tumors were detected and the transplanted tumor volume was compared on the 21st day. Dual luciferase reporter experiment was applied to verify the targeted regulatory effect of miR-424 on FBXW7 in U266 cells. Results In comparisonwith those in the normal human bone marrow plasma cells, the expression of miR-424 in theMM. 1S, RPMI 8226, and U266 cells were increased ( P < 0. 05 ), while the expression of FBXW7 mRNA were decreased ( P < 0. 05). In addition, when compared with the control group, the miR-424 inhibitor group and the FBXW7 overexpression group showed decreased cell proliferation rate, lower protein expression levels of Cyclin D1, PCNA and Bcl-2, and decreased transplanted tumor volume on the 21st day (P < 0. 05), and increased apoptosis rate, FBXW7 mRNA and protein expression levels, and Bax protein expression level ( P < 0. 05). There was no significant difference in the indicators in cells of the negative control group (P > 0. 05). Moreover, when compared with the miR-424 inhibitor group, the miR-424 inhibitor + FBXW7 knockdown group exhibited increased cell proliferation rate, Cyclin D1, PCNA and Bcl-2 protein expression, and transplanted tumor volume on the 21st day (P < 0. 05), and decreased apoptosis rate, FBXW7 mRNA and protein expression levels, and Bax protein expression level ( P < 0. 05). It was also observed that miR-424 was able to targetly downregulate FBXW7 expression in U266 cells. Conclusion Down-regulation of miR-424 can inhibit MM cell proliferation and growth in nude mice, and promote the apoptosis by up-regulating FBXW7 expression.
Nerve Growth Factor Combined with BMSCs Exosomes Alleviates Neural Injury in Rats with Intracerebral Haemorrhage through Keap1 / NQO1 / Nrf2 Signaling Pathway #br#
LI Fang, TANG Shijun, Maimaitiyiming Tuoheti
2024, 21(4):  341-346.  doi:10.3870/j.issn.1672-8009.2024.04.008
Abstract ( 76 )   PDF (3116KB) ( 37 )  
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Objective To explore the therapeutic effect and mechanisms of rat nerve growthfactor (RtNGF) combined with bone marrow mesenchymal stem cell-derived exosomes ( BMSCs exosomes) on neural injury of intracerebral haemorrhage (ICH) rats. Methods The BMSCs exosomes were prepared for the following experiments. Sixty rats were randomly divided into 5 groups: Sham group, ICH group, ICH + RtNGF group, ICH + BMSCs exosomes group, and ICH + RtNGF + BMSCs exosomes group, with 12 rats in each group. A ICH rat model was established and RtNGF or BMSCs exosomes were treated alone or in combination. Paraffin embedded tissue sections of rat brain tissues in each group were prepared and HE staining was performed. qPCR and Immunohistochemistry were used to determine the mRNA and protein expression levels of genes in the Keap1 / NQO1 /Nrf2 signaling pathway. Results Significant existence of tissue lacunes and blood clots were observed in the ICH group rather than in the Sham group. RtNGF or / and BMSCs treatments improved that situation, and the combination of RtNGF and BMSCs exosomes treatment had the best effect on alleviating neural injury. The mRNA expression levels of Keap1, NQO1 and Nrf2 in the brain tissues, and the IHC relative staining scores of the three proteins in the ICH group were increasedwhen compared with those in the Sham group ( allP < 0. 05). The levels of the above indicators inthe ICH + RtNGF group, ICH + BMSCs exosomes group, and ICH + RtNGF + BMSCs exosomesgroup were decreased when compared with those in the ICH group (P< 0. 05), with the values the lowest in the ICH + RtNGF + BMSCs exosomes group ( P < 0. 05). Conclusion RtNGF combinedwith BMSCs exosomes has significant effect on reducing oxidative stress and alleviating neural injury through Keap1 / NQO1 / Nrf2 signaling pathway in ICH rats.

hsa_ circRNA_ 002178 Gene Interference Inhibits Malignant Biological Behavior of Ovarian Cancer Cells #br#
PENG Hu, LONG Chenglan, LUO Ting, YIN Bangchao, ZHOU Jian
2024, 21(4):  347-353.  doi:10.3870/j.issn.1672-8009.2024.04.009
Abstract ( 53 )   PDF (4081KB) ( 26 )  
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Objective To study the effect of circRNA_ 002178 gene interference on malignant biological behavior of ovarian cancer cells. Methods Human ovarian cancer SKOV3 cells were divided into 4 groups: control group, short hairpin RNA negative control (shRNA-NC) group, circRNA_ 002178-shRNA 1 group and circRNA_ 002178-shRNA 2 group. The expression level of circRNA_ 002178 was detected by real-time fluorescence quantitative polymerase chain reaction (RTPCR). Flow cytometry was used to detect the cell apoptosis and mitochondrial membrane potential and to select the stem cell positive (CD44, CD133) cell lines. The stem cell spheroidization test was used to detect the sphere formation rate and the diameter of spheres. Transwell assay was used to detect the cell invasion. Western blotting was used to detect the expression levels of the proteins. Thetransplanted tumor model was constructed to observe the effect of circRNA_ 002178 gene interference on tumor formation. Results CircRNA_ 002178 interference significantly promoted the apoptosis ofSKOV3 cells, decreased the number of CD44 and CD133 positive cells, the rate of sphere formation, the diameter of spheres and the number of invasive cells, intensified the changes of mitochondrial membrane potential, and inhibited tumor growth and Akt / mTOR pathway activation in transplanted tumor rats. Conclusion CircRNA_ 002178 interference can inhibit the malignant biologicalbehavior of ovarian cancer cells. The mechanism may be related to the inhibitory effect on Akt / mTOR pathway.
 
Anti-Tumor Effect of Kaempferol on Esophageal Squamous Cell Carcinoma through PI3K / AKT Signaling Pathway #br#
YANG Zhao, ZANG Ting , MA Kai , WANG Zhuangzhuang , LI Wenhai , ZHOU Jincai
2024, 21(4):  354-360.  doi:10.3870/j.issn.1672-8009.2024.04.010
Abstract ( 61 )   PDF (5418KB) ( 26 )  
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Objective To investigate the anti-tumor effect and potential mechanism ofkaempferol on esophageal squamous cell carcinoma (ESCC) cells. Methods CCK-8, colony formation and flow cytometry were used to determine the effect of kaempferol on the proliferation andapoptosis of ECA-109 cells. Transwell assay was used to detect cell invasion. Western blotting wasemployed to measure the protein expression levels. Results Compared with the 0 μmol / L kaempferol group, the 40 μmol / L and 60 μmol / L kaempferol groups had significantly inhibited proliferationand invasion of ECA-109 cells and enhanced apoptosis. Moreover, kaempferol (40 μmol / L and 60μmol / L ) had significantly decreased expression levels of proliferating cell nuclear antigen (PCNA) and Ki67, and lower phosphorylation levels of phosphatidylin-ositol-3-kinase ( PI3K) and protein kinase B ( AKT), and increased expression levels of pro-apoptosis-related proteins. In addition, PI3K activator 740Y-P reversed the regulatory effect of kaempferol on proliferation, invasion and apoptosis of ECA-109 cells. Conclusion Kaempferol inhibits the proliferation, invasion and inducesthe apoptosis of ECA-109 cells by inhibiting PI3K / AKT signaling pathway.
Expression of MyD88 / IL-23 and Liver Regeneration after Hepatectomy in Mice with Subcutaneous Infection of E. granulosus #br#
CHEN Jun, YU Peng
2024, 21(4):  361-365.  doi:10.3870/j.issn.1672-8009.2024.04.011
Abstract ( 81 )   PDF (1999KB) ( 31 )  
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Objective To explore the influence of Echinococcus granulosus, (E. granulosus)infection on liver regeneration in hepatectomy model in mice, and to investigate the expression ofMyD88 / IL-23 in the liver regeneration of E. granulosus-infected mice post hepatectomy and its significance. Methods A mouse model with 70 % hepatectomy following subcutaneous infection of E- . granulosus was established. A total of 18 E. granulosus-infected mice and 18 healthy mice as controls were chosen for the surgery. The amount and rate of liver regeneration at different time points post-surgery in mice between the two groups were analyzed. The expression levels of MyD88 and IL-23 in mouse serum at different time points were measured by ELISA. The changes in hepatic functionindicators AST and ALT were also monitored. Results Compared to the control mice, the E-. granulosus -infected mice demonstrated decreased liver regeneration amount and regeneration ratepost hepatectomy, with significant differences apparent at the time points of 12 hours, 1 day, and2 days post-surgery. In comparison to the control mice, the E. granulosus-infected mice exhibitedmarkedly increased levels of AST and ALT in peripheral blood 1 day post-surgery, and notably increased levels of MyD88 and IL-23 2 hours post-surgery. Conclusions E. granulosus infection significantly decelerates the liver regeneration process following hepatectomy in mice, which maythrough increasing the levels of MyD88 and IL-23.
Bioinformatics Analysis of circRNA-miRNA-mRNA ceRNA Network for Prognosis in Gastric Cancer #br#
HUANG Xinyi, ZHOU Jintao, JIANG Chenshan
2024, 21(4):  366-373.  doi:10.3870/j.issn.1672-8009.2024.04.012
Abstract ( 114 )   PDF (10124KB) ( 14 )  
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Objective To construct a prognostic circRNA-miRNA-mRNA ceRNA network ingastric cancer ( GC) and explore the diagnostic and therapeutic targets. Methods Differentiallyexpressed circular RNAs (circRNA), related microRNAs (miRNA) and mRNAs in GC were obtained from GEO and TCGA databases. Cytoscape was utilized to construct the circRNA-miRNA-mRNA ceRNA network, to understand the biological functions of differentially expressed mRNAs and identifying the hub genes. Kaplan-Meier survival analysis was used to verify the prognostic values. Results The ceRNA network was consisted of 2 circRNAs, 5 miRNAs and 349 mRNAs thatwere differentially expressed. Functional enrichment analysis revealed that mRNAs were significantly enriched in terms and pathways like “ muscle system process”, “ metal ion transmembrane transporter activity”, “synaptic membrane” and “calcium signaling pathway” . A PPI network containing 125 nodes and 165 edges was constructed and 10 hub genes were identified. Survival analysis implied that low ADAR1D or PTGFR expression levels might lead to poor prognosis of GC patients. Conclusion The circRNA-miRNA-mRNA ceRNA network involved in prognosis of GC issuccessfully constructed. Two axes, the hsa _ circ _ 0001190 / hsa-miR-7-5p / ADRA1D and the hsa_ circ_ 0036287 / hsa-miR-3127-5p / PTGFR, are identified with potential prognostic values in GC, providing a new target for diagnosis andtreatment of GC.
Bioinformatics Analysis of Common Key Genes and Signal Pathways in Liver Cancer and Diabetes #br#
ZHOU Yilin, JI Haitao, WANG Yanfeng
2024, 21(4):  374-379.  doi:10.3870/j.issn.1672-8009.2024.04.013
Abstract ( 82 )   PDF (5268KB) ( 184 )  
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Objective To explore the gene features and pathogenic mechanisms shared byhepatocellular carcinoma and diabetes mellitus using bioinformatics methods. Methods The hepatocellular carcinoma dataset (GSE121248) and diabetes mellitus dataset ( GSE29221) were downloaded from the GEO (Gene Expression Omnibus) database, and were analyzed by R. Venn diagrams were used to obtain the shared differentially expressed genes (DEGs). GO (gene ontology) and KEGG ( kyoto encyclopedia of genes and genomes) enrichment analyses were performed on DEGs, and Cytoscape software was used to obtain the key modules and core genes in the proteinprotein interaction (PPI) network. The network interaction analyses of genes, transcription factors and mi-RNAs were performed in NetworkAnalyst database. DGIdb database was used for gene-drug interaction analysis. The prognostic values of the core genes were analyzed by Kaplan-Meier Plotterdatabase. Results A total of 39 DEGs were screened out, which were significantly enriched inpathways such as extracellular matrix, positive regulation of insulin-like growth factor receptor signaling pathway, heparin binding, and P53 signaling pathway. 6 core genes ( THBS1, DCN, BGN, COL14 A1, LUM and PCOLC) were screened out, of which two core genes (DCN and THBS1) could interacted with some tumor therapeutic agents and one core gene (DCN) was associated with the prognosis of hepatocellular carcinoma patients. Conclusion DCN may be a potentialdrug therapeutic target for patients with both diabetes and hepatocellular carcinoma.

Relationship between Serum Hcy, CysC, D-D Levels and Condition of Patients with Acute Ischemic Stroke and Their Short-term Prognosis after Intravenous Thrombolysis #br#
WANG Wenjing, LI Lina, WANG Jicun
2024, 21(4):  380-385.  doi:10.3870/j.issn.1672-8009.2024.04.014
Abstract ( 79 )   PDF (1105KB) ( 28 )  
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Objective To investigate the relationship between serum homocysteine ( Hcy),cystatin C (CysC) and D-dimer ( D-D) levels and the condition and short-term prognosis of patients with acute ischemic stroke ( AIS) after intravenous thrombolysis. Methods A total of 100AIS patients who received intravenous thrombolytic therapy in Shunyi District Hospital from October2019 to June 2023 were selected. According to the National Institutes of Health Stroke Scale (NIHSS) score, the patients were divided into 3 groups: mild defect group (1-4 points, 44 cases), moderate defect group (5-15 points, 29 cases) and severe defect group (16-42 points, 27 cases). According to the volume of cerebral infarction, the patients were divided into 3 groups: small infarction group ( < 5 cm3, 40 cases), moderate infarction group (5 ~ 15 cm3, 37 cases), and large infarction group ( > 15 cm3, 23 cases). Three months after intravenous thrombolysis, the patients were divided into 2 groups: good prognosis group (≤2 points, 75 cases) and poor prognosis group ( > 2 points, 25 cases), according to the modified Rankin scale score. Baseline data of patients were collected, and serum Hcy, CysC and D-D levels were detected. The changes of serum Hcy, CysC and D-D levels in AIS patients with different degrees of neurological deficit, cerebral infarction volume and short-term prognosis were compared. Pearson correlation coefficient was used to analyze the correlation between serum Hcy, CysC and D-D levels and AIS condition. Multivariate logistic regression was used to analyze the independent influencing factors of short-term prognosis of AIS. The receiver operating characteristic (ROC) curve was used to evaluate the predictive value of serum Hcy, CysC and D-D levels for short-term prognosis after AIS intravenous thrombolysis. Results The levels of serum Hcy, CysC and D-D in the mild defect group were the lowest, followed by the moderate defect group, and the severe defect group was the highest, with statisticallysignificant (P< 0. 05). The levels of serum Hcy, CysC and D-D in the small infarction group werethe lowest, followed by the moderate infarction group, and the large infarction group was the highest, the difference between the groups was statistically significant (P < 0. 05). Pearson correlationcoefficient analysis showed that serum Hcy, CysC and D-D levels were positively correlated withNHISS score (r = 0. 424, 0. 573, 0. 716, all P < 0. 001) and cerebral infarction volume ( r =0. 633, 0. 479, 0. 548, all P< 0. 001). Univariate analysis showed that the levels of serum Hcy,CysC and D-D in the good prognosis group were lower than those in the poor prognosis group (all P< 0. 05). Multivariate logistic regression analysis showed that Hcy, CysC and D-D (OR = 1. 093,1. 343, 1. 146) were independent predictors of short-term prognosis of AIS (P< 0. 05). ROC curveanalysis showed that the area under the curve of serum Hcy, CysC, D-D and the combination of thethree in predicting the short-term prognosis of AIS was 0. 853, 0. 873, 0. 792 and 0. 946, respectively, and the combination of the three had the highest predictive value. Conclusion The levels ofserum Hcy, CysC and D-D are positively correlated with the severity of AIS patients, which can beused as predictors of short-term prognosis after intravenous thrombolysis in AIS patients.


Progress in the Application of Lipidomics in Lung Cancer Research #br#
LIANG Yi, YU Wanjun, LI Jiawei, XU Tao
2024, 21(4):  386-390.  doi:10.3870/j.issn.1672-8009.2024.04.015
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In recent years, the application of lipidomics in lung cancer research has receivedincreasing attention, providing new perspectives on understanding the pathogenesis and therapeutic strategies of lung cancer. With technological advances, lipidomics will play a more critical role in lung cancer research and provide more specific biomarkers and pharmacodynamic evaluation tools for early diagnosis, condition monitoring, and personalized treatment of lung cancer. This review discusses the critical roles of core technologies like mass spectrometry and bioinformatics in lung cancer research. It also emphasizes the importance of serum and tissue-based lipidomics analysis in exploring specific biomarkers and differences between subtypes of lung cancer. Novel lipidomics strategies provide new directions for elucidating lung cancer pathogenesis and therapeutic strategy selection.