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30 September 2024, Volume 21 Issue 5
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Effect of Acteoside on Lung Injury in Rats with Severe Acute Pancreatitis by Regulating IRE1α/ TXNIP / NLRP3 Signaling Pathway #br#
WEN Cai, ZHOU Jing , WAN Xiaoqin
2024, 21(5):  391-398.  doi:10.3870/j.issn.1672-8009.2024.05.001
Abstract ( 104 )   PDF (3881KB) ( 74 )  
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Objective This study aims to investigate the effect of acteoside on lung injury inrats with severe acute pancreatitis ( SAP ) by regulating the inositol-requiring enzyme 1α(IRE1α) / thioredoxin interacting protein ( TXNIP) / nucleotide binding oligomerization domain-like receptor protein 3 ( NLRP3 ) pathway. MethodsRats were randomly separated into SAPgroup, normal group, acteoside low-dose ( ACT-L ) group, acteoside high-dose ( ACT-H )group, ulinastatin group, ACT-H + empty-vector group, and ACT-H + Ad-IRE1α group, with 12rats in each group. SAP model were constructed by injecting 5 % sodium taurocholate solution into the bile duct of rats. SAP model rats were then administered with acteoside, ulinastatin or AdIRE1α once a day for 2 days. The changes in serum lipase and amylase levels, and lung wet weight / dry weight ratio were detected. HE staining was used to detect the pathological changes of pancreas and lung tissues and to evaluate the pathological scores. Levels of reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase ( SOD) in lung tissues were detected by kits. ELISA was applied to detect the levels of interleukin-18 and IL-1β in lung tissues. Western blotting was applied to detect the levels of IRE1α, TXNIP, NLRP3, and caspase-1 proteins inlung tissues. Results Pancreatic edema and a large number of cell necrosis and inflammatory cellinfiltration were observed in rats in the SAP group, the inflammatory cell infiltration in lung tissues was observed, and alveolar congestion and alveolar wall edema were severe when compared with those in the normal group. The pancreatic and lung histological scores, the levels of lipase and amylase in serum, the wet / dry lung weight ratio, the levels of MDA, ROS, IL-18, IL-1β in lung tissues, and the expression levels of IRE1α, TXNIP, NLRP3, and caspase-1 proteins were elevated in the SAP group, and the level of SOD in lung tissues was decreased when compared with those inthe normal group (P< 0. 05). The pancreatic and lung tissue damages in rats in the ACT-L group,ACT-H group, and ulinastatin group were improved when compared with those in the SAP group. The pancreatic and lung histological scores, the levels of lipase and amylase in serum, the wet / dry lung weight ratio, the levels of MDA, ROS, IL-18, IL-1β in lung tissues, and the expression levels of IRE1α, TXNIP, NLRP3, and caspase-1 proteins were decreased, and the level of SOD in lung tissues was increased in the ACT-L group, ACT-H group, and ulinastatin groupwhen compared with those in the SAP group (P< 0. 05). The pancreatic and lung tissue damages inthe ACT-H + Ad-IRE1α group were aggravated, and the pancreatic and lung histological scores, the levels of lipase and amylase in serum, the wet / dry lung weight ratio, the levels of MDA, ROS, IL-18, IL-1β in lung tissues, and the expression levels of IRE1α, TXNIP, NLRP3, and caspase-1 proteins were increased, while the level of SOD in lung tissues was decreased when compared withthose in the ACT-H + empty vector group (P< 0. 05). Conclusion The mechanism by which acteoside improves lung injury in SAP rats may be related to the inhibition of IRE1α / TXNIP / NLRP3pathway activation.

Inhibition of Survivin Alleviates Etoposide Resistance in Small Cell Lung Cancer and Its Mechanism#br#
Kadilia Abuduweili, Aziguli Tuersunmaimaiti, HUI Jing, Mairehaba Halike
2024, 21(5):  399-404.  doi:10.3870/j.issn.1672-8009.2024.05.002
Abstract ( 93 )   PDF (2948KB) ( 81 )  
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Objective To investigate the effect and mechanism of Survivin on the proliferationand apoptosis of etoposide resistant small cell lung cancer cell lines. Methods Etoposide resistancesmall cell lung cancer cell lines were constructed in NCI-H82 and NCI-H446 cell lines (NCI-H82 /ER and NCI-H446 / ER), the IC50 and resistance index of NCI-H82 / ER and NCI-H446 / ER weredetermined. qRT PCR and Western blotting assay were used to detect the expression level of Survivinin the cell lines. Survivin siRNA (si-Survivin group) and Survivin siRNA Negative Control (si-NCgroup) were transfected into NCI-H82 / ER and NCI-H446 / ER cells. Cell proliferation was determined by CCK8, apoptosis was determined by flow cytometry, and phosphorylation levels of PI3K,AKT, and mTOR were detected by Western blotting. Results The IC50 of NCI-H82 / ER and NCIH446 / ER were 154. 5 μmol / L and 130. 5 μmol / L, respectively, with resistance indices of 5. 40and 6. 21. Compared with the NCI-H82 and NCI-H446 cells, the NCI-H82 / ER and NCI-H446 / ERcells had significantly increased expression levels of Survivin mRNA and protein ( P < 0. 001 ).Compared with the cells in the si-NC group, NCI-H82 / ER and NCI-H446 / ER cells in the si-Survivin group had significantly reduced proliferation abilities (P< 0. 05), and significantly increased level of apoptosis ( P < 0. 001), and significantly reduced phosphorylation levels of PI3K, AKT, and mTOR (P< 0. 001). Conclusion Inhibiting Survivin can inhibit the PI3K / AKT / mTOR signaling and affect the proliferation and apoptosis of etoposide resistant small cell lung cancer cells.
miR-542-5p Inhibits Proliferation, Migration and Invasion of Hepatocellular Carcinoma by Targeting ENSA #br#
DAI Hanli, WANG Guohua, XU Xiangyong
2024, 21(5):  405-412.  doi:10.3870/j.issn.1672-8009.2024.05.003
Abstract ( 98 )   PDF (6876KB) ( 53 )  
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Objective To explore the effect of miR-542-5p on proliferation, migration and invasion of hepatocellular carcinoma (HCC) by targeting ENSA. Methods The expression of miR-542-5p in HCC tissues and para-carcinoma tissues was analyzed by GSE36915 data matrix. miR-542- 5p overexpression were performed in the HCC cell lines HepG2 and Hep3B and verified by RTPCR. The proliferation, migration and invasion of cells were detected by CCK-8, wound healing and Transwell assays. miR-542-5p overexpressed Hep3B cells were used to establish the transplanted tumor model in nude mice. The volume and weight of transplanted tumors were measured. The miR- 542-5p expression level in transplanted tumors was detected by RT-PCR. The differential expression genes of GSE101728 and GSE7642 were analyzed by GEO2R, and the target genes of miR-542-5pwere predicted by miRWalk, ENSA gene was then screened out. The expression level of ENSA inHCC tissues and para-carcinoma tissues was analyzed by TCGA HCC data. The expression level of ENSA in miR-542-5p overexpressed HepG2 and Hep3B cells was detected by RT-PCR. The cell proliferation, migration and invasion were detected in miR-542-5p overexpressed HepG2 and Hep3Bcells after transfected with ENSA overexpression plasmid. Results The expression level of miR-542-5p in the HCC tissues was significantly lower than that in the para-carcinoma tissues (P < 0. 01).The proliferation rate, migration rate and relative number of invasion cells in the miR-542-5p overexpressed cells were significantly lower than those in miR-NC overexpressed cells (P < 0. 01). The results ofin vivoexperiments showed that the volume and weight of tumors in the miR-542-5p overexpression group were significantly lower than those in the miR-NC overexpression group (P< 0. 01).The expression level of ENSA in the HCC tissues was significantly higher than that in the para-carcinoma tissues (P< 0. 01), and ENSA could promote HCC progression. The protein expression levelof ENSA in the miR-542-5p overexpressed cells were significantly lower than that in the miR-NCoverexpressed cells (P< 0. 01). The proliferation rate, migration rate and relative number of invasion cells in cells with miR-542-5p + ENSA overexpression were significantly higher than those incells with miR-542-5p overexpression (P< 0. 01). Conclusion miR-542-5p can inhibit the proliferation, migration and invasion of HCC cells by inhibiting ENSA.

Asiaticoside Inhibits Cell Growth and Invasion of Imatinib-resistant K562 Cells #br#
ZHENG Runtao, ZHUANG Minli, ZHANG Wenxia
2024, 21(5):  413-418.  doi:10.3870/j.issn.1672-8009.2024.05.004
Abstract ( 61 )   PDF (2229KB) ( 47 )  
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Objective To study the effect of asiaticoside on the proliferation, invasion and cellcycle arrest of chronic myelogenous leukemia (CML) cells, and to explore its regulation on GATA-1 expression. Methods CML cell line K562, imatinib (IM) -resistant K562 cells (K562r) andhuman original CML cells were used for experiments. Cell viability was determined by CCK-8 assay. K562r cells were treated with 0, 25, 50, 100 μmol / L asiaticoside, then cell proliferation wasdetermined by colony formation assay, cell migration was determined by transwell assay, the cell cycle was measured by flow cytometry, the expression levels of cyclin A, CDK2, CDK4, cyclinD1, Ki67, PCNA, VEGF, MMP-9 and MMP-14 were detected by Western blotting. Results Compared with the control group, asiaticoside treatment significantly reduced the number of K562rcell colonies and migration cells, and induced the cell cycle arrest. In addition, the expression levelof GATA-1 in K562r cells was significantly up-regulated after asiaticoside treatment. Conclusion Asiaticoside can inhibit the proliferation and migration of K562r cells and induce cell cycle arrest,and the mechanism may be related to the up-regulation of GATA-1 expression.
Prognostic Value of Interleukin-4 Combined with APACHE Ⅱ Score for Carbapenem-resistant Acinetobacter baumannii Infection #br#
YUAN Zhifa, QIU Jingxing, WU Kefeng
2024, 21(5):  419-424.  doi:10.3870/j.issn.1672-8009.2024.05.005
Abstract ( 64 )   PDF (946KB) ( 49 )  
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Objective To analyze the prognostic value of interleukin-4 (IL-4) combined withacute physiology and chronic health evaluation ( APACHE Ⅱ ) in the infection of carbapenem-resistant Acinetobacter baumannii ( CRAB). Methods A total of 143 patients with CRAB infectiontreated in Affiliated Hospital of Guangdong Medical University from November 2021 to October 2023were set as the study group, and 49 patients with carbapenem-sensitive Acinetobacter baumannii infection treated in the same period were taken as the control group. According to the clinical outcome of the patients in the study group, they were divided into 2 groups: death group (n = 46) and survival group (n = 97), and the differences of IL-4 and APACHE Ⅱ scores between the study groupand the control group, as well as the death group and the survival group were compared. Pearson correlation analysis was used to calculate the correlation between serum IL-4 level and APACHE Ⅱ score in patients with CRAB infection. Receiver operating characteristic curves (ROC) was used to evaluate the application value of IL-4, APACHE Ⅱ score and joint diagnosis in predicting the adverse clinical outcome of patients with CRAB infection. Results The level of IL-4 and the APACHEⅡ score in the death group were significantly higher than those in the survival group (P < 0. 05).The results of Pearson correlation analysis showed that the two indexes (the level of IL-4 and the APACHE Ⅱ score) had obvious positive correlation ( r = 0. 093, P < 0. 001) . The AUC of serumIL-4, APACHE Ⅱ score and the combined index in evaluating the prognosis of patients with CRABinfection were 0. 712 (95 % CI = 0. 606-0. 817, P < 0. 001), 0. 849 (95 % CI = 0. 763-0. 936, P < 0. 001) and 0. 956 (95 % CI = 0. 927-0. 985, P < 0. 001), respectively. Conclusion Theserum IL-4 and APACHE Ⅱ scores of CRAB patients with poor prognosis are significantly higher than those of survival patients. The combination of serum IL-4 and APACHE Ⅱ scores can be used in the prognosis evaluation of such patients, which is helpful to provide reference for their clinical treatment.

Long Non-coding RNA B3GALT5-AS1 Inhibits Proliferation, Invasion and Tumorigenicity of Non-small Cell Lung Cancer A549 Cells #br#
PENG Qiang, ZHAO Hui, YAO Qiuying
2024, 21(5):  425-431.  doi:10.3870/j.issn.1672-8009.2024.05.006
Abstract ( 79 )   PDF (4032KB) ( 61 )  
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Objective To explore the effect of overexpression of long non-coding RNA ( lncRNA) B3GALT5-AS1 on the growth and invasion ability in non-small cell lung cancer (NSCLC).Methods qRT-PCR was employed to examine the expression level of B3GALT5-AS1 in clinicalsamples. A549 cells were divided into 3 groups: control group, pcDNA-scramble group, and pcDNA-B3GALT5-AS1 group, the pcDNA-scramble and pcDNA-B3GALT5 AS1 vectors were transfected into cells respectively. The colony formation experiment was employed to evaluate the colony-forming ability of A549 cells, qRT-PCR was used to detect the mRNA expression level of Ki67 and Survivin. Flow cytometry was used to analyse cell apoptosis, Transwell assay was used to test cell invasion, and Western blotting was used to detect the expression level of P27, P53, VEGF and Vimentin proteins. A549 cells transfected with pcDNA-scramble or pcDNA-B3GALT5-AS1 were injected subcutaneously into nude mice. The tumor volume and weight were measured, the expression level of B3GALT5-AS1 in tumor tissues was detected by qRT-PCR, and the expression of Ki67 and VEGF were determinded by immunohistochemistry. Results The relative mRNA expression level ofB3GALT5-AS1 in the lung cancer tissues was significantly lower than that in the adjacent normal tissues when compared with that in the paracancerous tissues (P< 0. 05). The colony forming ability of cells in the pcDNA-B3GALT5-AS1 group was reduced ( P < 0. 05), the expression of Ki67 and Survivin was obviously down-regulated (P< 0. 05), the apoptosis rate of cell was clearly increased (P< 0. 05), and the number of invasion cells was evidently reduced (P < 0. 05), the expression level of P27 and P53 proteins was up-regulated (P< 0. 05), and the expression of VEGF and Vimentin protein was significantly down-regulated (P< 0. 05). The results of in vivo xenotransplantationexperiments showed that overexpression of B3GALT5-AS1 clearly reduced tumor volume and weight(P< 0. 05), and the numbers of Ki67 and VEGF positive cells in tumor tissues were obviously reduced (P< 0. 05) when compared with that in the pcDNA-scramble group. Conclusion Overexpression of B3GALT5-AS1 obviously inhibits the proliferation and invasion of NSCLC cells and induces apoptosis, it also blocks the growth of tumor tissues in vivo and plays an anti-cancer effect in NSCLC.

Canagliflozin Alleviates Kidney Damage in STZ-induced Diabetic Nephropathy Mice by TGF-β/ STAT3 #br#
ZENG Weixin, YUN Chuan, LI Xiaoyan, LI Dawei
2024, 21(5):  432-436.  doi:10.3870/j.issn.1672-8009.2024.05.007
Abstract ( 67 )   PDF (1041KB) ( 47 )  
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Objective To explore the potential mechanism by which canagliflozin alleviateskidney injury in streptozotocin ( STZ ) -induced diabetic nephropathy mice through TGF-β /STAT3. Methods A diabetic nephropathy mouse model was established using STZ. Mice were divided into 5 groups: control group, STZ-induced diabetic nephropathy mice group, canagliflozintreated group, TGF-β inhibitor-treated group, and STAT3 inhibitor-treated group. Renal weight / body weight ratio, urinary albumin, renal function parameters, serum TGF-β level and the phosphorylation level of STAT3 in the kidney tissues were measured. Results Mice with diabetic nephropathy exhibited signs of renal injury, including a significant increase in renal weight / bodyweight ratio and urinary albumin (P < 0. 05), whereas these indices returned to normal levels aftercanagliflozin treatment. The serum TGF-β level and phosphorylation level of STAT3 in tissues wereelevated in diabetic nephropathy mice (P < 0. 05), while they returned to similar levels as that inthe control after canagliflozin treatment. In addition, the TGF-β expression level was positively correlated with the STAT3 phosphorylation level (P < 0. 05). Conclusion Canagliflozin attenuated renal injury in diabetic nephropathy by modulating TGF-β and STAT3 pathways.
miR-139-5p Targets Notch1 to Inhibit Proliferation, Migration and Invasion of Lung Adenocarcinoma Cells #br#
DONG Yuehua, WANG Guigang, YANG Yanjun, WEI Yulei, GAO Yongshan, JIANG Weihua
2024, 21(5):  437-444.  doi:10.3870/j.issn.1672-8009.2024.05.008
Abstract ( 73 )   PDF (4431KB) ( 45 )  
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Objective To investigate the role and regulatory mechanism of miR-139-5p in the progression of lung adenocarcinoma (LUAD). Methods The expression levels of miR-139-5p andNotch homolog 1 (Notch1) in LUAD tissues and cells were detected and the transfection efficiency after cell transfection was verified by Quantitative real-time PCR ( qRT-PCR) and Western blotting. The proliferation, migration and invasion of LUAD cells were determined by CCK-8, wound healing and Transwell assay. The targeting relationship of miR-139-5p to Notch1 was analyzed using a dual luciferase reporter gene assay. Western blotting was employed to detect the expression levels ofPI3K / AKT / mTOR signaling pathway related proteins. Results miR-139-5p was significantly downregulated (P < 0. 01) and Notch1 was significantly up-regulated in the LUAD tissues and cells (P < 0. 01), when compared with those in the normal tissues and human normal bronchial epithelialcells. miR-139-5p overexpression suppressed the proliferation, migration and invasion of LUADcells, and down-regulated the expression levels of p-PI3K, p-AKT and p-mTOR ( P < 0. 01 ).Notch1 was identified as a target of miR-139-5p that could directly bind to it. Overexpression of Notch1 attenuated the inhibitory effects of miR-139-5p on proliferation, migration and invasion ofLUAD cells (P < 0. 05). In vivo experiment showed that the overexpression of miR-139-5p inhibited the growth of xenograft tumor in nude mice when compared with that in the control group ( P < 0. 05). Conclusion miR-139-5p inhibits the proliferation, migration and invasion of LUAD cellsby targeting Notch1 and inactivation of PI3K / Akt / mTOR pathway.
Value of miR-550a-5p in Diagnosis of Spinal Bone Metastasis of Nonsmall Cell Lung Cancer #br#
XU Kun, AO Man, HAO Jiaying, CAO Sheng, ZHANG Yilong, WANG Jianhua
2024, 21(5):  445-451.  doi:10.3870/j.issn.1672-8009.2024.05.009
Abstract ( 65 )   PDF (1156KB) ( 40 )  
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Objective To explore the value of microRNAs (miR-550a-5p) in the diagnosis ofspinal bone metastases in non-small cell lung cancer (NSCLC), and to provide reference for clinical prevention and treatment. Methods Sixty-two NSCLC patients with the presence of spinal bonemetastasis and 44 NSCLC patients without spinal bone metastasis admitted to the Affiliated Hospital of Chengde Medical College from January 2019 to January 2023 were selected and included in the spinal bone metastasis group and the no spinal bone metastasis group, respectively, based on the confirmation of magnetic resonance imaging or CT examination. Serum miR-550a-5p, lung tumor markers [ carcinoembryonic antigen ( CEA ), cytokeratin-19 soluble fragment ( CYFRA21-1 ), neuron-specific enolase (NSE)], bone metabolism markers [type I collagen pyridine cross-linked amino-terminal peptide (NTx), bone transmutation alkaline phosphatase (BALP), Type I collagen carboxyl terminal peptide (ICTP)] were detected and compared between the two groups. The level of serum miR-550a-5p in NSCLC patients with different clinical characteristics was compared, and the association between the grade of NSCLC spine bone metastasis and the level of serum miR- 550a-5p was analyzed. The diagnostic value of serum miR-550a-5p in NSCLC spine bone metastasiswas analyzed by receiver operating characteristic curve (ROC). Results The levels of serum miR-550a-5p, CEA, NSE, CYFRA21-1, BALP, ICTP and NTx in the spinal bone metastasis groupwere higher than those in the non-spinal bone metastasis group (P < 0. 05). There were statisticallysignificant differences in the level of miR-550a-5p among NSCLC patients in spinal bone metastasis group with different tumor diameter, degree of differentiation, TNM stage, number of bone metastases, lymph node metastases, bone-related events and symptoms of bone pain (P< 0. 05). There weresignificant differences in the level of serum miR-550a-5p, NSE, BALP, CEA, ICTP, CYFRA21-1and NTx among NSCLC patients with different bone metastasis grades (P< 0. 05). The levels of serummiR-550a-5p, lung tumor markers and bone metabolism markers were increased with the increase of bone metastasis grade. Spearman correlation analysis showed that the level of serum miR-550a-5p was positively correlated with bone metastasis grade, and the levels of CEA, NSE, CYFRA21-1, BALP,ICTP and NTx (P< 0. 05). The AUC value of serum miR-550a-5p combined with lung tumor markers and bone metabolic markers was 0. 941 (95 % CI: 0. 878-0. 978) (P < 0. 05), which was higher than that of lung tumor markers combined with bone metabolic markers only [0. 902 (95 % CI:0. 829-0. 951)]. Conclusion miR-550a-5p has a high value in the diagnosis of spinal bone metastasisof NSCLC, and its level is closely related to bone metastasis grade, and level of lung tumor markers,and bone metabolic markers. Application of miR-550a-5p combined with lung tumor markers and bonemetabolic markers can improve the diagnostic value.

Expression of FtMt Protein in Non-small Cell Lung Cancer and Its Clinicopathological Significance #br#
XU Meirong, SHEN Xiaowen, GU Lingli, SHEN Hongmei, HUANG Linling
2024, 21(5):  452-457.  doi:10.3870/j.issn.1672-8009.2024.05.010
Abstract ( 67 )   PDF (1497KB) ( 39 )  
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Objective To study the relationships between the expression level of mitochondrialferritin (FtMt) and the clinical pathology and molecular characteristics in non-small cell lung cancer (NSCLC). Methods A total of 154 surgical specimens with pathologically confirmed NSCLCfrom September 2018 to December 2020 were selected. Immunohistochemistry was used to determine the expression of FtMt protein. Amplification refractory mutation system was used to detect the mutations of EGFR, ALK, and KRAS genes. Fluorescence quantitative PCR was used to detect the mRNA expression levels of epithelial-mesenchymal transformation markers N-cadherin, E-cadherin, Vimentin, and mitochondrial pathway apoptotic proteins B-lymphoblastoma-2 (Bcl-2), Bcl2-associated X-protein ( Bax), caspase-3, and ferroptosis markers glutathione peroxidase 4 ( GPX4), solute carrier family 7 member 11 (SLC7A11). Patients with NSCLC were followed-up for the tumorfree survival and overall survival. Results The positive expression rate of FtMt in the NSCLC tissueswas higher than that in the adjacent tissues ( P < 0. 05). The positive expression rates of FtMt inNSCLC tissues with low differentiation, pTNM stage Ⅲ , and lymph node metastasis were higherthan those with high differentiation, pTNM stage Ⅰ -Ⅱ , and no lymph node metastasis ( P <0. 05). The mRNA expression levels of N-cadherin, Vimentin, Bcl-2, GPX4, SLC7A11 and the mutant rate of EGFR in the NSCLC tissues with positive FtMt expression were increased, while themRNA expression levels of E-cadherin, Bax, and Caspase-3, as well as the tumor free survival rate and overall survival rate were decreased when compared with those in the NSCLC tissues withnegative FtMt expressions (P < 0. 05). Conclusion The positive expression of FtMt in NSCLC isassociated with pathological progression, EGFR mutation, and reduced survival. The biologicalmechanisms may associate with abnormal epithelial mesenchymal transformation, ferroptosis and mitochondrial pathway apoptosis.

Expression of C-C Motif Chemokine Receptor 2 and Th1 / Th2 Cells in Renal Interstitial Fibrosis of Rats with IgA Nephropathy and Its Significance #br#
ZHU Jianping, HE Linghui, XIANG Yong
2024, 21(5):  458-463.  doi:10.3870/j.issn.1672-8009.2024.05.011
Abstract ( 77 )   PDF (4061KB) ( 49 )  
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Objective To investigate the expression of C-C motif chemokine receptor 2(CCR2) and the numbers of helper T cell 1 / 2 (Th1 / Th2) in renal interstitial fibrosis of rats withIgA nephropathy and their significance. Methods A total of 40 male SD rats were randomly dividedinto 2 groups, each group included 20 rats. Immunoglobulin A (IgA) nephropathy in rats was induced by using a combined treatment of lipopolysaccharide (LPS), modified bovine serum albumin (BSA), and carbon tetrachloride ( CCl4 ). The pathological changes and IgA deposition were observed, the percentage of collagen fibers in renal tissues was calculated, and the Katafuchi score was used to evaluate the degree of tubulointerstitial injury. Western blotting was used to detect the expression level of CCR2 in renal tissues. Serum levels of interleukin-4 ( IL-4) and interferon-γ (IFN-γ) were measured by double-antibody sandwich enzyme-linked immunosorbent assay. Flowcytometry was used to measure the proportion of Th1 / Th2 cells. Results The percentage of collagenfiber area and the Katafuchi score in the model group were significantly higher than those in the control group (P < 0. 05). The expression level of CCR2 in renal tissues, the serum level of IL-4, thenumber of Th2 cells and the ratio of IL-4 / IFN-γ in the model group were significantly higher than those in the control group, while the serum level of IFN-γ and the number of Th1 cells were significantly lower than those in the control group (P< 0. 05). The levels of CCR2 and IL-4 and the ratioof IL-4 / IFN-γ were positively correlated with the collagen fiber area percentage and the Katafuchiscore (P< 0. 05), while the level of IFN-γ was negatively correlated with collagen fiber area percentage and the Katafuchi score ( P < 0. 05). Conclusion The abnormal expression of CCR2 andthe Th1 / Th2 Imbalance are involved in the occurrence and development of renal interstitial fibrosis in IgA nephropathy rats, meanwhile, antagonizing CCR2 and regulating Th1 / Th2 balance may reduce the changes of renal fibrosis in IgA nephropathy rats.

Protective Effect of Hypericum perforatumExtract on Myocardial Injury in Rats with Autoimmune Myocarditis and Its Influence on Myocardial Collagen Metabolism #br#
WANG Xiufang, LI Yanjun, LI Hongzhong
2024, 21(5):  464-469.  doi:10.3870/j.issn.1672-8009.2024.05.012
Abstract ( 70 )   PDF (1816KB) ( 63 )  
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Objective To explore the protective effect of Hypericum perforatum extract (HPE)on myocardial injury in rats with autoimmune myocarditis and its influence on myocardial collagenmetabolism. Methods Six-week-old Lewis rats were enrolled as the research subjects. The experimental autoimmune myocarditis (EAM) rat model was established by subcutaneous injection of porcine cardiac myosin emulsion into the hind foot pad. The EAM model rats were randomly classifiedinto 4 groups: model group, and low-dose, middle-dose and high-dose HPE groups, with 10 ratsin each group. The rats in each group were given intragastric administration of normal saline, 20mg / kg HPE, 50 mg / kg HPE or 100 mg / kg HPE, with twice a day for 28 days. The blank control group was additionally set and was given normal saline according to the same course of treatment. The clinical manifestations of rats were observed, and the heart weight ( HW) and body weight (BW) were measured, and BW/ HW ratio was calculated. The pathological changes of heart were observed under optical microscope after HE staining. Cardiac parameters such as left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF) were measured by echocardiography. The levels of serum myocardial injury indicators [creatine kinase isoenzyme MB (CK-MB), cardiac troponin T ( cTnT)] and collagen metabolism indicators ( type I collagen, type Ⅲ collagen) were detected, and tumor necrosis factor-alpha ( TNF-α) and transforminggrowth factor-β1 (TGF-β1) protein level was determined by Western blotting. Results The valuesof LVEDD, LVESD, HW/ BW, and the expression levels of CK-MB, cTnT, type I collagen, type Ⅲ collagen, TNF-α protein and TGF-β1 protein in the EAM model rats were increased, the pathological score of myocardial tissues were enhanced, while the values of LVFS and LVEF weredecreased, when compared with those in the blank control group (P < 0. 05). After HPE administration, the values of LVEDD, LVESD, HW/ BW, and the expression levels of CK-MB, cTnT, type I collagen, type Ⅲ collagen, TNF-α protein and TGF-β1 protein were reduced in the lowdose, middle-dose and high-dose HPE groups, and the myocardial tissue pathological score weredeclined, while the values of LVFS and LVEF were risen (P< 0. 05). Conclusion The traditionalChinese medicine Hypericum perforatum extract can improve myocardial injury in EAM model rats,which may be related to its inhibition of myocardial tissue inflammation and reduction of collagen deposition.

Predictive Value of Keratin17 Combined with HPV E6 / E7 mRNA in the Outcome of Cervix Low-grade Squamous Intraepithelial Lesions #br#
WU Ying, LI Yuan, WANG Xiaoyan
2024, 21(5):  470-474.  doi:10.3870/j.issn.1672-8009.2024.05.013
Abstract ( 62 )   PDF (825KB) ( 48 )  
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Objective To study the predictive value of Keratin17 (Krt17) combined with human papillomavirus (HPV) E6 / E7 mRNA in the prognosis of cervical low-grade squamous intraepithelial lesions (LSIL). Methods Patients diagnosed with LSIL from January 2020 to September2021 and completed 24 months of follow-up were selected and grouped according to the histologicalfindings of the lesions at the 24th month of return visit. Patients with LSIL regression or maintenancewere classified as the non-lesion progression group, and patients with LSIL progression to a highergrade were classified as the lesion progression group. The clinical data, Krt17 mRNA expression level and E6 / E7 copy number of the two groups were compared at the time of first diagnosis. The riskfactors of LSIL lesion progression were analyzed by multivariate logistic step-by-step regression, andthe predictive value of Krt17 combined with E6 / E7 on LSIL lesion progression was analyzed by ROCcurve. Results Among the 98 LSIL patients, 19 cases ( 19. 39 % ) progressed and 79 cases(80. 61 % ) did not progress. The age, smoking rate, menopause rate, Krt17 mRNA expressionlevel and E6 / E7 copy number of LSIL patients in the lesion progression group were higher than thosein the non-lesion progression group (P < 0. 05). Multivariate logistic regression analysis showed that age ≥ 45 years, smoking, increased Krt17 mRNA expression level and E6 / E7 copy number were risk factors for the progression of LSIL lesions. ROC curve analysis showed that Krt17 and E6 / E7had predictive value for the progression of LSIL lesions, and the sensitivity and specificity of thecombined prediction of the two indexes were respectively 81. 01 % and 94. 74 % . Conclusion Krt17 combined with HPV E6 / E7 can predict the progression of LSIL lesions.

Effect of Shikonin on Proliferation and Apoptosis of Ovarian Cancer Cells #br# #br#
JIAO Peiying, DU Qiaoqian, LI Na, WANG Jiao
2024, 21(5):  475-480.  doi:10.3870/j.issn.1672-8009.2024.05.014
Abstract ( 65 )   PDF (2677KB) ( 42 )  
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Objective To explore the effect of shikonin on the proliferation and apoptosis of ovarian cancer cells and the expression of c-Jun N-terminal kinase ( JNK) signaling pathway.Methods Human ovarian cancer cell ( SKOV-3 ) cells cultured in vitro were divided into 4groups: control group ( 0 μmol / L ), low-dose Shikonin group ( 2. 5 μmol / L ), middle-dose Shikonin group (5 μmol / L) and high-dose Shikonin group (10 μmol / L). Cell proliferation and apoptosis were detected in each group. The expression levels of proliferating cell nuclear antigen (PCNA), cleaved Caspase-9 and Caspase-3 proteins, and c-Jun N-terminal kinase 1 / 2 ( JNK1 /2) phosphorylation were detected by Western blotting. Results The inhibitory effect of shikoninon the proliferation of SKOV-3 cells showed dependence of drug concentration, with the semi-inhibitory concentration (IC50) of 10. 59 μmol / L. The cells survival rate and colony formation rate weresignificantly decreased in the middle-dose Shikonin group and high-dose Shikonin group ( P <0. 05), the apoptosis rate was significantly increased (P < 0. 05), the expression levels of PCNAand (p-JNK1 / 2) / (JNK1 / 2) were significantly decreased (P < 0. 05), and the levels of cleavedCaspase-9 / Caspase-9 and cleaved Caspase-3 / Caspase-3 were significantly increased (P < 0. 05), ifcompared with those in the control group. Conclusion Shikonin can inhibit the proliferation ofSKOV-3 cells, inhibit JNK signaling pathway, and induce apoptosis.
Downregulation of Long Non-coding RNA XIST Alleviates IL-1β-induced Chondrocyte Apoptosis by Targeting miR-124 / NF-κB Axis #br#
TAN Jifeng, YAN Hong, JIANG Luoyong
2024, 21(5):  481-486.  doi:10.3870/j.issn.1672-8009.2024.05.015
Abstract ( 65 )   PDF (3012KB) ( 44 )  
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Objective To explore the effect of long non-coding RNA ( lncRNA) X inactivespecific transcript ( XIST) on interleukin-1β ( IL-1β ) -induced chondrocyte apoptosis and itsmechanism. Methods The targeting relationship between XIST and miR-124 was predicted bybioinformatics and verified by dual luciferase reporter gene assay. Ten experimental groups were set as follows: normal group, IL-1β group, si-NC group, si-XIST group, miR-124-NC group, miR-124 mimics group, si-NC + inhibitor-NC group, si-XIST + inhibitor-NC group, si-NC + miR-124inhibitor group, si-XIST + miR-124 inhibitor group. qRT-PCR was used to detect the expression levels of XIST and miR-124 in cells. Western blotting was used to detect the expression level of nuclearfactor kappa B P65 ( NF-κB P65 ) protein. Flow cytometry was used to detect cell apoptosis. Results There was a targeting relationship between lncRNA XIST and miR-124. The expressionlevels of lncRNA XIST and NF-κB P65 protein and the apoptosis rate in the IL-1β-induced chondrocytes were increased, while the expression level of miR-124 was decreased when compared withthose in the normal group (P < 0. 05). The expression level of NF-κB P65 protein and the apoptosisrate in the si-XIST group and the miR-124 mimics group were reduced when compared with those inthe IL-1β group (P < 0. 05). The expression level of NF-κB P65 protein and the cell apoptosis rate in the si-XIST + inhibitor-NC group were reduced when compared with those in the si-NC + inhibitorNC group. The expression level of NF-κB P65 protein and the apoptosis rate in the si-XIST + miR-124 inhibitor group were decreased when compared with those in the si-NC + miR-124 inhibitorgroup, ( P < 0. 05). Conclusion Down-regulation of lncRNA XIST can target and regulate themiR-124 / NF-κB axis, thereby alleviating the apoptosis of chondrocytes induced by IL-1β.

Research Progress of KCNQ1 Channel Structure and Function #br#
LIU Hongyu , XIE Jinyan ,
2024, 21(5):  487-491.  doi:10.3870/j.issn.1672-8009.2024.05.016
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The KCNQ1 channel is a voltage-gated potassium channel subunit, which is assembled with the proteins of KCNE family to form a functional potassium channel. Changes in the structure and function of KCNQ1 channels affect the pathophysiological processes of various diseases in vivo. In this paper, the structure of KCNQ1, its role in various molecular biological processes, andthe interaction between KCNQ1 and the KCNE family or non-KCNE family are discussed, and the biophysical research progress on KCNQ1 channels are summarized systematically.
Research Progress on Mechanism of Scutellaria baicalensis and Its Compounds Preparations against Candida albicans Infection #br#
NIU Chunyu, FENG Wenli
2024, 21(5):  497-500.  doi:10.3870/j.issn.1672-8009.2024.05.018
Abstract ( 104 )   PDF (693KB) ( 58 )  
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In recent years, the incidence of candidiasis has increased significantly due to the COVID-19 pandemic. Candida albicans infection and resistance of commonly used therapeutic drugs have become increasingly serious public health problems globally. The extract of Scutellaria baicalensis, its monomer components and the traditional Chinese medicine compounds preparations have been proved to have good anti- Candida albicans activities in experiments and clinics. However, themechanisms seem to be very complex, which may be related to inhibiting adhesion and invasion, affecting biofilm formation, inducing apoptosis, disrupting calcium homeostasis, disrupting glycolysis, inhibiting effecting pump, fighting inflammation and improving immunity.