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    Chinese Hepatolgy    2019, 24 (9): 975-983.  
    Abstract283)      PDF (915KB)(523)      
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    Chinese Hepatolgy    2021, 26 (8): 939-942.  
    Abstract856)      PDF (839KB)(846)      
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    Regulation of microRNA-21 for cisplatin resistance in Huh7 cells by PTEN and Wnt signaling pathways
    LU Tian-fei, ZHONG Cheng-peng, GU Guang-xiang, HAO Jun, ZHANG Jian-jun , XU Ning
    Chinese Hepatolgy    2018, 23 (1): 31-36.  
    Abstract180)      PDF (2814KB)(375)      
    Objective To investigate the mechanism of microRNAs in mediating cisplatin resistance in hepatocellular carcinoma (HCC).Methods MicroRNA-21 (miR-21) level was determined in HCC patients after cisplatin chemotherapy. miR-21 mimics and miR-21 inhibitor were used to upregulate or downregulate miR-21 level in Huh-7 cells. Human dickkopf-1(DKK-1) and bpV (phen) were used as Wnt inhibitor and phosphate and tension homology deleted on chromsome ten (PTEN) inhibitor, respectively. Relative mRNA level and protein expression were detected by real-time polymerase chain reaction (RT-PCR) and western blot, respectively. Results The results showed that overexpression of miR-21 decreased cisplatin (5 and 10 μg/mL)-induced inhibition of cell proliferation in Huh7 cells. Both mRNA level and protein expression of Wnt4 were elevated remarkably when Huh7 cells were treated with miR-21 mimics. Moreover, inhibition of Wnt4 and cell proliferation by DKK-1 was reversed using overexpression of miR-21. In addition, miR-21 mimics increased both mRNA level and protein expression of PTEN, and overexpression of miR-21 increased cell proliferation rate which was inhibited using bpV (phen, 100 and 200 nmol/L) in Huh7 cells. Conclusion miR-21 was involved in regulating resistance to cisplatin in Huh7 cells by activating Wnt and PTEN signaling pathways.
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    Chinese Hepatolgy    2018, 23 (12): 1090-1092.  
    Abstract234)      PDF (673KB)(1510)      
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    Chinese Hepatolgy    2019, 24 (11): 1319-1322.  
    Abstract340)      PDF (690KB)(1636)      
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    Chinese Hepatolgy    2016, 21 (9): 746-747.  
    Abstract453)      PDF (925KB)(1308)      
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    Chinese Hepatolgy    2017, 22 (11): 1032-1035.  
    Abstract155)      PDF (1325KB)(648)      
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    Chinese Hepatolgy    2019, 24 (2): 196-199.  
    Abstract96)      PDF (639KB)(585)      
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    Chinese Hepatolgy    2018, 23 (2): 171-176.  
    Abstract222)      PDF (1217KB)(1390)      
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    Chinese Hepatolgy    2018, 23 (11): 1029-1031.  
    Abstract192)      PDF (683KB)(1132)      
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    Chinese Hepatolgy    2019, 24 (3): 327-328.  
    Abstract178)      PDF (1051KB)(712)      
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    Chinese Hepatolgy    2017, 22 (9): 857-858.  
    Abstract279)      PDF (625KB)(1370)      
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    Chinese Hepatolgy    2023, 28 (1): 16-20.  
    Abstract108)      PDF (760KB)(209)      
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    Chinese Hepatolgy    2017, 22 (4): 339-341.  
    Abstract391)      PDF (700KB)(1322)      
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    Chinese Hepatolgy    2021, 26 (2): 205-210.  
    Abstract266)      PDF (1146KB)(796)      
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    Chinese Hepatolgy    2018, 23 (10): 852-855.  
    Abstract142)      PDF (634KB)(580)      
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    Chinese Hepatolgy    2021, 26 (10): 1079-1081.  
    Abstract397)      PDF (788KB)(437)      
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    Chinese Hepatolgy    2019, 24 (10): 1194-1195.  
    Abstract146)      PDF (661KB)(564)      
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    Chinese Hepatolgy    2017, 22 (2): 178-178.  
    Abstract157)      PDF (645KB)(311)      
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    Effects of short chain fatty acids on metabolism of glucose and lipid in obese mice induced by high fat diet
    LIU Qian, CHENG Chen, XIN Xin, HU Yi-yang, FENG Qin
    Chinese Hepatolgy    2018, 23 (7): 591-595.  
    Abstract267)      PDF (1896KB)(434)      
    Objective To observe the effects of short chain fatty acids (SCFAs) on metabolism of glucose and lipid in obese mice induced by high fat diet (HFD), and to investigate the possible mechanisms from the perspective of intestinal epithelial barrier function. Methods Forty C57BL/6J mice were equally randomly divided into normal diet (ND) group, HFD model group, SCFAs treatment (HFD+SCFAs) group and lactulose (LA) treatment (HFD+LA) group. Mice were fed a HFD for 14 weeks, and treated with corresponding drugs or distilled water since week 10. After 4-week treatment, mice were sacrificed for observing body weight, food intake, liver weight, ratio of liver weight to body weight, morphology and diameter of adipocytes after epididymis, fasting plasma glucose (FBG), fasting serum insulin (FINS), homeostatic model assessment insulin resistance (HOMA-IR), serum triglyceride (TG), serum cholesterol (TC), low density lipoprotein, hepatic TG, serum alanine aminotransferase, aspartate aminotransferase, and hepatic and colonic tissue pathological changes. Results The body weight, liver weight, ratio of liver weight to body weight, FBG, FSI, HOMA-IR, serum TG, serum TC and hepatic TG in HFD+SCFAs group were significantly lower than those in the HFD group (P<0.01). SCFAs was superior to LA in reducing FSI, HOMA-IR, serum TG, serum TC, and hepatic TG (P<0.01 or P<0.05). Moreover, hepatic steatosis, inflammation and ballooning were significantly improved in HFD+SCFAs group than those in HFD group, and disease activity score was decreased (P<0.01). SCFAs intervention could significantly improve colonic pathology, including colonic epithelial damage, glandular disorder and inflammatory cell infiltration induced by HFD. Conclusion SCFAs can effectively reduce body weight, improve the metabolism of glucose and lipid and decrease hepatic fat deposition in obese mice induced by HFD. Reducing intestinal inflammatory response and enhancing intestinal epithelial barrier function maybe one of the possible mechanisms.
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