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Metabolic changes of macrophages in LPS-induced liver failure GUO Jin, SHI Chun-xia, DENG Wei, ZHANG Lu-yi, CHEN Qian, WANG Yao, GONG Zuo-jiong Chinese Hepatolgy    2022, 27 (9): 973-977.   Abstract （174）      PDF （651KB）（744）       Knowledge map    Objective During the process of acute liver failure (ALF), endotoxin activated macrophages to release cytokines and induced changes in cellular metabolism. The aim of this study was to investigate the change of the substrates and products of malate dehydrogenase, and to analyze the metabolic changes of mice ANA-1 macrophages in response to lipopolysaccharide (LPS). Methods A total of 16 subjects were enrolled, including 8 ALF cases and 8 were healthy controls. Liquid Chromatograph Mass Spectrometer (LC-MS) was used to analyze the level of the substrates and related metabolite (malate and oxaloacetate). The Mice ANA-1 macrophages cultured in vitro were divided into normal control group and LPS group [treated by LPS (5μg/ml)]. The levels of tumor necrosis factor-α (TNF-α), malate dehydrogenase 1 (MDH1), lactic acid, glucose, adenosine-5'-triphosphate (ATP) were tested. Western-blot was used to detect the intracellular MDH1 protein content. Results Compared with the normal group, the malate increased and oxaloacetate decreased in ALF group (P<0.05). In LPS-induced mice ANA-1 macrophages, the level of TNF-α in supernatant increased [(1722.501 ± 76.261) pg/mL vs (255.010 ± 16.139) pg/mL], P<0.05, which indicates that LPS stimulated macrophages release cytokines. Compared with the control group (15.710 ± 0.302) ng/mL, the level of MDH1(11.831 ± 0.335) ng/mL and protein content in the LPS group were reduced (P<0.05). In addition, the levels of lactate and glucose in ANA-1 cells treated by LPS increased [(0.281 ± 0.016) mmol/L vs (0.081±0.012) mmol/L, (0.081 ± 0.006) μmol/mL vs (0.033 ± 0.004) μmol/mL], and the ATP levels decreased [(61.766 ± 11.982) μmol/gprot VS (130.786 ± 25.386) μmol/gprot], P<0.05. Conclusion During the process of ALF, LPS suppressed the activity of MDH1 in macrophages, induced mitochondrial-related metabolism disorders, resulted in the increase of lactate and glucose, and decrease of ATP production. Reference | Related Articles | Metrics

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Chinese Hepatolgy    2019, 24 (9): 975-983.   Abstract （454）      PDF （915KB）（2840）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2023, 28 (2): 148-151.   Abstract （831）      PDF （723KB）（830）       Knowledge map    Reference | Related Articles | Metrics

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Effects of prohibitin 1 on cell proliferation of human hepatocellular carcinoma cells and its mechanism SHI Juan-juan, ZHANG Xin, WU Feng-ping, WANG Mu-qi, LI Ya-ping, WANG Wen-jun, GAO Ning, DANG Shuang-suo Chinese Hepatolgy    2019, 24 (8): 864-870.   Abstract （196）      PDF （1238KB）（575）       Knowledge map    Objective To investigat the effects of prohibitin1 (PHB1) on cell proliferation of human hepatocellular? carcinoma (HCC) cells, and to elucidate the mechanism of PHB1 in the occurrence and development of HCC.Methods HepG2 and SMMC-7721 cells were transfected with enhanced green fluorescent protein plasmid-PHB1 and PHB1-specific short hairpin ribonucleic acid (RNA) to induce the up-regulation and down-regulation of PHB1 expression. The cell proliferation, cell cycle and key regulators of cell cycle were investigated by MTT assay, flow cytometry, real-time polymerase chain reaction and western blot. Results Overexpression of PHB1 arrested the HepG2 and SMMC-7721 cell cycle in G0/G1 phase (67.28%±2.94 vs 56.71% ± 2.56, t=6.64, P=0.00; 69.48%±3.82 vs 60.43%±2.59, t=4.80, P=0.00), decreased the proportion of cells in S phase (14.74%±1.45 vs 24.13%±1.92, t=9.54, P=0.00; 13.73%±1.26 vs 25.50% ± 2.30, t=10.99, P=0.00), and inhibited cell proliferation. Furthermore, as PHB1 overexpressed, the messenger RNA and protein levels of p53 and p21CIP1 were increased, while those of cyclin A2, cyclin E1 and cyclin-dependent kinase 2 were decreased in the HepG2 and SMMC-7721cells (P<0.01). Conversely, these results were reversed when the expression of PHB1 was inhibited.Conclusion Overexpression of PHB1 arrested the HCC cell cycle in G0/G1 phase, thus inhibit cell proliferation, which might be related to p53-mediated G0/G1 phase-related cell cycle protein. Reference | Related Articles | Metrics

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Chinese Hepatolgy    2020, 25 (1): 98-99.   Abstract （273）      PDF （891KB）（1061）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2022, 27 (1): 12-14.   Abstract （545）      PDF （660KB）（836）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2018, 23 (3): 266-268.   Abstract （207）      PDF （627KB）（1042）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2019, 24 (9): 991-996.   Abstract （129）      PDF （792KB）（1111）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2016, 21 (6): 493-500.   Abstract （173）      PDF （864KB）（878）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2018, 23 (12): 1090-1092.   Abstract （278）      PDF （673KB）（1902）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2021, 26 (6): 579-584.   Abstract （487）      PDF （887KB）（1909）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2019, 24 (8): 910-914.   Abstract （178）      PDF （1275KB）（457）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2018, 23 (5): 378-379.   Abstract （207）      PDF （659KB）（1331）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2021, 26 (9): 1046-1051.   Abstract （188）      PDF （677KB）（446）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2019, 24 (4): 418-420.   Abstract （659）      PDF （862KB）（986）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2019, 24 (10): 1194-1195.   Abstract （177）      PDF （661KB）（1360）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2019, 24 (8): 918-920.   Abstract （164）      PDF （681KB）（528）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2021, 26 (7): 802-803.   Abstract （182）      PDF （675KB）（334）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2021, 26 (5): 568-570.   Abstract （223）      PDF （787KB）（520）       Knowledge map    Reference | Related Articles | Metrics

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Dynamic changes of intrahepatic T cell receptor repertoires before and after nucleos(t)ide analogues treatment in patients with chronic hepatitis B WU Hong-kai, DENG Hao-hui, GONG Ming-xing, GAO Hong-bo, WANG Zhan-hui, YU Le-cheng Chinese Hepatolgy    2021, 26 (7): 742-746.   Abstract （333）      PDF （971KB）（447）       Knowledge map    Objective To investigate the dynamic changes of intrahepatic T cell receptor (TCR) repertoires before and after nucleos(t)ide analogues (NUCs) antiviral therapy in chronic hepatitis B (CHB) patients. Methods A total of ten CHB patients with tebivudine (LDT) based therapy were subdivided to two groups on HBeAg status after 104 treatment. The TCRβ complementarity determining region 3 (CDR3) of liver biopsies before and after 2-year NUCs treatment was analyzed by high-throughput sequencing. The TCR repertoire profiles and their correlations with serological parameters were analyzed. Results After LDT-based treatment for 104 weeks, the diversity of intrahepatic TCR repertoires in patients with HBeAg seroconversion decreased significantly on the number of unique VJ combinations (151.0 比 71.0, P=0.043), CDR3 clonotypes (223.0 比 109.0, P=0.043), and the values of normalized Shannon diversity entropy (0.58 比 0.17, P=0.045). The decline of HBsAg levels in these patients was positively correlated with the elevation of ablated clonetype frequency (r=0.9, P=0.037). Conclusion NUCs antiviral therapy may induce changes of intrahepatic TCR repertoires. T cell clone expansion plays an important role in HBeAg seroconversion, suggesting that oral antiviral therapy combined with immunotherapy may be more conducive to the control of HBV. Reference | Related Articles | Metrics