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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    2021, 26 (6): 579-584.   Abstract （487）      PDF （887KB）（1909）       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    2021, 26 (8): 939-942.   Abstract （1260）      PDF （839KB）（1592）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2016, 21 (9): 781-783.   Abstract （155）      PDF （618KB）（1379）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2019, 24 (11): 1319-1322.   Abstract （407）      PDF （690KB）（2302）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2021, 26 (9): 1044-1046.   Abstract （535）      PDF （620KB）（975）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2019, 24 (10): 1202-1204.   Abstract （201）      PDF （839KB）（1191）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2017, 22 (9): 857-858.   Abstract （398）      PDF （625KB）（2017）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2018, 23 (4): 316-318.   Abstract （186）      PDF （621KB）（415）       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    2022, 27 (12): 1340-1343.   Abstract （758）      PDF （795KB）（862）       Knowledge map    Reference | Related Articles | Metrics

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Chinese Hepatolgy    2017, 22 (2): 172-175.   Abstract （122）      PDF （668KB）（812）       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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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