The Journal of international medical research · 2020
Oxymatrine exerts anti-fibrotic effects in a rat model of hepatic fibrosis by suppressing endoplasmic reticulum stress.
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Liu Xiaodong, Wang Dong, Yang Wenping, Wu Xiaomeng
Аннотация
OBJECTIVE: This study evaluated the anti-fibrotic effects of oxymatrine and the role of endoplasmic reticulum (ER) stress in hepatic fibrosis (HF) in animal models.
METHODS: The HF rat model was established by exposure to NaAsO2, followed by treatment with oxymatrine. Biomarkers of HF and ER stress were measured. The difference in protein expression between groups was evaluated using isobaric tag for relative and absolute quantification (iTRAQ) analysis. The mechanism by which oxymatrine modulated ER stress to alleviate arsenic-induced HF was evaluated using LX2 hepatic stellate cells in vitro.
RESULTS: The rat model mimicked the pathological and physical phenotypes of HF including ER stress, oxidative stress, impaired liver function, and fibrosis. Treatment with oxymatrine suppressed these responses. Moreover, apoptosis, inflammation, and hepatic stellate cell activation were also inhibited by oxymatrine treatment. The differentially expressed proteins and pathways related to ER stress were identified in the HF and oxymatrine-treated groups via iTRAQ analysis combined with liquid chromatography-mass spectrometry. LX2 cells were activated by NaAsO2 in vitro. Meanwhile, oxymatrine suppressed the activation of LX2 cells by alleviating ER stress and regulating cellular calcium homeostasis.
CONCLUSIONS: Oxymatrine could reverse NaAsO2-induced HF by alleviating ER stress.
METHODS: The HF rat model was established by exposure to NaAsO2, followed by treatment with oxymatrine. Biomarkers of HF and ER stress were measured. The difference in protein expression between groups was evaluated using isobaric tag for relative and absolute quantification (iTRAQ) analysis. The mechanism by which oxymatrine modulated ER stress to alleviate arsenic-induced HF was evaluated using LX2 hepatic stellate cells in vitro.
RESULTS: The rat model mimicked the pathological and physical phenotypes of HF including ER stress, oxidative stress, impaired liver function, and fibrosis. Treatment with oxymatrine suppressed these responses. Moreover, apoptosis, inflammation, and hepatic stellate cell activation were also inhibited by oxymatrine treatment. The differentially expressed proteins and pathways related to ER stress were identified in the HF and oxymatrine-treated groups via iTRAQ analysis combined with liquid chromatography-mass spectrometry. LX2 cells were activated by NaAsO2 in vitro. Meanwhile, oxymatrine suppressed the activation of LX2 cells by alleviating ER stress and regulating cellular calcium homeostasis.
CONCLUSIONS: Oxymatrine could reverse NaAsO2-induced HF by alleviating ER stress.