nonalcoholic 英 [,nɒnælkə'hɒlɪk] 美 [,nɑn,ælkə'hɑlɪk]
释义 adj. 不含酒精的
例句 Insulin resistance, diabetes and high levels of cholesterol all contribute to the development of nonalcoholic fatty liver disease and its complications. 胰岛素抵抗、糖尿病及高水平的胆固醇均导致非酒精性脂肪肝的发展及并发症的产生。
steatohepatitis 英 [,stiə'to ˌhepəˈtaɪtɪs] 美 [,stiə'to ˌhɛpəˈtaɪtɪs]
释义 n. 脂肪性肝炎
例句 To explore the risk factors of non-alcoholic steatohepatitis(NASH) in children. 探讨儿童非酒精性脂肪性肝炎（NASH）的危险因素。
作者： Kapil K. Upadhyay
Nuclear factor-erythroid 2 related factor 2 (Nrf2)-mediated signaling plays a central role in maintaining cellular redox homeostasis of hepatic cells. Carbon monoxide releasing molecule-A1 (CORM-A1) has been reported to stimulate up-regulation and nuclear translocation of Nrf2 in hepatocytes. However, the role of CORM-A1 in improving lipid metabolism, antioxidant signaling and mitochondrial functions in nonalcoholic steatohepatitis (NASH) is unknown. In this study, we report that CORM-A1 prevents hepatic steatosis in high fat high fructose (HFHF) diet fed C57BL/6J mice, used as model of NASH. The beneficial effects of CORM-A1 in HFHF fed mice was associated with improved lipid homeostasis, Nrf2 activation, upregulation of antioxidant responsive (ARE) genes and increased ATP production. As, mitochondria are intracellular source of reactive oxygen species (ROS) and important sites of lipid metabolism, we further investigated the mechanisms of action of CORM-A1-mediated improvement in mitochondrial function in palmitic acid (PA) treated HepG2 cells. Cellular oxidative stress and cell viability were found to be improved in PA + CORM-A1 treated cells via Nrf2 translocation and activation of cytoprotective genes. Furthermore, in PA treated cells, CORM-A1 improved mitochondrial oxidative stress, membrane potential and rescued mitochondrial biogenesis thru upregulation of Drp1, TFAM, PGC-1α and NRF-1 genes. CORM-A1 treatment improved cellular status by lowering glycolytic respiration and maximizing OCR. Improvement in mitochondrial respiration and increment in ATP production in PA + CORM-A1 treated cells further corroborate our findings. In summary, our data demonstrate for the first time that CORM-A1 ameliorates tissue damage in steatotic liver via Nrf2 activation and improved mitochondrial function, thus, suggesting the anti-NASH potential of CORM-A1.