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野生淫羊藿黄酮对 CCl4 诱导的急性肝损伤的保肝作用评价。

The evaluation of hepatoprotective effects of flavonoids from Wild against CCl-induced acute liver injury and .

机构信息

School of Pharmaceutical Sciences, Jilin University, Changchun, China.

Department of Pharmacy, the First Hospital of Jilin University, Changchun, China.

出版信息

Drug Chem Toxicol. 2022 May;45(3):1284-1294. doi: 10.1080/01480545.2020.1815763. Epub 2020 Sep 14.

Abstract

Wild is a traditional herbal medicine; however, little is known with regard to the effect of flavonoids from S. (FSA) on liver injury induced by Carbon tetrachloride (CCl), especially the mechanism remains unknown. Therefore, our paper was designed to investigate the hepatoprotective effect of FSA against CCl-induced acute liver injury and , with focus on its potential mechanism. The purity of FSA prepared by using polyporous resin column chromatography could reach 94.5%, and seven flavonoid compounds in FSA were identified by using LC-ESI-MS analysis. results showed that FSA markedly decreased the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and malonaldehyde (MDA) and increased the contents of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Furthermore, and results confirmed that FSA could inhibit inflammatory response, as evidenced by decreasing the levels of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) through inactivating toll-like receptor-4/nuclear factor-κB (TLR4/NF-κB) signaling pathway. FSA activated autophagy by increasing the ratio of LC3B-II/I and decreasing the protein level of p62 so as to exert its hepatoprotective effect. In general, these evidences suggested that FSA is likely to serve as a potential material for the drugs against chemical hepatic injury.

摘要

野生是一种传统的草药;然而,关于黄酮类化合物从 S. (FSA)对四氯化碳(CCl)诱导的肝损伤的影响知之甚少,特别是其机制尚不清楚。因此,我们的论文旨在研究 FSA 对 CCl 诱导的急性肝损伤的保护作用,并重点研究其潜在机制。采用大孔树脂柱层析法制备的 FSA 纯度可达 94.5%,并用 LC-ESI-MS 分析鉴定出 FSA 中的 7 种黄酮类化合物。结果表明,FSA 能显著降低天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、乳酸脱氢酶(LDH)和丙二醛(MDA)的水平,增加超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的含量。此外,Western blot 结果证实,FSA 可通过抑制 Toll 样受体 4/核因子-κB(TLR4/NF-κB)信号通路,降低肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的水平,从而抑制炎症反应。FSA 通过增加 LC3B-II/I 的比值和降低 p62 蛋白水平来激活自噬,从而发挥其肝保护作用。总之,这些证据表明,FSA 可能是一种治疗化学性肝损伤的潜在药物。

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