牛蒡子苷通过抑制MAPK通路减轻非酒精性脂肪肝的脂质积累、炎症和氧化应激

Lin Li, Ying Zhang, Fang-xi Xiao, Zhigang Wang, Ju Liu
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摘要

非酒精性脂肪性肝病(NAFLD)是一种常见的慢性肝病,主要影响成年人。据报道,牛动素通过多种途径改善肝脏功能,但其确切的分子机制尚不清楚。首先,成功构建小鼠肥胖模型,采用苏木精染色、伊红染色和酶联免疫吸附血清学法(ELISA)分别检测肝组织损伤中丙氨酸转氨酶和天冬氨酸转氨酶的水平。免疫组化(IHC)染色检测肝组织脂质积累,检测试剂盒检测血清甘油三酯和总胆固醇水平。Western blotting检测肝脏组织中脂肪合成蛋白、甾醇调节元件结合蛋白-1、茶royl- coa去饱和酶-1、脂肪酸合成酶的表达。采用ELISA法和免疫组化法分别检测大鼠肝组织中谷胱甘肽过氧化物酶、丙二醛、超氧化物歧化酶、过氧化氢酶、活性氧以及白细胞介素2 (IL-2)、IL-1β、IL-6、肿瘤坏死因子-α的水平和p-P65、P65的表达。最后,WB检测肝组织中细胞外信号调节激酶(ERK)、磷酸化ERK、Jun n末端激酶、磷酸化jnk、p38和磷酸化p38蛋白的表达水平。结果表明,与正常饮食相比,高脂饮食小鼠的体重和肝组织脂肪含量增加,肝组织损伤加重,氧化应激能力降低,炎症反应增强,而牛蒡子肽改变了这些不良反应,抑制了丝裂原活化蛋白激酶(MAPK)途径。牛蒡子苷通过抑制MAPK通路、改善脂质积累、炎症反应和氧化应激发挥肝脏保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Arctiin attenuates lipid accumulation, inflammation and oxidative stress in nonalcoholic fatty liver disease through inhibiting MAPK pathway
Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease that predominantly affects the adult population. It was reported that arctiin improves functioning of the liver through multiple pathways, but the exact molecular mechanism is not clear yet. First, a mouse obesity model was successfully constructed, and hematoxylin and eosin staining and enzyme-linked-immunosorbent serologic assay (ELISA) were used to assess the levels of alanine aminotransferase and aspartate aminotransferase, respectively, in liver tissue damage. Then lipid accumulation in liver tissues was detected by immunohistochemistry (IHC) staining, and detection kits were used to determine the levels of triglycerides and total cholesterol in serum. Western blotting was used to detect the expression of adipose synthesis proteins, sterol regulatory element-binding protein-1, stea-royl-CoA desaturase-1 and fatty acid synthase, in liver tissues. Further, the levels of glutathione peroxidase, malondialdehyde, superoxide dismutase, catalase and reactive oxygen species as well as that of interleukin 2 (IL-2), IL-1β, IL-6 and tumor necrosis factor-α, and the expression of p-P65 and P65, in liver tissues were mea-sured by ELISA and IHC, respectively. Finally, the protein expression levels of extracellular signal-regulated kinase (ERK), phospho-ERK, Jun N-terminal kinase, phospho-JNK, p38 and phospho-p38 in liver tissues were examined by WB. The results showed that relative to normal diet, mice on high-fat diet had increased body weight as well as fat content in liver tissues, increased liver tissue damage, decreased oxidative stress capacity and enhanced inflammatory response, while arctiin changed these adverse effects and inhibited mitogen-activated protein kinase (MAPK) pathway. Arctiin exerts hepatoprotective effects by inhibiting MAPK pathway and improving lipid accumulation, inflammatory response and oxidative stress.
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