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Boletus aereus protects against acute alcohol-induced liver damage in the C57BL/6 mouse via regulating the oxidative stress-mediated NF-κB pathway
Pharmaceutical Biology ( IF 3.9 ) Pub Date : 2020-01-01 , DOI: 10.1080/13880209.2020.1812672
Luping Zhang 1 , Bo Meng 1, 2 , Lanzhou Li 2 , Yanzhen Wang 2, 3 , Yuanzhu Zhang 2 , Xuexun Fang 1, 2 , Di Wang 2, 3
Affiliation  

Abstract Context Alcoholic liver disease, caused by abuse and consumption of alcohol, exhibits high morbidity and mortality. Boletus aereus Bull. (Boletaceae) (BA) shows antioxidant, anti-inflammatory and antimicrobial effects. Objectives To investigate the hepatoprotective effects of BA using an acute alcohol-induced hepatotoxicity mice model. Materials and methods The composition of BA fruit body was first systematically analyzed. Subsequently, a C57BL/6 mice model of acute alcohol-induced liver injury was established by intragastrically administration of alcohol, which was intragastrically received with BA powder at 200 mg/kg and 800 mg/kg for 2 weeks, 60 mg/kg silybin treatment was used as positive control group. By employing the pathological examination, ELISA, RT-PCR and western blot, the regulation of BA on oxidative stress signals was investigated. Results The LD50 of BA was much higher than 4 g/kg/p.o. In acute alcohol-damaged mice, BA reduced the levels of alanine aminotransferase (>18.3%) and aspartate aminotransferase (>27.6%) in liver, increased the activity of liver alcohol dehydrogenase (>35.0%) and serum acetaldehyde dehydrogenase (>18.9%). BA increased the activity of superoxide dismutase (>13.4%), glutathione peroxidase (>11.0%) and 800 mg/kg BA strongly reduced chemokine (C-X-C motif) ligand 13 (14.9%) and chitinase-3 like-1 protein (13.4%) in serum. BA reversed mRNA over-expression (>70%) and phosphor-stimulated expression (>45.0%) of an inhibitor of nuclear factor κ-B kinase (NF-κB, an inhibitor of nuclear factor κ-B α and nuclear factor κ-B in the liver. Conclusions BA is effective in ameliorating alcohol-induced liver injury through regulating oxidative stress-mediated NF-κB signalling, which provides a scientific basis for further research on its clinical applications.

中文翻译:

牛肝菌通过调节氧化应激介导的 NF-κB 通路保护 C57BL/6 小鼠免受急性酒精性肝损伤

摘要背景酒精性肝病是由滥用和饮酒引起的,发病率和死亡率都很高。牛肝菌牛肝菌。(牛肝菌科) (BA) 显示抗氧化、抗炎和抗菌作用。目的 使用急性酒精性肝毒性小鼠模型研究 BA 的保肝作用。材料与方法首先系统地分析了BA子实体的组成。随后,通过灌胃酒精建立C57BL/6小鼠急性酒精性肝损伤模型,给予BA粉200mg/kg和800mg/kg灌胃2周,60mg/kg水飞蓟宾治疗用作阳性对照组。通过病理检查、ELISA、RT-PCR和蛋白质印迹,研究了 BA 对氧化应激信号的调节。结果 BA的LD50远高于4 g/kg/po 在急性酒精中毒小鼠中,BA降低肝脏中丙氨酸转氨酶(>18.3%)和天冬氨酸转氨酶(>27.6%)的水平,增加肝脏活性乙醇脱氢酶 (>35.0%) 和血清乙醛脱氢酶 (>18.9%)。BA 增加了超氧化物歧化酶 (>13.4%)、谷胱甘肽过氧化物酶 (>11.0%) 和 800 mg/kg BA 的活性,强烈降低了趋化因子(CXC 基序)配体 13(14.9%)和几丁质酶-3 样 1 蛋白(13.4%) ) 在血清中。BA 逆转了核因子 κ-B 激酶抑制剂(NF-κB,核因子 κ-B α 和核因子 κ- 的抑制剂)的 mRNA 过表达(>70%)和磷刺激的表达(>45.0%) B 在肝脏。
更新日期:2020-01-01
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