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Protective effects of alpha-lipoic acid and coenzyme Q10 on lipopolysaccharide-induced liver injury in rats

机译:α-硫辛酸和辅酶Q10对脂多糖诱导的大鼠肝损伤的保护作用

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Lipopolysaccharide (LPS) is a major cell wall component of gram-negative bacteria known to stimulate the synthesis and secretion of several toxic metabolites, such as reactive oxygen species and cytokines. In this study, the protective effect of alpha-lipoic acid (ALA) and coenzyme Q10 (CoQ10) were evaluated in LPS-induced hepatic injury in rats. To this end, male adult Sprague Dawley rats were divided into five groups; normal control, LPS control where rats were injected with an initial dose of LPS (4 mg/kg; i.p.) on the 1stday of the experiment followed by a challenging dose (2 mg/kg; i.p.) on the 8th day, ALA (50 mg/kg), CoQ10 (10 mg/kg) and ALA plus CoQ10. Treatments continued for 15 days and the last three groups also received LPS. At the end of the study, liver function tests, as well as interleukin-6 (IL-6) were estimated in serum. Liver lipid peroxides (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and total antioxidant capacity (TAC) were also assessed, in addition to histological examination of liver sections from all groups. The obtained data revealed that LPS markedly elevated activities of serum aminotransferases, alkaline phosphatase and gamma-glutamyl transferase, as well as, total bilirubin and interleukin-6 levels. LPS-treated rats showed an increase in MDA liver content versus decrease in GSH content, SOD activity and TAC. Oral administration of ALA, CoQ10 and their combination ameliorated LPSinduced increases in liver function enzymes and IL-6, coupled by hampering of oxidative biomarkers. This was supported by histopathological evaluation results. In conclusion, administration of ALA, CoQ10 and their combination improved pathological abnormalities in liver tissues and reversed the deleterious effects induced by LPS.
机译:脂多糖(LPS)是革兰氏阴性细菌的主要细胞壁成分,已知能刺激多种有毒代谢产物的合成和分泌,例如活性氧和细胞因子。在这项研究中,评估了LPS诱导的大鼠肝损伤中α-硫辛酸(ALA)和辅酶Q10(CoQ10)的保护作用。为此,将成年成年雄性Sprague Dawley大鼠分为五组。正常对照,LPS对照,其中在实验的第一天给大鼠注射初始剂量的LPS(4 mg / kg; ip),然后在第8天注射挑战剂量(2 mg / kg; ip),ALA(50 mg / kg),辅酶Q10(10 mg / kg)和ALA加辅酶Q10。治疗持续了15天,最后三组也接受了LPS。在研究结束时,评估血清中的肝功能测试以及白介素6(IL-6)。除了对所有组的肝脏切片进行组织学检查外,还评估了肝脂质过氧化物(MDA),还原型谷胱甘肽(GSH),超氧化物歧化酶(SOD)和总抗氧化能力(TAC)。获得的数据表明,LPS显着提高了血清氨基转移酶,碱性磷酸酶和γ-谷氨酰转移酶的活性,以及​​总胆红素和白介素6的水平。 LPS处理的大鼠显示MDA肝含量增加,而GSH含量,SOD活性和TAC下降。口服ALA,辅酶Q10及其组合可改善LPS诱导的肝功能酶和IL-6的增加,同时还会阻碍氧化性生物标记物的表达。这得到了组织病理学评估结果的支持。总之,施用ALA,辅酶Q10及其组合改善了肝组织的病理学异常并逆转了LPS诱导的有害作用。

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