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首页> 外文期刊>Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie >Hepatoprotective effect of alpha-mangostin against lipopolysaccharide/D-galactosamine-induced acute liver failure in mice
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Hepatoprotective effect of alpha-mangostin against lipopolysaccharide/D-galactosamine-induced acute liver failure in mice

机译:α-脑霉素对脂多糖/ D-半乳糖胺诱导的小鼠急性肝衰竭的肝脏保护作用

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摘要

The purpose of this study was to investigate the hepatoprotective effect of alpha-mangostin (alpha-MG) on lipopolysaccharide/D-galactosamine (LPS/D-Ga1N)-induced acute liver failure and discover its potential mechanisms in mice. The results showed that alpha-MG could attenuate LPS/D-Ga1N-induced liver pathological injury, and decrease the hepatic malondialdehyde (MDA) level, serum alanine aminotransferase (ALT), aspartate transaminase (AST), tumor necrosis factor (TNF-alpha), interleukin-1 beta and 6 (IL-1 beta, IL-6) levels and recovery hepatic glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) activities. The results also indicated that alpha-MG inhibited LPS/D-Ga1N-induced toll-like receptor 4 (TLR4) expression and NF-kappa B activation. In addition, alpha-MG up-regulated the expressions of Nrf2 and heme oxygenase-1 (HO-1). In conclusion, the results indicated that alpha-MG could protect against LPS/D-Ga1N-induced liver failure by activating Nrf2 to induce antioxidant defense and inhibiting TLR4 signaling pathway to induce anti-inflammatory effect
机译:本研究的目的是探讨α-山底蛋白(α-Mg)对脂多糖/ D-半乳糖胺(LPS / D-GA1N)诱导的急性肝功能衰竭的肝脏保护作用,并发现其小鼠的潜在机制。结果表明,α-Mg可以衰减LPS / D-GA1N诱导的肝脏病理损伤,降低肝丙醛(MDA)水平,血清丙氨酸氨基转移酶(ALT),天冬氨酸转氨酶(AST),肿瘤坏死因子(TNF-α ),白细胞介素-1β和6(IL-1β,IL-6)水平和回收肝谷胱甘肽(GSH),超氧化物歧化酶(SOD),过氧化氢酶(猫)活性。结果还表明,α-Mg抑制LPS / D-GA1N诱导的Toll样受体4(TLR4)表达和NF-Kappa B活化。此外,α-Mg上调NRF2和血红素氧酶-1(HO-1)的表达。总之,结果表明,通过激活NRF2来诱导抗氧化防御和抑制TLR4信号通路以诱导抗炎作用来保护α-Mg抗LPS / D-Ga1N诱导的肝功能衰竭

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