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Protective effects of geniposide against Tripterygium glycosides (TG)-induced liver injury and its mechanisms

机译:gen子苷对雷公藤多甙(TG)诱导的肝损伤的保护作用及其机制

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摘要

Tripterygium glycosides (TG) are commonly used for basic medicine in curing rheumatoid arthritis but with a high incidence of liver injury. Geniposide (GP) has broad and diverse bioactivities, but until now it is still unknown whether GP can protect against TG-induced liver injury. This study, for the first time, observed the possible protection of GP against TG-induced liver injury in mice and its mechanisms underlying. Oral administration of TG (270 mg/kg) induced significant elevation in the levels of serum alanine / aspartate transaminase (ALT/AST), hepatic malondialdehyde (MDA) and pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) (all P < 0.01). On the other hand, remarkably decreased biomarkers, including hepatic glutathione (GSH) level, activities of glutathione transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT), and anti-inflammatory cytokine interleukin (IL)-10, were observed following TG exposure (all P < 0.01). Nevertheless, all of these phenotypes were evidently reversed by pre-administration of GP for 7 continuous days. Further analysis showed that the mRNA expression of hepatic growth factor-betal (TGF-beta 1), one of tissue repair and regeneration cytokines, was enhanced by GP. Taken together, the current research suggests that GP protects against TG-induced liver injury in mice probably involved during attenuating oxidative stress and inflammation, and promoting tissue repair and regeneration.
机译:雷公藤多甙(TG)通常用于治疗类风湿关节炎的基础药物,但肝损伤的发生率很高。 ip子苷(GP)具有广泛而多样的生物活性,但是直到现在,GP能否预防TG引起的肝损伤仍是未知的。这项研究首次观察到GP对TG诱导的小鼠肝损伤的可能保护作用及其潜在机制。口服TG(270 mg / kg)导致血清丙氨酸/天冬氨酸转氨酶(ALT / AST),肝丙二醛(MDA)和促炎性细胞因子肿瘤坏死因子-α(TNF-α)的水平显着升高(全部P <0.01)。另一方面,生物标志物显着下降,包括肝谷胱甘肽(GSH)水平,谷胱甘肽转移酶(GST),谷胱甘肽过氧化物酶(GPx),超氧化物歧化酶(SOD)和过氧化氢酶(CAT)以及抗炎细胞因子白介素(IL) TG暴露后,观察到)-10)(所有P <0.01)。尽管如此,通过连续连续7天的GP预先给药,所有这些表型均被明显逆转。进一步的分析表明,GP可以增加肝修复因子-β1(TGF-beta 1)的mRNA表达,TGF-β1是组织修复和再生细胞因子之一。综上所述,当前的研究表明,GP可以防止可能引起衰减氧化应激和炎症并促进组织修复和再生的小鼠受TG诱导的肝损伤。

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