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Protective effects of pentoxifylline on acute liver injury induced by thioacetamide in rats

机译:己酮可可碱对硫代乙酰胺致大鼠急性肝损伤的保护作用

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摘要

Pentoxifylline (PTX) is a non-selective phosphodiesterase inhibitor with the effects of antioxidation, anti-inflammation and anti-fibrosis that has been shown to induce damage in liver. The purpose of this study is to investigate the effects and possible mechanisms of PTX on thioacetamide (TAA)-induced acute liver injury in rats. Male Sprague-Dawley (SD) rats were divided into four groups: control, PTX, TAA and PTX+TAA treated groups. Rats were administrated TAA together with or without PTX for a week and sacrificed 24 h after the last intragastric administration of PTX. Histopathological analysis was carried out. The liver function, the indices of oxidative stress including malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) in liver tissues, and pro-inflammatory cytokines expressions were examined. The mRNA level of NF-κB p65 in liver was also determined. PTX significantly attenuated TAA-induced liver injury. The serum transaminase and MDA levels were reduced while the levels of SOD and GSH were increased, as compared with the TAA-treated group. PTX also remarkably suppressed the secretions of pro-inflammatory cytokines and the nuclear factor-κB (NF-κB) activation induced by TAA. In addition, the histopathological analysis showed that the range and degree of liver tissue lesions were improved obviously in PTX treated group. Pentoxifylline could ameliorate the effects of thioacetamide-induced acute liver injury in rats by inhibiting oxidative stress, expressions of pro-inflammatory cytokines and NF-κB activation.
机译:己酮可可碱(PTX)是一种非选择性磷酸二酯酶抑制剂,具有抗氧化,抗发炎和抗纤维化的作用,已证明可引起肝脏损害。本研究的目的是研究PTX对硫代乙酰胺(TAA)诱导的大鼠急性肝损伤的影响及其可能的机制。将雄性Sprague-Dawley(SD)大鼠分为四组:对照组,PTX,TAA和PTX + TAA治疗组。大鼠接受TAA联合或不联合PTX一周,并在最后一次胃内施用PTX后24小时处死。进行了组织病理学分析。检查肝组织中的肝功能,氧化应激指数,包括丙二醛(MDA),超氧化物歧化酶(SOD)和谷胱甘肽(GSH),以及促炎性细胞因子的表达。还测定了肝中NF-κBp65的mRNA水平。 PTX显着减轻了TAA诱导的肝损伤。与TAA治疗组相比,血清转氨酶和MDA水平降低,而SOD和GSH水平升高。 PTX还显着抑制TAA诱导的促炎性细胞因子的分泌和核因子-κB(NF-κB)活化。另外,组织病理学分析表明,PTX治疗组肝组织病变范围和程度明显改善。己酮可可碱可通过抑制氧化应激,促炎细胞因子的表达和NF-κB的活化来改善硫代乙酰胺诱导的大鼠急性肝损伤的作用。

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