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首页> 外文期刊>Cellular Physiology and Biochemistry >TP-58, a Novel Thienopyridine Derivative, Protects Mice from ConcanavalinA-Induced Hepatitis by Suppressing Inflammation
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TP-58, a Novel Thienopyridine Derivative, Protects Mice from ConcanavalinA-Induced Hepatitis by Suppressing Inflammation

机译：TP-58，一种新型噻吩并吡啶衍生物，通过抑制炎症反应，保护小鼠免受刀豆素A诱导的肝炎的侵袭。

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Hepatitis represents a ubiquitous human health problem but effective therapies with limited side effects are still lacking. In this study, we investigated the effect and mechanism of TP-58, a novel thienopyridine derivative, on a murine fulminant hepatitis model induced by concanavalin A (ConA). We found TP-58 markedly alleviated ConA-caused liver injury and increased survival ratio of mice injected with a lethal dose of ConA. Oral administration of TP-58 significantly alleviated ConA-caused liver injury in mice by the reduction of serum aminotransferases and liver necrosis.The analysis of proinflammatory cytokines showed that TP-58 decreased both hepatic mRNA expressions and serum protein levels of TNF-α and IL-6. And the result from LPS-stimulated RAW 264.7 cells showed TP-58 suppressed the production of TNF-α, IL-6, and Nitro Oxide (NO) in the supernatant of LPS-stimulated RAW 264.7 cells. The study of activation of nuclear factor-?B (NF-?B) by electrophoretic mobility shift assay (EMSA) showed that TP-58 inhibited the activation of NF-?B both iin vivo/i and iin vitro/i. The inhibitory effect was also accompanied by a parallel reduction of I?B phosphorylation. These results indicate that TP-58 protects against liver injury by inhibition of the NF-?B-mediated inflammation and suggest a potential role of TP-58 against acute liver injury and other inflammatory diseases.
机译：肝炎代表了普遍存在的人类健康问题，但仍然缺乏副作用有限的有效疗法。在这项研究中，我们调查了新型噻吩并吡啶衍生物TP-58在伴刀豆球蛋白A（ConA）诱导的鼠暴发性肝炎模型中的作用和机制。我们发现TP-58显着减轻了由ConA致死剂量注射的小鼠的ConA引起的肝损伤并提高了存活率。口服TP-58可通过减少血清中的氨基转移酶和肝坏死来减轻ConA所致的小鼠肝损伤。促炎细胞因子分析显示TP-58可以降低肝mRNA表达以及TNF-α和IL的血清蛋白水平-6。 LPS刺激的RAW 264.7细胞的结果表明TP-58抑制了LPS刺激的RAW 264.7细胞上清液中TNF-α，IL-6和一氧化氮（NO）的产生。电泳迁移率迁移分析（EMSA）对核因子-βB（NF-βB）活化的研究表明，TP-58抑制体内和体外。抑制作用还伴随着I 2 B磷酸化的平行降低。这些结果表明，TP-58通过抑制NF-κB介导的炎症而防止肝损伤，并暗示TP-58对急性肝损伤和其他炎性疾病的潜在作用。

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