传统中药配方姜仙护肝素通过NF-κB和Nrf2信号通路对伴刀豆球蛋白A诱导的小鼠肝炎的保护作用。,Journal of Ethnopharmacology

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传统中药配方姜仙护肝素通过NF-κB和Nrf2信号通路对伴刀豆球蛋白A诱导的小鼠肝炎的保护作用。
Journal of Ethnopharmacology ( IF 4.8 ) Pub Date : 2018-02-09 , DOI: 10.1016/j.jep.2018.02.003
Huan-Huan Tang ₁ , Hai-Long Li ₂ , Yue-Xuan Li ₃ , Yan You ₃ , Yun-Yun Guan ₃ , Su-Lin Zhang ₃ , Li-Xin Liu ₃ , Wei-Lian Bao ₃ , Yong Zhou ₂ , Xiao-Yan Shen ₃

Affiliation

人类药理学关系江鲜护肝（JXHG）由淡水蛤（Corbicula fluminea），姜黄，女贞，女贞，草c和five药五种天然产物配制而成，具有很好的保肝作用。。这项研究的目的我们调查了JXHG对伴刀豆球蛋白A（ConA）诱导的小鼠急性活体损伤的影响，并阐明其潜在的分子机制。材料与方法降康灵胶囊（900 mg / kg），小剂量JXHG（LJXHG，700 mg / kg），大剂量JXHG（HJXHG，1400 mg / kg）于灌胃前20天每天口服给小鼠一次静脉注射ConA（20 mg / kg）。通过测量血清中酶和细胞因子的水平以及肝脏组织学分析来评估肝损伤。我们还测量了mRNA水平上细胞因子的肝表达以及与NF-κB和核因子（类胡萝卜素衍生的2）样2（Nrf2）信号通路相关的蛋白。结果我们的结果表明，JXHG预处理可显着减轻ConA诱导的活伤，这可通过降低血清谷氨酸-丙酮酸转氨酶（ALT）和谷氨酸草酰转氨酶（AST）以及降低肝细胞凋亡和死亡率来证明。此外，JXHG能够显着降低血清促炎细胞因子水平，下调白介素6（IL-6）和干扰素-γ（IFN-γ）的mRNA表达，并上调IL-10和Con A注射后肝脏组织中的超氧化物歧化酶1（SOD1），谷胱甘肽还原酶（GSR）和谷胱甘肽过氧化物酶2（GPX2）mRNA的表达。此外，JXHG预处理可显着抑制NF-κBp65（p65）的磷酸化，增加Nrf2表达，并降低肝组织中裂解的caspase-3 / caspase-3的表达率。结论这些结果表明，JXHG通过抑制NF-κB介导的炎症途径和促进Nrf2介导的抗氧化应激信号通路来预防ConA诱导的急性活伤。

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Protective effects of a traditional Chinese herbal formula Jiang-Xian HuGan on Concanavalin A-induced mouse hepatitis via NF-κB and Nrf2 signaling pathways.

ETHNOPHARMACOLOGICAL RELEVANCE Jiang-Xian HuGan (JXHG) formulated by five natural products including Freshwater clam (Corbicula fluminea), Curcuma longa L., Ligustrum lucidum, Eclipta prostrata (L.) L. and Paeonia lactiflora Pall., has exhibited a great hepatoprotective effect. AIM OF THIS STUDY We investigated the effect of JXHG on concanavalin A (ConA)-induced acute live injury in mice, and to elucidate its underlying molecular mechanisms. MATERIALS AND METHODS Jiangkanling Capsule (900 mg/kg), low-dose JXHG (LJXHG, 700 mg/kg), high-dose JXHG (HJXHG, 1400 mg/kg) were administered to mice by oral gavage daily for 20 days prior to a single intravenous injection of ConA (20 mg/kg). Liver injury was evaluated by measuring the serum levels of enzymes and cytokines as well as liver histological analysis. We also measured the hepatic expression of cytokines at mRNA levels and the proteins related to NF-κB and Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling pathways. RESULT Our results showed that JXHG pretreatment significantly alleviated ConA-induced live injury as evidenced by decreased serum levels of glutamic-pyruvic transaminase (ALT) and glutamic oxalacetic transaminase (AST), and reduced hepatocyte apoptosis and mortality. Furthermore, JXHG was able to significantly reduce the serum levels of proinflammatory cytokines, down-regulate the mRNA expression of interleukin-6 (IL-6) and interferon-γ (IFN-γ), and up-regulate IL-10 as well as superoxide-dimutase-1 (SOD1), glutathione reductase (GSR) and Glutathione peroxidase 2 (GPX2) mRNA in the liver tissues after Con A injection. In addition, JXHG pretreatment dramatically suppressed the phosphorylation of NF-κB p65 (p65), increased Nrf2 expression, and decreased the expression ratio of cleaved caspase-3/caspase-3 in liver tissues. CONCLUSION These results suggest that JXHG protects against ConA-induced acute live injury through inhibiting NF-κB mediated inflammatory pathway and promoting Nrf2 mediated anti-oxidative stress signaling pathway.

更新日期：2019-11-01

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