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徐杰, 高雅, 吉燕萍, 连苑宇, 张可锋. 岩白菜素对D-GalN诱导大鼠急性肝损伤影响[J]. 中国公共卫生, 2022, 38(1): 70-74. DOI: 10.11847/zgggws1131528
引用本文: 徐杰, 高雅, 吉燕萍, 连苑宇, 张可锋. 岩白菜素对D-GalN诱导大鼠急性肝损伤影响[J]. 中国公共卫生, 2022, 38(1): 70-74. DOI: 10.11847/zgggws1131528
XU Jie, GAO Ya, JI Yan-ping, . Effect of bergenin on D-galactosamine-induced acute liver injury in rats[J]. Chinese Journal of Public Health, 2022, 38(1): 70-74. DOI: 10.11847/zgggws1131528
Citation: XU Jie, GAO Ya, JI Yan-ping, . Effect of bergenin on D-galactosamine-induced acute liver injury in rats[J]. Chinese Journal of Public Health, 2022, 38(1): 70-74. DOI: 10.11847/zgggws1131528

岩白菜素对D-GalN诱导大鼠急性肝损伤影响

Effect of bergenin on D-galactosamine-induced acute liver injury in rats

  • 摘要:
      目的  了解岩白菜素对D-GalN诱导急性肝损伤的保护作用及其作用机制。
      方法  将60只SD大鼠随机分为对照组、模型组、水飞蓟素组(120 mg/kg)及岩白菜素低、中、高剂量组(20、40、80 mg/kg),每组10只,各剂量组大鼠每天同一时间按10 mL/kg灌胃给药,对照组和模型组大鼠灌胃相应体积蒸馏水,每天1次,连续7 d。末次给药2 h后,按4 mL/kg腹腔注射D-GalN(700 mg/kg)建立动物急性肝损伤模型。16 h后,收集血液,采集肝组织。生化法检测大鼠血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)、总抗氧化能力(T-AOC)、总胆红素(TBIL)、总超氧化物歧化酶(T-SOD)、丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-Px)活性或含量;酶联免疫吸附法(ELISA)检测大鼠肝组织中γ – 干扰素(IFN-γ)、肿瘤坏死因子 – α(TNF-α)、白介素 – 1β(IL-1β)和IL-6含量;蛋白免疫印记法(Western blot)分析肝组织p-JNK、JNK、c-Jun、p-AMPK和AMPK的蛋白表达情况;HE染色检查肝组织病变程度。
      结果  与对照组比较,模型组大鼠血清中AST、ALT、TBIL活性和MDA含量明显升高(P < 0.01);与模型组比较,各岩白菜素组大鼠血清中AST、ALT、TBIL活性和MDA含量明显降低(P < 0.05),岩白菜素高、中剂量组大鼠血清中T-AOC、T-SOD和GSH-Px含量均升高(P < 0.01);与模型组比较,岩白菜素高、中剂量组大鼠肝组织中TNF-α、IL-1β和IL-6含量下降、IFN-γ含量升高(P < 0.01),p-JNK和c-Jun蛋白表达下调(P < 0.05)、p-AMPK表达上调(P < 0.01)。
      结论  岩白菜素对D-GalN诱导的大鼠急性肝损伤具有保护作用,其作用机制可能与激活AMPK/JNK信号通路抑制氧化应激与炎症反应有关。

     

    Abstract:
      Objective  To study protective effect and mechanism of bergenin on D-galactosamine (D-GalN)-induced acute liver injury in rats.
      Methods  Totally 60 Sprague-Dawley (SD) rats were randomly assigned into 6 groups (10 in each group): a control and a model group with saline, a silymarin group (120 mg/kg), and low, moderate and high bergenin groups (20, 40, 80 mg/kg). All the treatments were carried out by intragastric administration (10 mL/kg) once a day consecutively for 7 days. Two hours after the last administration, D-GalN (700 mg/kg) was intraperitoneally administered for all the rats to establish acute liver injury model, excepted for the control rats. Sixteen hours after the D-GalN injections, all rats′ blood and liver tissue specimens were collected. Biochemical methods were used to detect serum content or activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total antioxidant capacity (T-AOC), total bilirubin (TBIL), total superoxide dismutase (T-SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px); enzyme-linked immunosorbent assay (ELISA) was adopted to measure contents of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in liver tissues; and Western blot analysis was performed to determine phosphorylated c-Jun N-terminal kinase (p-JNK), JNK, c-Jun, phospharylated adenosine monophosphate-activated protein kinase (p-AMPK), and AMPK protein expressions in liver tissues, respectively. Pathological changes of liver tissues were observed with hematoxillin-eosin (HE) staining.
      Results  Compared with those in the control rats, serum activity of AST, ALT, TBIL and MDA were significantly increased in the model rats (all P < 0.01). In contrast to those in the model rats, serum AST, ALT, TBIL, and MDA were significantly reduced in the rats of the three bergenin groups (all P < 0.05) and the activity of serum T-AOC, T-SOD, and GSH-Px were significantly increased in the rats of moderate and high bergenin groups (all P < 0.01); in addition, significantly decreased TNF-α, IL-1β, IL-6 and increased IFN-γ (all P < 0.01), down-regulated p-JNK and c-Jun expressions (both P < 0.05) but up-regulated p-AMPK expression (P < 0.01) were detected in liver tissues of the rats of moderate and high bergenin groups.
      Conclusion  Bergenin possesses a protective effect on D-GalN-induced acute liver injury in rats and the mechanism of the effect may be related to the inhibition of oxidative stress and the regulation of AMPK/JNK signaling pathway.

     

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