Baicalin protects against ethanol-induced chronic gastritis in rats by inhibiting Akt/NF-κB pathway
Baicalin protects against ethanol-induced chronic gastritis in rats by inhibiting Akt/NF-κB pathway
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黄芩苷通过抑制 Akt/NF-kappa B 通路预防乙醇诱导的大鼠慢性胃炎
DOI：
10.1016/j.lfs.2019.117064
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发表时间：
2019-12-15
期刊：
影响因子：
6.1
通讯作者：
Wang, Xinhong
中科院分区：
文献类型：
--
作者：
Ji, Wanli;Liang, Kun;Wang, Xinhong
目的：目前，慢性胃炎是一种高发的消化系统疾病，常伴有食欲不振、腹痛和腹泻。黄芩苷属于黄芩的主要生物活性黄酮类化合物，具有抗炎和抗菌活性。然而，黄芩苷对乙醇诱导的胃炎的保护作用尚未完全阐明。我们的研究旨在评估黄芩苷对乙醇诱导的慢性胃炎的保护作用。
主要方法：通过给予56%乙醇4周诱导大鼠慢性胃炎模型。分别口服给予黄芩苷（50和100mg/kg）7天以评估其疗效。采用酶联免疫吸附测定（ELISA）法测定肿瘤坏死因子 -α（TNF -α）、白细胞介素（IL）- 8、IL - 1β、一氧化氮（NO）、内皮素 - 1（ET - 1）、前列腺素E2（PGE2）、乳酸脱氢酶（LDH）和环氧化酶 - 2（COX - 2）的产生量。通过蛋白质印迹法检测Akt、磷酸化Akt（p - Akt）、IκBα、磷酸化IκBα（p - IκBα）、核因子 -κBp65和磷酸化核因子 -κBp65（NF -κBp - p65）的活性。采用免疫荧光染色评估核因子 -κBp65的定位。
关键发现：组织病理学分析的变化以及NO、ET - 1、PGE2、LDH和COX - 2水平表明，黄芩苷治疗可改善乙醇诱导的胃炎。ELISA分析显示黄芩苷抑制了TNF -α、IL - 8和IL - 1β的水平。此外，黄芩苷显著抑制了Akt、p - Akt、IκBα、p - IκBα、NF -κBp65和NF -κBp - p65的表达。同时，通过免疫荧光染色，黄芩苷抑制了NF -κBp65向细胞核的转位，分子对接分析表明黄芩苷与Akt和NF -κBp65具有亲和力。
意义：所有结果表明，黄芩苷通过抑制炎症调节因子的水平和抑制Akt/核因子 -κB的激活，有效缓解慢性胃炎。
Aims: Currently, chronic gastritis is a high incidence of digestive diseases, along with loss of appetite, abdominal pain and diarrhea. Baicalin belongs to the major bioactive flavonoids compounds from Scutellariae Radix, it exhibited anti-inflammatory and anti-bacteria activities. Nonetheless, the protective effects of baicalin on ethanol-induced gastritis have not been completely clarified. Our study was designed to evaluate the protective activity of baicalin on ethanol-induced chronic gastritis.Main methods: Rat with chronic gastritis model was induced by the administration of 56% ethanol for four weeks. Baicalin (50 and 100 mg/kg) were orally administered for seven days to evaluate its curative effect, respectively. The production of TNF-alpha, interleukin (IL)-8, IL-1 beta, NO, ET-1, PGE2, LDH and COX-2 were determined by ELISA. The activities of Akt, p-Akt, I kappa B alpha, p-I kappa B alpha, NF-kappa Bp65 and NF-kappa Bp-p65 were tested by western blot. Immunofluorescence staining was employed to assess the location of NF-kappa Bp65.Key findings: The changes of the histopathological analysis and the levels of NO, ET-1, PGE2, LDH and COX-2 demonstrated that baicalin treatment ameliorated ethanol-induced gastritis. ELISA analysis showed that baicalin inhibited the levels of TNF-alpha, IL-8 and IL-1 beta. Besides, Akt, p-Akt, I kappa B alpha, p-I kappa B alpha, NF-kappa Bp65 and NF-kappa Bp-p65 expression were significantly suppressed by baicalin. Meanwhile, baicalin suppressed the translocation of NF-kappa Bp65 to the cell nucleus through immunofluorescence staining, molecular docking analysis showed that baicalin had affinity with Akt and NF-kappa Bp65.Significance: All results demonstrated that baicalin effectively alleviated chronic gastritis via suppressing the levels of inflammatory regulators and inhibiting Akt/NF-kappa B activation.