| 李有连,张秉丽,霍成英,朱海宏.吴茱萸碱对酒精性胃溃疡大鼠胃黏膜上皮细胞的保护作用.[J].中南医学科学杂志.,2022,(2):184-189. |
| 吴茱萸碱对酒精性胃溃疡大鼠胃黏膜上皮细胞的保护作用 |
| Protective effect of evodiamine on gastric mucosal epithelial cells in rats with alcoholic gastric ulcer |
| 投稿时间：2021-01-17 修订日期：2021-05-20 |
| DOI：10.15972/j.cnki.43-1509/r.2022.02.007 |
| 中文关键词: 吴茱萸碱 酒精性胃溃疡 胃黏膜上皮细胞 JAK2/STAT3信号通路 |
| 英文关键词:evodiline alcoholic gastric ulcer gastric mucosal epithelial cells JAK2/STAT3 signal pathway |
| 基金项目:青海省卫生计生指导性科研课题(【2015】18-17) 作者简介:李有连,主治医师,研究方向为消化系统疾病的治疗,E-mail为liyou741lian@163.com。 |
|
| 摘要点击次数: 430 |
| 全文下载次数: 246 |
| 中文摘要: |
| 目的观察吴茱萸碱(EVO)对酒精性胃溃疡大鼠胃黏膜上皮细胞的保护作用及机制。方法将实验大鼠随机分为对照组、模型组、奥美拉唑组、EVO高剂量组、EVO低剂量组和酪氨酸蛋白激酶2特异性抑制剂(AG490)组。使用药物预处理7天后,除对照组外的大鼠通过灌胃无水乙醇(5 mL/kg)造成酒精性胃溃疡模型。计算各组大鼠胃溃疡面积及胃溃疡抑制率；HE和TUNEL染色检测胃黏膜病变和细胞凋亡,ELISA法检测胃黏膜组织中氧化应激指标超氧化物歧化酶(SOD)、丙二醛(MDA)和肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)的水平,Western blotting法检测胃黏膜组织B淋巴细胞瘤-2基因(Bcl-2)、Bcl-2关联X蛋白(Bax)、酪氨酸蛋白激酶2(JAK2)、磷酸化的JAK2(p-JAK2)、信号转导与转录激活因子3(STAT3)及磷酸化的STAT3(p-STAT3)蛋白表达。结果与对照组比较,模型组大鼠胃黏膜组织溃疡面积和炎症浸润程度增加,血清TNF-α、IL-6含量增加,IL-10含量降低,胃黏膜上皮凋亡细胞数量增加,胃黏膜组织SOD活力和Bcl-2表达降低,MDA含量和Bax表达增加,JAK2和STAT3磷酸化水平增加(P＜0.05)。EVO可减轻胃溃疡模型大鼠胃黏膜组织损伤和炎症浸润,降低血清TNF-α、IL-6含量,增加IL-10含量,减少胃黏膜上皮凋亡细胞数量,增加胃黏膜组织SOD活力和Bcl-2表达,降低MDA含量和Bax表达,抑制JAK2和STAT3磷酸化。结论EVO能够抑制酒精性胃溃疡炎症反应、氧化应激和细胞凋亡,减轻组织损伤,其作用可能与调节JAK2/STAT3通路蛋白的表达有关。 |
| 英文摘要: |
| To observe the protective effect and mechanism of evodialine (EVO) on gastric mucosal epithelial cells in rats with alcoholic gastric ulcer. MethodsExperimental rats were randomly divided into control group, model group, omeprazole group, EVO high-dose group, EVO low-dose group and the specific inhibitor of tyrosine protein kinase 2 (AG490) group, 10 animals in each group. In addition to control group, after 7 days of drug pretreatment, rats in each group were given ethanol (5 mL/kg) by gavage to establish alcoholic gastric ulcer model. The area of gastric ulcer and the inhibition rate of gastric ulcer were calculated. HE and TUNEL staining was used to detect gastric mucosal lesions and cell apoptosis. ELISA was used to detect the levels of oxidative stress indicators, superoxide dismutase (SOD), malondialdehyde (MDA), and tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and interleukin 10 (IL-10). Western blotting was used to detect the expression of B-cell lymphoma-2 (Bcl-2), BCL2-associated X protein (Bax), Janus activated kinase 2 (JAK2), phospho-JAK2 (p-JAK2), signal transducer and activator of transcription 3 (STAT3) and phospho-STAT3 (p-STAT3). ResultsCompared with the control group, the gastric mucosal tissue of the model group was significantly damaged, the ulcer area and the degree of inflammatory infiltration increased, the serum TNF-α, IL-6 content increased, the IL-10 content decreased, and the number of gastric mucosal epithelial apoptotic cells increased, SOD activity and Bcl-2 expression of gastric mucosal tissue decreased, MDA content and Bax expression increased, JAK2 and STAT3 phosphorylation levels increased(P＜0.05). EVO improved gastric mucosal tissue damage and inflammation of gastric ulcer model rats, reduced serum TNF-α, IL-6 content, increased IL-10 content, reduced the number of gastric mucosal epithelial apoptotic cells, and increased SOD activity and Bcl-2 expression of gastric mucosal tissues, reduced MDA content and Bax expression, inhibited JAK2 and STAT3 phosphorylation. ConclusionsEVO can inhibit alcoholic gastric ulcer inflammation, oxidative stress, cell apoptosis, and reduce tissue damage. Its effect may be related to the regulation of the expression of JAK2/STAT3 pathway proteins. |
| 查看全文 查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|