参灵方对药源性胃黏膜损伤大鼠Bcl-2和Bax表达的影响

目的研究预先给予参灵方对佐剂性关节炎(adjuvant arthritis,AA)大鼠药源性胃黏膜损伤的保护作用。方法建立AA大鼠模型,造模成功后随机分为参灵方小、大剂量组、模型组、雷尼替丁组,每组10只,分别灌胃治疗(雷尼替丁组给予30mg·kg-1·d-1;参灵方2组分别给予参灵方3.5g·kg-1·d-1、7g·kg-1·d-1,28d后采用皮下注射消炎痛进一步诱导药源性胃黏膜损伤的动物模型,光学显微镜观察胃黏膜组织病理变化。免疫组织化学ABC法对大鼠胃黏膜组织凋亡相关蛋白Bcl-2、Bax的表达进行细胞计算机医学图像分析及统计学处理。结果参灵方可明显抑制消炎痛致AA大鼠损伤胃黏膜的细胞凋亡,诱导损伤的胃黏膜细胞增殖,上调Bcl-2表达、下调Bax表达,与模型组比较,差异有统计学意义(P<0.05)。结论参灵方抑制细胞凋亡,对AA大鼠药源性胃黏膜损伤有保护作用。

Effects of Cenling decoction on the expression of Bcl-2 and Bax in damaged gastric mucosa induced by drugs in AA rats

Objective To investigate the protective effect of Cenling decoction on damaged gastric mucosa induced by drugs in （ adjuvant arthritis） AA rats. Methods The AA models were established in rats, then the rats were randomly divided into model group, ranitidine group, Cenling decoction low-dose group, Cenling decoction high-dose group,with 10 rats in each group. The rats were given different drugs by gavage once a day, for 28 days （ ranitidine group 30mg ·kg - 1 ·d - 1 ; Cenling decoction groups 3.5 g·kg - 1 ·d - 1,7g ·kg - 1 ·d - l respectively）. The animal models of gastric mucous membrane injury were further induced by subcutaneous injections with indomethaein, then the pathological changes of gastric mucous membrane were observed under light microscope and by HE staining. The expressions of Bcl-2 and Bax protein were detected by immunohistochemical method, and the results were analyzed by cytocomputer image analysis and were treated statistically. Results As compared with model group, Cenling decoction could inhibit obviously the cell apoptosis of damaged gastric mucosa caused by indomethacin in AA rats, induce cell proliferation of damaged gastric mucosa, up-regulate expression of Bcl-2 protein and down-regulate expression of Bax protein, and there were significant differences between Cenling decoction groups and model group（ P 〈 0.05 ）. Conclusion Cenling decoction can obviously inhibit the apoptosis of gastric mucosal cells and has protective effect on the damaged gastric mucous membrane induced by drugs in AA rats.