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目的:探讨萎胃康颗粒对大鼠慢性萎缩性胃炎(CAG)的治疗作用及其机制。方法:90只SD大鼠随机取出18只为正常对照组,其余鼠造模后随机分为4组,模型组、萎胃康高、低剂量组、三九胃泰组均采用多重刺激复制大鼠CAG模型。在造模成功后分别ig萎胃康6,3 g.kg-1,三九胃泰1.6 g.kg-1,0.9%的生理盐水20 mL.kg-1。用药30 d后HE染色、透射电镜观察大鼠胃黏膜萎缩情况,免疫组化法观察胃黏膜上皮细胞中增殖细胞核抗原(PCNA)和表皮生长因子受体(EGFR)的表达。结果:光镜和电镜下均显示,萎胃康高、低剂量组胃黏膜病理变化比模型组明显减轻。模型组PCNA标记指数44.96%和EGFR的平均吸光度(A)0.183±0.030,明显高于正常组PCNA标记指数29.30%和EGFR的A 0.125±0.039。萎胃康高、低剂量组PCNA标记指数分别为29.58%,29.97%,EGFR的A分别为0.100±0.023,0.104±0.027,与模型组比较,表达降低(P<0.05或P<0.01)。结论:中药萎胃康颗粒对慢性萎缩性胃炎大鼠胃黏膜有明显修复作用,其作用机制可能是通过抑制胃黏膜PCNA和EGFR的过度表达而抑制细胞增殖和恶性转化实现的。
Objective: To investigate the therapeutic effect of Weiweikang Granules on chronic atrophic gastritis (CAG) in rats and its mechanism. Methods: Totally 18 SD rats were randomly divided into normal control group and other rats were randomly divided into 4 groups. The model group, Weiweikang high, low dose and Sanjiuweitai groups were all duplicated by multiple stimulation Mouse CAG model. After successful model were ig Weiweikang 6,3 g.kg-1, Sanjiuweitai 1.6 g.kg-1, 0.9% saline 20 mL.kg-1. After 30 days of treatment, HE staining and transmission electron microscopy were used to observe the gastric mucosal atrophy in rats. The expression of proliferating cell nuclear antigen (PCNA) and epidermal growth factor receptor (EGFR) in gastric mucosal epithelial cells were observed by immunohistochemistry. Results: Both light and electron microscopy showed that the pathological changes of gastric mucosa in wuweikang high and low dose groups were significantly alleviated compared with model group. The PCNA labeling index (44.96%) and EGFR (A) 0.183 ± 0.030 in model group were significantly higher than those in normal group (29.30%) and EGFR (0.125 ± 0.039). The scores of PCNA were 29.58% and 29.97% respectively in the Wudangkang high and low dose groups, and were respectively 0.100 ± 0.023,0.104 ± 0.027 in the EGFR group (P <0.05 or P <0.01). Conclusion: Weiweikang Granule can obviously repair gastric mucosa in rats with chronic atrophic gastritis, and its mechanism may be through inhibition of overexpression of PCNA and EGFR in gastric mucosa and inhibition of cell proliferation and malignant transformation.