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目的 :探讨胃炎消逆转胃癌癌前病变 (PL GC)的作用机制。方法 :采用链霉素抗生物素蛋白 -过氧化酶(L SAB)免疫组化法检测胃炎消治疗组及维酶素对照组共 35例胃癌癌前病变患者治疗前后 P1 6、周期素(Cyclin D1 )、视网膜母细胞瘤 (p Rb)的变化。结果 :抑癌基因 Rb、P1 6蛋白表达阳性率均随着胃粘膜病变的进展逐渐递减。癌基因 Cyclin D1 蛋白表达阳性率随着胃粘膜病变的进展逐渐递增。治疗后治疗组可使 Rb蛋白的表达率及表达强度明显增强 (P <0 .0 1) ,余无显著变化 (P >0 .0 5 ) ;对照组各指标的表达情况未有明显变化 (P >0 .0 5 )。结论 :胃炎消可能通过调整 P1 6 和 (或 ) Cyclin D1 异常基因的表达 ,使 p Rb处于低磷酸化状态 ,以利于病变的逆转。
Objective: To explore the mechanism of gastritis in reversing gastric precancerous lesions (PL GC). Methods: Serum levels of P1 6, cyclin (IL-6, IL-6, IL-6 and IL-6) in 35 patients with precancerous lesions of gastric cancer treated by Weishanxiao and Weizhi Su were detected by streptavidin-peroxidase D1), retinoblastoma (p Rb) changes. Results: The positive rate of tumor suppressor gene Rb and P1 6 protein gradually decreased with the progress of gastric mucosal lesions. The positive rate of oncogene Cyclin D1 protein gradually increases with the progress of gastric mucosal lesions. After treatment, the expression of Rb protein and the intensity of expression of Rb protein in the treatment group were significantly increased (P <0.01), while no significant changes were found in the treatment group (P> 0.05). The expression of Rb protein in the control group did not change significantly P> 0 .0 5). CONCLUSION: Gastritis can reduce the expression of p16 and / or cyclin D1 and make p Rb be in a state of hypophosphorylation to facilitate the reversal of the pathological changes.