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目的观察复方蜥蜴散不同微粒组合剂(下文简称蜥蜴散)对胃癌前病变(PLGC)大鼠Wnt信号通路下游靶蛋白C-Myc、Cyclin-D1表达的影响,从分子生物学水平对治疗PLGC进行探讨。方法 120只SD雄性大鼠随机分为空白组、模型组、蜥蜴散80目、100目、80+100目混合组及维酶素组6组,后五组采取MNNG配合饥饱失常及情绪刺激综合因素8周制备PLGC模型。造模成功后,治疗组分别用蜥蜴散不同组合剂及维酶素混悬液进行治疗,模型组给予生理盐水。通过光学显微镜来观察大鼠治疗前后胃黏膜的病理组织学变化,采用免疫组织化学法来检测大鼠胃组织C-Myc、Cyclin-D1靶蛋白的表达。结果 C-Myc、Cyclin-D1蛋白表达:模型组与空白组对比,差异具有统计学意义(P<0.05);各治疗组与模型组对比,差异具有统计学意义(P<0.05);蜥蜴散各治疗组与维酶素组对比,差异有统计学意义(P<0.05);蜥蜴散80目组、蜥蜴散100目组与蜥蜴散80+100目混合组对比,差异具有统计学意义(P<0.05)。结论蜥蜴散可以降低或抑制PLGC大鼠胃组织中增殖蛋白C-Myc和Cyclin-D1的表达,部分逆转其胃黏膜病理变化,揭示了其治疗PLGC的作用机制,可能是通过干预其黏膜增生、分化,促进其细胞凋亡,抑制细胞增殖,恢复其细胞增殖与凋亡之间的平衡,从而阻断胃癌前病变的,同时对胃黏膜的损害具有一定的保护与修复作用。
Objective To observe the effects of different composition of compound lizards (Lizard Powder) on the expressions of C-Myc and Cyclin-D1 in Wnt signaling pathway of gastric precancerous lesions (PLGC) rats. Discussion. Methods 120 SD male rats were randomly divided into blank group, model group, lizards scattered 80 mesh, 100 mesh, 80 + 100 mesh mixed group and vitamin enzyme group 6 group, followed by MNNG with MNNG disorders and emotional stimulation Comprehensive factors 8 weeks to prepare PLGC model. After successful modeling, the treatment group were treated with different combinations of lizard powder and vitamin enzyme suspension, the model group given saline. The histopathological changes of gastric mucosa before and after treatment were observed by light microscopy. The expression of C-Myc and Cyclin-D1 target proteins in gastric tissues of rats were detected by immunohistochemistry. Results The expressions of C-Myc and Cyclin-D1 in the model group were significantly lower than those in the blank group (P <0.05). The differences between the two groups were statistically significant (P <0.05) There was significant difference between each treatment group and Vitexin group (P <0.05), and the difference was statistically significant (P <0.05). Conclusion Lizzy Powder can reduce or inhibit the expression of proliferating proteins C-Myc and Cyclin-D1 in gastric mucosa of PLGC rats and partially reverse the pathological changes of gastric mucosa. The mechanism of action of lizards on PLGC may be related to the intervention of mucosal hyperplasia, Differentiation, promoting its apoptosis, inhibiting cell proliferation, restoring the balance between cell proliferation and apoptosis, thus blocking the precancerous lesions of gastric cancer, and at the same time having certain protective and repair effects on gastric mucosal damage.