慢性萎缩性胃炎大鼠血瘀证的微观辨证研究

Study the pathogenesis of blood stasis syndrome in rats with chronic atrophic gastritis by microcosmic syndrome differentiation

[目的]通过微观辨证探讨慢性萎缩性胃炎(CAG)的主要病机以及活血化瘀中药的合理应用。[方法]采用N-甲基-N-硝基-N-亚硝基胍(MNNG)合并胃黏膜机械损伤方法制作CAG大鼠模型。选用具有活血化瘀作用的中药制剂阻癌胃泰进行预防和治疗给药,观察模型大鼠胃黏膜病理形态变化,同时检测血浆血栓素A2(TXA2)、前列环素(PGI2)在血液中的稳定代谢产物血栓素B2(TXB2)、6-酮-前列腺素F1α(6-keto-PGF1α)、血小板α颗粒膜蛋白(GMP-140)变化。[结果]活血化瘀中药组能明显阻断化学致癌物对黏膜的炎症损伤,改善癌前病变组织黏膜不典型增生程度,同时中药治疗后TXB2、、GMP-140水平明显低于病理对照组,6-keto-PGF1α明显高于对照组(P<0.05)。[结论]血瘀是CAG主要病机之一,活血化瘀中药可以广泛应用于CAG,不必拘泥于经典的血瘀证的症状和体征。

[Objective]To explore the pathogenesis of blood stasis syndrome in rats with CAG by microcosmic syndrome differentiation and the mechanism of the traditional Chinese medicine used to promote blood circulation and remove blood stasis. [Methods]Models of CAG were build by MNNG combined with mechanical injury of gastric mucosa in rats. Chinese drugs Zuaiweitai with action of promoting blood circulation and removing blood stasis, were chosen to prevent and treat CAG in rats. Pathologic change in gastric mucosa of rats were observed and TXB2, 6-keto-PGF1α, GMP-140 were detected [ Results] Traditional Chinese medicine used to promote blood circulation and remove blood stasis was able to block the inflammatory injury on mucosa caused by chemcial carcinogens, relieve atypical hyperplasia in mucosa of precancerous lesions. TXB2and GMP-140 in rats treated by Chinese medicine were obviously lower than those in pathological control group（P〈0.05）. The level of 6-keto-PGF1αwas significantly higher than that of control group（P〈0. 05）. [Conclusion ]Blood stasis is the main pathogenesis of CAG. The traditional Chinese medicine used to promote blood circulation and remove blood stasis was able to widely used in CAG and should not be restricted by the traditional symptoms and signs of blood stasis.