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【目的】探讨血瘀热毒证型患者凋亡相关基因的表达,观察善胃Ⅰ号治疗血瘀热毒型胃癌前病变、促使胃癌前病变向正常胃黏膜逆转的作用,并从细胞凋亡和相关基因表达方面探讨其作用机理。【方法】82例患者均经胃镜与病理检查证实为胃癌前病变,随机分成2组,光镜观察治疗前后胃黏膜的增生情况,并采用原位末端标记法(Tunel)检测细胞凋亡,免疫组化检测fas、fas-L、bcl-2、bax的表达。【结果】治疗组(善胃Ⅰ号,血瘀热毒型)有效率85.29%(34例),优于对照组(猴头菌片)29.17%(48例)。治疗组细胞凋亡率和fas、fas-L表达率分别从(20.13±11.23)%、42.88%、40.00%升高至(39.45±16.24)%、72.00%、60.00%;而bcl-2表达率从88.46%下降至24%(P<0.05)。对照组猴头菌片无明显作用。【结论】血瘀热毒证型的发生可能与细胞凋亡相关基因有关,善胃Ⅰ号能有效治疗血瘀热毒型胃癌前病变,明显诱导胃癌前病变细胞凋亡,增强fas、fas-L表达而抑制bcl-2表达。
【Objective】 To investigate the expression of apoptosis-related genes in patients with syndrome of blood stasis and heat toxicity, observe the effect of Shanwei I on the treatment of blood stasis and heat-toxic precancerous lesions, and promote the reversion of gastric precancerous lesions to normal gastric mucosa, and from apoptosis The mechanism of action is discussed in relation to gene expression. 【Methods】 All the 82 patients were diagnosed as gastric precancerous lesions by gastroscopy and pathological examination. They were randomly divided into 2 groups. The proliferation of gastric mucosa was observed by light microscopy before and after treatment. The apoptosis was detected by in vitro endoscopy (Tunel). The expression of fas, fas-L, bcl-2 and bax was detected by histochemistry. [Results] The effective rate was 85.29% (34 cases) in the treatment group (good stomach I, blood stasis and heat-toxic type), which was better than 29.17% (48 cases) in the control group (heron head tablets). The rate of apoptosis and fas and fas-L expression in the treatment group increased from (20.13±11.23)%, 42.88%, 40.00% to (39.45±16.24)%, 72.00%, 60.00%, respectively; and the expression rate of bcl-2 was increased. From 88.46% to 24% (P<0.05). The control group of Hericium has no obvious effect. 【Conclusion】 The occurrence of blood stasis type syndrome may be related to apoptosis-related genes, Shanwei I can effectively treat blood stasis and heat-toxic precancerous lesions, significantly induce apoptosis of gastric precancerous lesions, and enhance fas and fas- L expression inhibits bcl-2 expression.