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作 者:代二庆[1] 赵占考[1] 张明华[1] 张磊[1] 孙捍卫[1] 郑东明[1] 李翠翠[1]
出 处:《武警医学院学报》2009年第3期180-183,共4页Acta Academiae Medicinae CPAPF
基 金:天津市科委应用基础研究计划面上项目(05YFJMJC08400)
摘 要:【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 explore expression of apoptosis - related genes in the blood stasis and heat toxicity pattern patients. To study the effect of "Benefiting 5tomach I" on the treating of precancerosis gastric cancer, and the mechanism of apoptosis and its relatied genes expression. [Methods] A total of 82 cases of precancerous lesions of gastric cancer were divided into 2 groups at random, treatment group (pattern of blood stasis and heat toxicity group, treated with chinese herb) and control group (treated with hericium tablet). The hyperplasia of gastric epithelial cell was observed by microscope. The apoptosis and expression of fas , fas-L, bcl-2, and bax were detected by Tunel and immunohistochemical mcthod respectively, [ Results] The efficiency rate of treatment group (85.29%, n = 34) was higher than that of control group (29.17%, n = 48) .Apoptosis, fas and fas-L expression rate were significantly increased from (20.13 ± 11.23)%, 42.88%, 40.00% to (39.45 ± 16.24)%, 72.00%, 60.00%, but bcl- 2 expression rate was significantly decreased from 88.46% to 24% in treatment group (P 〈 0.05) . Control group didn't display obvious effect on gene expression. [ Conclusions] Genesis of the pattern of blood stasis and heat toxicity may be related with the apoptosis- related genes, Benefiting Stomach I is effective to precancerosis of gastric cancer (the pattem of blood stasis and heat toxicity), induce significantly gastric epithelial apoptosis , increese fas and fas-L expression but supprcss bcl-2 cxpression.
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