Objective: To explore the effects of Anwei decoction (AD) on the protein expression of TFF in rats with chronic atrophic gastritis(CAG). Methods: Forty-eight healthy rats were randomly divided into 4 groups: normal co...Objective: To explore the effects of Anwei decoction (AD) on the protein expression of TFF in rats with chronic atrophic gastritis(CAG). Methods: Forty-eight healthy rats were randomly divided into 4 groups: normal control group, pathologic model group, Anwei Decoction group, and Weifuchun group. CAG was induced in rats with N-methy-N-nitro-N-nitrogua-nidine (MNNG). The protein expression of TFF in rats’ gastric mucosa was determined by immunohistochemistry. Results: Compared with that in the normal control group, the protein expression of TFF1 was significantly enhanced in the pathologic model, Anwei Decoction and Weifuchun groups (both P TFF1 was significantly higher in the Anwei Decoction group than in the Weifuchun group (P < 0.01). Compared with the normal control group, the protein expression of TFF2 was significantly enhanced in the pathologic model, Anwei Decoction and Weifuchun groups (both P < 0.01). The protein expression level of TFF2 was significantly higher in the Anwei Decoction group than in the Weifuchun group (P < 0.01). In comparison with the pathologic model group, the protein expression of TFF3 was remarkably reduced in Anwei Decoction and Weifuchun groups (both P < 0.01). but there was no difference between the group of Anwei decoction and the group of Weifuchun (P > 0.05). Conclusion: Anwei decoction may be effective in the treatment of CAG by enhancing the protein expression of TFF1, TFF2 while reducing that of TFF3 in gastric mucosas.展开更多
背景众多证据表明免疫逃逸在肿瘤形成过程中扮演重要角色,慢性萎缩性胃炎(chronic atrophic gastritis,CAG)是胃癌的癌前疾病.安胃汤被发现可改善CAG临床症状及病理表现,实现CAG的逆转,该作用是否与免疫逃逸机制相关有待进一步研究.目...背景众多证据表明免疫逃逸在肿瘤形成过程中扮演重要角色,慢性萎缩性胃炎(chronic atrophic gastritis,CAG)是胃癌的癌前疾病.安胃汤被发现可改善CAG临床症状及病理表现,实现CAG的逆转,该作用是否与免疫逃逸机制相关有待进一步研究.目的从细胞免疫逃逸角度,探讨程序性死亡受体-1(programmed cell death protein 1,PD-1)/程序性死亡受体配体-1(programmed cell death ligand 1,PD-L1)信号轴与安胃汤对CAG模型大鼠疗效之间的关系.方法采用1-甲基-3-硝基-1-亚硝基胍(1-Methyl-3-nitro-1-nitrosoguanidine,MNNG)慢性萎缩性胃炎大鼠模型,应用不同剂量安胃汤及维酶素片进行干预;HE染色观察安胃汤对CAG模型大鼠胃黏膜炎症细胞浸润及组织形态改变的影响;免疫组化检测CAG模型大鼠胃黏膜组织PD-1、PD-L1蛋白表达;ELISA检测血清CD4^(+)、CD8^(+)水平变化;qPCR检测CAG模型大鼠胃黏膜PD-1mRNA、PD-L1mRNA表达;Western-blot检测CAG模型大鼠胃黏膜组织PD-1、PD-L1蛋白表达.结果免疫组化结果示:与模型组和维酶素组比较,安胃汤高、低剂量组PD-L1表达均较低(P<0.01,P<0.05).ELISA实验结果示:与模型组比较,安胃汤高剂量组CD4^(+)表达及CD4^(+)/CD8^(+)比值升高(P<0.01,P<0.05),安胃汤各组和维酶素组CD8^(+)表达降低(P<0.01);与维酶素组比较,安胃汤高剂量组CD8^(+)表达降低(P<0.05).qPCR实验结果显示:与模型组比较,安胃汤高剂量组和维酶素组PD-1mRNA表达下降(P<0.01),安胃汤高、中剂量组PD-L1mRNA表达下降(P<0.01,P<0.05).Western-blot实验结果显示:与模型组比较,安胃汤高、中剂量组PD-1/Actin,PD-L1/Actin表达下降(P<0.01,P<0.05).结论安胃汤抗CAG作用可能与抑制PD-1/PD-L1信号通路诱导的细胞免疫逃逸有关.展开更多
目的探讨安胃汤对实验性慢性萎缩性胃炎大鼠模型的TFF1 mRNA表达的影响。方法采用甲基硝基亚硝基胍(MNNG)慢性萎缩性胃炎大鼠模型,48只清洁级健康雄性Wistar大鼠随机分为空白组、病理模型组、安胃汤组、胃复春对照组共4组。光学显微镜...目的探讨安胃汤对实验性慢性萎缩性胃炎大鼠模型的TFF1 mRNA表达的影响。方法采用甲基硝基亚硝基胍(MNNG)慢性萎缩性胃炎大鼠模型,48只清洁级健康雄性Wistar大鼠随机分为空白组、病理模型组、安胃汤组、胃复春对照组共4组。光学显微镜观察胃黏膜病理变化,实时定量PCR方法观察安胃汤对实验性慢性萎缩性胃炎大鼠模型胃黏膜TFF1 mRNA表达的影响。结果安胃汤与胃复春均能改善胃黏膜的病理形态,但以安胃汤效果为佳。与病理模型组相比,安胃汤组和胃复春对照组均显著提高TFF1 mRNA/-βactin相对表达量比值(0.86±0.13 vs 0.54±0.10and 0.83±0.10 vs 0.54±0.10,P<0.01),安胃汤组优于胃复春对照组(0.86±0.13 vs 0.83±0.10,P<0.01)。结论安胃汤能够改善慢性萎缩性胃炎大鼠模型胃黏膜的病理形态,可能通过增加胃黏膜TFF1 mRNA表达而起到治疗CAG作用。展开更多
文摘Objective: To explore the effects of Anwei decoction (AD) on the protein expression of TFF in rats with chronic atrophic gastritis(CAG). Methods: Forty-eight healthy rats were randomly divided into 4 groups: normal control group, pathologic model group, Anwei Decoction group, and Weifuchun group. CAG was induced in rats with N-methy-N-nitro-N-nitrogua-nidine (MNNG). The protein expression of TFF in rats’ gastric mucosa was determined by immunohistochemistry. Results: Compared with that in the normal control group, the protein expression of TFF1 was significantly enhanced in the pathologic model, Anwei Decoction and Weifuchun groups (both P TFF1 was significantly higher in the Anwei Decoction group than in the Weifuchun group (P < 0.01). Compared with the normal control group, the protein expression of TFF2 was significantly enhanced in the pathologic model, Anwei Decoction and Weifuchun groups (both P < 0.01). The protein expression level of TFF2 was significantly higher in the Anwei Decoction group than in the Weifuchun group (P < 0.01). In comparison with the pathologic model group, the protein expression of TFF3 was remarkably reduced in Anwei Decoction and Weifuchun groups (both P < 0.01). but there was no difference between the group of Anwei decoction and the group of Weifuchun (P > 0.05). Conclusion: Anwei decoction may be effective in the treatment of CAG by enhancing the protein expression of TFF1, TFF2 while reducing that of TFF3 in gastric mucosas.
文摘背景众多证据表明免疫逃逸在肿瘤形成过程中扮演重要角色,慢性萎缩性胃炎(chronic atrophic gastritis,CAG)是胃癌的癌前疾病.安胃汤被发现可改善CAG临床症状及病理表现,实现CAG的逆转,该作用是否与免疫逃逸机制相关有待进一步研究.目的从细胞免疫逃逸角度,探讨程序性死亡受体-1(programmed cell death protein 1,PD-1)/程序性死亡受体配体-1(programmed cell death ligand 1,PD-L1)信号轴与安胃汤对CAG模型大鼠疗效之间的关系.方法采用1-甲基-3-硝基-1-亚硝基胍(1-Methyl-3-nitro-1-nitrosoguanidine,MNNG)慢性萎缩性胃炎大鼠模型,应用不同剂量安胃汤及维酶素片进行干预;HE染色观察安胃汤对CAG模型大鼠胃黏膜炎症细胞浸润及组织形态改变的影响;免疫组化检测CAG模型大鼠胃黏膜组织PD-1、PD-L1蛋白表达;ELISA检测血清CD4^(+)、CD8^(+)水平变化;qPCR检测CAG模型大鼠胃黏膜PD-1mRNA、PD-L1mRNA表达;Western-blot检测CAG模型大鼠胃黏膜组织PD-1、PD-L1蛋白表达.结果免疫组化结果示:与模型组和维酶素组比较,安胃汤高、低剂量组PD-L1表达均较低(P<0.01,P<0.05).ELISA实验结果示:与模型组比较,安胃汤高剂量组CD4^(+)表达及CD4^(+)/CD8^(+)比值升高(P<0.01,P<0.05),安胃汤各组和维酶素组CD8^(+)表达降低(P<0.01);与维酶素组比较,安胃汤高剂量组CD8^(+)表达降低(P<0.05).qPCR实验结果显示:与模型组比较,安胃汤高剂量组和维酶素组PD-1mRNA表达下降(P<0.01),安胃汤高、中剂量组PD-L1mRNA表达下降(P<0.01,P<0.05).Western-blot实验结果显示:与模型组比较,安胃汤高、中剂量组PD-1/Actin,PD-L1/Actin表达下降(P<0.01,P<0.05).结论安胃汤抗CAG作用可能与抑制PD-1/PD-L1信号通路诱导的细胞免疫逃逸有关.
文摘目的探讨安胃汤对实验性慢性萎缩性胃炎大鼠模型的TFF1 mRNA表达的影响。方法采用甲基硝基亚硝基胍(MNNG)慢性萎缩性胃炎大鼠模型,48只清洁级健康雄性Wistar大鼠随机分为空白组、病理模型组、安胃汤组、胃复春对照组共4组。光学显微镜观察胃黏膜病理变化,实时定量PCR方法观察安胃汤对实验性慢性萎缩性胃炎大鼠模型胃黏膜TFF1 mRNA表达的影响。结果安胃汤与胃复春均能改善胃黏膜的病理形态,但以安胃汤效果为佳。与病理模型组相比,安胃汤组和胃复春对照组均显著提高TFF1 mRNA/-βactin相对表达量比值(0.86±0.13 vs 0.54±0.10and 0.83±0.10 vs 0.54±0.10,P<0.01),安胃汤组优于胃复春对照组(0.86±0.13 vs 0.83±0.10,P<0.01)。结论安胃汤能够改善慢性萎缩性胃炎大鼠模型胃黏膜的病理形态,可能通过增加胃黏膜TFF1 mRNA表达而起到治疗CAG作用。
