目的研究急性脑出血大鼠肝组织中IRAK-M表达的变化,并探讨涤痰通瘀方剂对急性脑出血大鼠肝损害的干预作用。方法通过建立SD大鼠急性脑出血模型,并随机分为中药组(酒大黄、胆南星、石菖蒲、蒲黄、三七、水蛭)、脑出血组、假手术组、正常...目的研究急性脑出血大鼠肝组织中IRAK-M表达的变化,并探讨涤痰通瘀方剂对急性脑出血大鼠肝损害的干预作用。方法通过建立SD大鼠急性脑出血模型,并随机分为中药组(酒大黄、胆南星、石菖蒲、蒲黄、三七、水蛭)、脑出血组、假手术组、正常组,每组分为24、48、72 h 3个时间亚组,检测每组肝脏组织IRAKM蛋白表达水平及肝组织肿瘤坏死因子-α(TNF-α)水平,并观察肝组织HE染色结果。结果脑出血模型组在造模后各个时间点IRAK-M蛋白表达水平较假手术组及正常组均明显降低(P<0.05);中药治疗组的IRAKM蛋白表达水平较脑出血模型组明显升高(P<0.05),与假手术组、正常组相比略有降低;中药治疗组及脑出血模型组肝脏IRAK-M蛋白表达水平与组织TNF-α水平呈负相关。结论 IRAK-M蛋白表达水平升高可能是抑制脑出血后诱发的LPS胞内信号转导炎性级联反应的重要因素;涤痰通瘀方剂可加强IRAK-M激酶活性,从而抑制炎症因子的释放,减轻急性脑出血大鼠肝脏损伤的程度。展开更多
目的:观察甲氨蝶呤(MTX)联合不同中药影响Ⅱ型胶原诱导关节炎(CIA)大鼠血清肿瘤坏死因子-α(TNF-α)以及孤核受体m RNA(RORγt m RNA)表达的差异。方法:将Waster大鼠随机分为5组,建立Ⅱ型胶原诱导关节炎模型,正常组和模型组给予0.9%氯...目的:观察甲氨蝶呤(MTX)联合不同中药影响Ⅱ型胶原诱导关节炎(CIA)大鼠血清肿瘤坏死因子-α(TNF-α)以及孤核受体m RNA(RORγt m RNA)表达的差异。方法:将Waster大鼠随机分为5组,建立Ⅱ型胶原诱导关节炎模型,正常组和模型组给予0.9%氯化钠溶液灌胃,各给药组分别给予对应药品,6周后,各组大鼠经腹主动脉取血,采用ELISA法检测大鼠中血清TNF-α,以荧光PCR法检测大鼠脾脏RORγt m RNA表达,评价MTX联合中药对类风湿性关节炎治疗差异。结果:与正常组比较,模型组大鼠血清TNF-α及脾脏RORγt m RNA表达水平均有所升高(P<0.01);与模型组比较,各治疗组大鼠血清TNF-α及脾脏RORγt m RNA表达水平降低(P<0.01)。与MTX组比较,MTX+雷公藤组和MTX+海蛇药酒组大鼠血清TNF-α及脾脏RORγt m RNA表达水平均明显降低(P<0.05)。结论:MTX、MTX联合雷公藤与海蛇药酒对CIA大鼠有一定的治疗作用,且MTX+雷公藤、MTX+海蛇药酒治疗效果最佳,能显著下调关节滑膜RORγt m RNA的表达,降低血清TNF-α水平,从而发挥抑制关节炎性反应的作用。展开更多
High mycoplasmal infection ratio in gastric cancer tissues suggests a possible association between my-coplasma infection and tumorigenesis. Because TNF-a plays an important role in carcinogenesis caused by microbes in...High mycoplasmal infection ratio in gastric cancer tissues suggests a possible association between my-coplasma infection and tumorigenesis. Because TNF-a plays an important role in carcinogenesis caused by microbes in-fection and P37 is a major immunogen of mycoplasma hy-orhinis (M. hyor.), investigating whether P37 could induceexpression and secretion of TNF-a will be very significant to elucidate the possible molecular mechanism of gastric car-cinogenesis involved with M. hyor. At the present study, we cloned full gene of p37 by PCR and mutated the 7 codes of TGA into TGG firstly, then expressed the P37 protein suc-cessfully with pGEX-4T-1 vector in E. coli, which was veri-fied with Western blot. By RT-PCR and sensitive L929 cell toxic assay, we found that P37 protein could induce expres-sion and secretion of TNF-a from human peripheral bloodmononuclear cells, and the inducing activity of P37 could be dramatically blocked by McAb PD4. These results suggestthat the induction of TNF-a secretion by P37 probably plays an important role in diseases caused by M. hyor. infectionand needs to be further investigated.展开更多
文摘目的研究急性脑出血大鼠肝组织中IRAK-M表达的变化,并探讨涤痰通瘀方剂对急性脑出血大鼠肝损害的干预作用。方法通过建立SD大鼠急性脑出血模型,并随机分为中药组(酒大黄、胆南星、石菖蒲、蒲黄、三七、水蛭)、脑出血组、假手术组、正常组,每组分为24、48、72 h 3个时间亚组,检测每组肝脏组织IRAKM蛋白表达水平及肝组织肿瘤坏死因子-α(TNF-α)水平,并观察肝组织HE染色结果。结果脑出血模型组在造模后各个时间点IRAK-M蛋白表达水平较假手术组及正常组均明显降低(P<0.05);中药治疗组的IRAKM蛋白表达水平较脑出血模型组明显升高(P<0.05),与假手术组、正常组相比略有降低;中药治疗组及脑出血模型组肝脏IRAK-M蛋白表达水平与组织TNF-α水平呈负相关。结论 IRAK-M蛋白表达水平升高可能是抑制脑出血后诱发的LPS胞内信号转导炎性级联反应的重要因素;涤痰通瘀方剂可加强IRAK-M激酶活性,从而抑制炎症因子的释放,减轻急性脑出血大鼠肝脏损伤的程度。
文摘目的:观察甲氨蝶呤(MTX)联合不同中药影响Ⅱ型胶原诱导关节炎(CIA)大鼠血清肿瘤坏死因子-α(TNF-α)以及孤核受体m RNA(RORγt m RNA)表达的差异。方法:将Waster大鼠随机分为5组,建立Ⅱ型胶原诱导关节炎模型,正常组和模型组给予0.9%氯化钠溶液灌胃,各给药组分别给予对应药品,6周后,各组大鼠经腹主动脉取血,采用ELISA法检测大鼠中血清TNF-α,以荧光PCR法检测大鼠脾脏RORγt m RNA表达,评价MTX联合中药对类风湿性关节炎治疗差异。结果:与正常组比较,模型组大鼠血清TNF-α及脾脏RORγt m RNA表达水平均有所升高(P<0.01);与模型组比较,各治疗组大鼠血清TNF-α及脾脏RORγt m RNA表达水平降低(P<0.01)。与MTX组比较,MTX+雷公藤组和MTX+海蛇药酒组大鼠血清TNF-α及脾脏RORγt m RNA表达水平均明显降低(P<0.05)。结论:MTX、MTX联合雷公藤与海蛇药酒对CIA大鼠有一定的治疗作用,且MTX+雷公藤、MTX+海蛇药酒治疗效果最佳,能显著下调关节滑膜RORγt m RNA的表达,降低血清TNF-α水平,从而发挥抑制关节炎性反应的作用。
基金supported by the National Natural Science Foundation of China(Grant No.30130190)Beijing Natural Science Foudation(Grant No.7012007)and Cancer Center of Peking University.
文摘High mycoplasmal infection ratio in gastric cancer tissues suggests a possible association between my-coplasma infection and tumorigenesis. Because TNF-a plays an important role in carcinogenesis caused by microbes in-fection and P37 is a major immunogen of mycoplasma hy-orhinis (M. hyor.), investigating whether P37 could induceexpression and secretion of TNF-a will be very significant to elucidate the possible molecular mechanism of gastric car-cinogenesis involved with M. hyor. At the present study, we cloned full gene of p37 by PCR and mutated the 7 codes of TGA into TGG firstly, then expressed the P37 protein suc-cessfully with pGEX-4T-1 vector in E. coli, which was veri-fied with Western blot. By RT-PCR and sensitive L929 cell toxic assay, we found that P37 protein could induce expres-sion and secretion of TNF-a from human peripheral bloodmononuclear cells, and the inducing activity of P37 could be dramatically blocked by McAb PD4. These results suggestthat the induction of TNF-a secretion by P37 probably plays an important role in diseases caused by M. hyor. infectionand needs to be further investigated.