This study investigated the expression of hemeoxygenase-1 （HO-1） in rats with acute lung rejection and its implication. A valid rat orthotopic left lung transplantation model （SD rat→Wistar rat） was established b...This study investigated the expression of hemeoxygenase-1 （HO-1） in rats with acute lung rejection and its implication. A valid rat orthotopic left lung transplantation model （SD rat→Wistar rat） was established by using an improved three-cuff anastomosis technique. The rats were divided into control group, CoPP （HO-1 inducer）-treated group and ZnPP （HO-1 inhibitor）-treated group. The severity of acute rejection was graded on the basis of the morphologic changes of the lung samples stained with HE. The expression of HO-1 protein in lung tissue was detected by using immunohistochemistry and Western blot, and HO-1 mRNA activity was assayed by RT-PCR. The results showed that the expression of HO-1 protein was significantly increased with the acute rejection grading in rats （P〈0.01）. As compared with control and ZnPP-treated groups, the severity of acute rejection was not alleviated and the grade not reduced significantly in CoPP-treated group （P〉0.05）. It was concluded that HO-1 protein might be involved in the pathological process of post-graft acute rejection. The expression of HO-1 protein was increased gradually with aggravation of acute rejection, and HO-1 protein might be used as an index to monitor acute rejection after lung transplantation.展开更多
目的:研究急性肝损伤时大鼠肝脏HO-1/CO系统的变化规律,探讨HO-1和内源性CO的作用机制及其病理生理意义.方法:采用D-氨基半乳糖(GalN)和脂多糖(LPS)联合腹腔注射制备大鼠急性肝损伤模型,动态测定各时间点(3,6,12,24,36h)大鼠肝脏HO-1活...目的:研究急性肝损伤时大鼠肝脏HO-1/CO系统的变化规律,探讨HO-1和内源性CO的作用机制及其病理生理意义.方法:采用D-氨基半乳糖(GalN)和脂多糖(LPS)联合腹腔注射制备大鼠急性肝损伤模型,动态测定各时间点(3,6,12,24,36h)大鼠肝脏HO-1活性和蛋白表达情况,测定肝脏CO浓度以及血清ALT,AST水平和肝组织SOD活性、MDA含量变化.结果:GalN和LPS联合注射成功诱导了大鼠急性肝损伤,表现为染毒24h时大鼠血清ALT,AST水平以及肝组织MDA浓度显著升高(10872.5±708.5nkat/L,9246.8±814.7nkat/L,5.06±1.21μmol/g vs 1043.5±247.4nkat/L,1278.6±273.8nkat/L,2.03±0.59μmol/g,均P<0.01),SOD活性明显下降(813.7±168.3nkat/mg vs 1248.2±84.9nkat/mg,P<0.01),HE染色显示肝细胞出现严重损伤.染毒3-24h大鼠肝脏HO-1活性明显增强,6-24h呈现一定的时间依赖方式(4.02±0.74,5.97±1.51,6.13±1.18μmol/g vs 2.86±0.41μmol/g);Western blot测定结果亦显示,HO-1蛋白表达显著增强,24h时明显高于正常对照组(1.87±0.39 vs 0.37±0.09,P<0.01).正常大鼠肝脏的CO浓度极低,染毒后以时间依赖方式开始升高,并显著高于正常对照组(0.373±0.112,0.474±0.152,0.513±0.193μmol/g vs 0.172±0.041μmol/g,P<0.01),这与HO-1表达情况相一致.结论:大鼠急性肝损伤时出现HO-1活性增加和蛋白表达持续上调以及CO浓度迅速增高,提示HO-1/CO系统参与急性肝损伤的病理生理过程,其表达增加可能对机体有重要调节作用.展开更多
文摘This study investigated the expression of hemeoxygenase-1 （HO-1） in rats with acute lung rejection and its implication. A valid rat orthotopic left lung transplantation model （SD rat→Wistar rat） was established by using an improved three-cuff anastomosis technique. The rats were divided into control group, CoPP （HO-1 inducer）-treated group and ZnPP （HO-1 inhibitor）-treated group. The severity of acute rejection was graded on the basis of the morphologic changes of the lung samples stained with HE. The expression of HO-1 protein in lung tissue was detected by using immunohistochemistry and Western blot, and HO-1 mRNA activity was assayed by RT-PCR. The results showed that the expression of HO-1 protein was significantly increased with the acute rejection grading in rats （P〈0.01）. As compared with control and ZnPP-treated groups, the severity of acute rejection was not alleviated and the grade not reduced significantly in CoPP-treated group （P〉0.05）. It was concluded that HO-1 protein might be involved in the pathological process of post-graft acute rejection. The expression of HO-1 protein was increased gradually with aggravation of acute rejection, and HO-1 protein might be used as an index to monitor acute rejection after lung transplantation.
文摘目的:研究急性肝损伤时大鼠肝脏HO-1/CO系统的变化规律,探讨HO-1和内源性CO的作用机制及其病理生理意义.方法:采用D-氨基半乳糖(GalN)和脂多糖(LPS)联合腹腔注射制备大鼠急性肝损伤模型,动态测定各时间点(3,6,12,24,36h)大鼠肝脏HO-1活性和蛋白表达情况,测定肝脏CO浓度以及血清ALT,AST水平和肝组织SOD活性、MDA含量变化.结果:GalN和LPS联合注射成功诱导了大鼠急性肝损伤,表现为染毒24h时大鼠血清ALT,AST水平以及肝组织MDA浓度显著升高(10872.5±708.5nkat/L,9246.8±814.7nkat/L,5.06±1.21μmol/g vs 1043.5±247.4nkat/L,1278.6±273.8nkat/L,2.03±0.59μmol/g,均P<0.01),SOD活性明显下降(813.7±168.3nkat/mg vs 1248.2±84.9nkat/mg,P<0.01),HE染色显示肝细胞出现严重损伤.染毒3-24h大鼠肝脏HO-1活性明显增强,6-24h呈现一定的时间依赖方式(4.02±0.74,5.97±1.51,6.13±1.18μmol/g vs 2.86±0.41μmol/g);Western blot测定结果亦显示,HO-1蛋白表达显著增强,24h时明显高于正常对照组(1.87±0.39 vs 0.37±0.09,P<0.01).正常大鼠肝脏的CO浓度极低,染毒后以时间依赖方式开始升高,并显著高于正常对照组(0.373±0.112,0.474±0.152,0.513±0.193μmol/g vs 0.172±0.041μmol/g,P<0.01),这与HO-1表达情况相一致.结论:大鼠急性肝损伤时出现HO-1活性增加和蛋白表达持续上调以及CO浓度迅速增高,提示HO-1/CO系统参与急性肝损伤的病理生理过程,其表达增加可能对机体有重要调节作用.
