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作 者:余娜[1] 张有才[1] 杜倩 权松霞[2] YU Na;ZHANG You-cai;DU Qian;QUAN Song-xia(The People′s Hospital of Jiaozuo,Department of Nephrology,Henan Jiaozuo 454000,China;不详)
机构地区:[1]焦作市人民医院肾内科,河南焦作454000 [2]郑州大学第一附属医院肾脏病理科
出 处:《江苏预防医学》2021年第3期296-300,共5页Jiangsu Journal of Preventive Medicine
摘 要:目的探究F630028O10Rik-siRNA对链脲佐菌素(STZ)诱导的大鼠糖尿病肾病(DN)损伤的保护作用及其机制。方法将30只经STZ(55mg/kg)注射处理后,造模成功的DN大鼠,随机平均分为模型组、空载体组和F630-siRNA组,10只未造模大鼠设为空白组。F630-siRNA组和空载体组分别注射200μl F630-siRNA(5×108 TU/ml)慢病毒载体和F630空载体。采用生化分析仪检测空腹血糖(FBG)、24h尿蛋白(mAlb)、血肌酐(Src)、血尿素氮(BUN),ELISA法检测血清中白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)和瘤坏死因子-α(TNF-α)含量,Western blot检测肾组织中NF-κB通路和肾脏纤维化相关蛋白水平。结果与空载体组比较,F630-siRNA组大鼠FBG、mAlb、Src和BUN水平明显下降,血清中IL-6、IL-1β和TNF-α含量,肾脏中IKKα/β、p-p65、p-IκBα、TGF-β1和α-SMA水平均显著下调(P值均<0.05)。模型组、空载体组和F630-siRNA组各项指标均高于空白组(P值均<0.05);模型组与空载体组差异均无统计学意义(P值均>0.05)。结论 F630028O10Rik-siRNA可能通过抑制NF-κB通路激活,抑制炎症因子的表达和改善肾纤维化,实现对糖尿病肾病大鼠的肾损伤保护。Objective To explore the protective effect and mechanism of F630028 O10 Rik-siRNA on streptozocin(STZ)-induced diabetic nephropathy(DN)damage in rats.Methods A total of 30 rats were injected with STZ(55 mg/kg)to establish DN models,which were randomly divided into model group,empty vector group and F630-siRNA group;while 10 rats not injected with STZ were set as blank group.The F630-siRNA group was injected with 200μl F630-siRNA(5×108 TU/ml)lentiviral vector,and the empty vector group was injected with the same amount of F630 empty vector.Biochemical analyzer was used to detect fasting blood glucose(FBG),24 hurine protein(mAlb),blood creatinine value(Src)and blood urea nitrogen(BUN)levels;while ELISA was used to detect serum levels of interleukin-6(IL-6),IL-1βand TNF-α;the Western blot was used to detect the levels of NF-κB pathway and renal fibrosis-related proteins in renal tissues.Results Compared with the empty vector group,the levels of FBG,mAlb,Src and BUN in F630-siRNA group significantly decreased,the serum levels of IL-6,IL-1βand TNF-αlevels and the kidney IKKα/β,p-p65,P-IκBα,TGF-β1 andα-SMA levels were also significantly downregulated(all P<0.05).All indexes of model group,empty vector group and F630-siRNA group were higher than those of blank group(all P<0.05).There were no significant differences of indexes between the model group and the empty vector group(all P>0.05).Conclusion F630028 O10 Rik-siRNA may inhibit the expression of inflammatory factors and improve renal fibrosis by inhibiting the activation of NF-κB pathway to protect the kidney from DN in rats.
关 键 词:糖尿病肾病 长链非编码RNA F630028O10Rik 炎症因子 NF-ΚB通路
分 类 号:R114[医药卫生—卫生毒理学]
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