摘要
目的探究基于PI3K/Akt/mTOR信号通路上调miR-155对糖尿病肾病大鼠的干预效果影响。方法选取40只SPF级Wistar大鼠,随机分为对照组、模型组、miR-155抑制剂组,miR-155模拟物组,每组10只,模型组、miR-155抑制剂组,miR-155模拟物组大鼠构建糖尿病肾病模型,成功后miR-155抑制剂组大鼠腹腔注射miR-155 inhibitor,miR-155模拟物组大鼠注射miR-155 mimic,对照组、模型组大鼠腹腔注射同剂量0.9%氯化钠溶液。结果与对照组相比,模型组、miR-155抑制剂组、miR-155模拟物组miR-155相对表达量下降(P<0.05),FPG、血肌酐、24 h尿蛋白、IL-6、TNF-α水平、肾组织细胞凋亡率、PI3K、Akt、mTOR表达量升高(P<0.05);与模型组相比,miR-155抑制剂组miR-155表达水平下降(P<0.05),FPG、血肌酐、24 h尿蛋白、IL-6、TNF-α水平、肾组织细胞凋亡率、PI3K、Akt、mTOR表达量升高(P<0.05),miR-155模拟物组miR-155相对表达量升高,FPG、血肌酐、24 h尿蛋白、IL-6、TNF-α水平、肾组织细胞凋亡率、PI3K、Akt、mTOR表达量降低(P<0.05);与miR-155抑制剂组相比,miR-155模拟物组miR-155相对表达量升高(P<0.05),FPG、血肌酐、24 h尿蛋白、IL-6、TNF-α水平、肾组织细胞凋亡率、PI3K、Akt、mTOR表达量降低(P<0.05)。结论上调miR-155表达,可使大鼠肾组织细胞凋亡率降低,使大鼠肾损伤降低,其机制可能与PI3K/Akt/mTOR信号通路被抑制有关。
Objective To explore the intervention effect of overexpressed miR-155 on diabetic nephropathy(DN)rats by regulating the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR)signaling pathway.Methods A total of 40 specific-pathogen-free(SPF)Wistar rats were selected and randomly divided into control group,model group,miR-155 inhibitor group,and miR-155 mimic group,with 10 in each group,rats in the latter three groups were subjected to the establishment of DN model,followed by intraperitoneally injected with normal saline,miR-155 inhibitor and miR-155 mimic,respectively.Rats in the control group were intraperitoneally injected with the same amount of normal saline.Results Compared with control group,significantly downregulated miR-155,and increased fasting plasma glucose(FPG),serum creatine,24-h urine protein,interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),apoptotic rate in the kidney tissues,PI3K,Akt and mTOR were detected in model group,miR-155 inhibitor group and miR-155 mimic group(P<0.05).Compared with model group,significantly downregulated miR-155,and increased FPG,serum creatine,24-h urine protein,IL-6,TNF-α,apoptotic rate in the kidney tissues,PI3K,Akt and mTOR were detected in miR-155 inhibitor group,and the opposite trends of them were detected in miR-155 mimic group(P<0.05).Compared with miR-155 inhibitor group,significantly upregulated miR-155,and decreased FPG,serum creatine,24-h urine protein,IL-6,TNF-α,apoptotic rate in the kidney tissues,PI3K,Akt and mTOR were detected in miR-155 mimic group(P<0.05).Conclusion Overexpression of miR-155 decreases apoptotic rate in the kidney tissues and protects kidney injury in DR rats by inhibiting the PI3K/Akt/mTOR signaling pathway.
作者
梁衍
朱燕亭
高妍婷
张琳萍
LIANG Yan;ZHU Yanting;GAO Yanting(Nephrotic Hemodialysis Center,Shaanxi Provincial People’s Hospital,Shaanxi,Xi’an 710068,China)
出处
《河北医药》
CAS
2023年第12期1785-1788,1793,共5页
Hebei Medical Journal
基金
陕西省自然科学基础研究计划项目(编号:2021JQ-905)。
