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作 者:聂鑫[1] 余益本[2,3] 文格波[3] NIE Xin YU Yi-Ben WEN Ge-Bo(Department of Gerontology, the Dongfeng Hospital Affiliated to Hubei University of Medicine, Shiyan 442000, Chin)
机构地区:[1]湖北医药学院附属东风医院老年病科,十堰442000 [2]南华大学病原生物学重点实验室,衡阳421001 [3]南华大学国家临床医学研究中心,衡阳421001
出 处:《中国免疫学杂志》2016年第12期1769-1772,共4页Chinese Journal of Immunology
摘 要:目的:探讨吡格列酮对糖尿病肾病大鼠肾组织中TOLL受体4/MAPKs信号通路的影响。方法:将雄性SD随机分为对照组(n=8)和试验组(n=32)。试验组SD鼠造模成功后随机分为3组进行干预,应用Western blot检测对照组和干预组大鼠肾组织中丝裂原活化蛋白激酶ERK1/2及p38MAPK磷酸化水平。结果:与对照组比较,各组大鼠肾组织中TOLL受体4表达增强,其中ERK1/2与JNK磷酸化水平明显升高(P<0.05),但p38MAPK水平变化不明显(P>0.05);与模型组比较,吡咯列酮干预组大鼠肾组织中ERK1/2与p38MAPK磷酸化水平降低(P<0.05)。结论:吡格列酮通过TOLL受体4/MAPKs/ERK1/2与TOLL受体4/MAPKs/JNK信号通路来完成,延缓糖尿病肾病的发生与发展。Objective: To study the role of TOLL-like receptor4 /MAPKs pathway of renal tissue in the diabetic rats treated with piogitazone. Methods: The male Sprague Dawlry rats were randomly selected as the control group( n = 8) and experimental group( n =32). The experimental rats were randomly divided into three groups. The expression of ERK1 /2,JNK and p38 MAPK,and levels of their phosphorylation in kidney were measured by Western blot in control group and experimental group. Results: The expression of TOLLlike receptor 4 in all renal tissue in the diabetic rats were significantlyincreased than those in control group( P〈0. 01). Compared with the control group. The activity of p-ERK1 /2 and p38 MAPK significantly increased in each experimental group( P〈0. 05),but the expression level of p-JNK was no statistical significance. TOLL-like receptor 4 could regulatory effect on the phorylation of ERK1 /2 and p38 MAPK. Compared with the model group,the expression of p-ERK1 /2 and p38 MAPK significantly decreased( P〈0. 05),moreover,these changes were more significant in high-dose treated group( P〈0. 05). Conclusion: Pioglitazone inhibits the expression of TOLLlike receptor 4 of renal tissue in the diabetic rats,and these effects may be related to TOLL-like receptor 4 / ERK1 /2 and TOLL-like receptor 4 / p38 MAPK pathways.
关 键 词:盐酸吡格列酮 糖尿病肾病 TOLL受体4/MAPKs信号通路
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