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罗格列酮通过抑制TLR4/NF-κB信号通路减轻急性心肌梗死大鼠的心肌细胞凋亡。

Rosiglitazone alleviates myocardial apoptosis in rats with acute myocardial infarction via inhibiting TLR4/NF-κB signaling pathway.

作者信息

Ma Hongzhong, Du Juan, Feng Xiaoli, Zhang Yingjun, Wang Haihuan, Ding Suchun, Huang Aijie, Ma Jiahai

机构信息

Department of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China.

Department of Pathology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China.

出版信息

Exp Ther Med. 2020 Apr;19(4):2491-2496. doi: 10.3892/etm.2020.8479. Epub 2020 Jan 30.

DOI:10.3892/etm.2020.8479
PMID:32256726
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7086202/
Abstract

Influence of rosiglitazone on the myocardial apoptosis in rats with acute myocardial infarction (AMI) via the Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway was explored. A total of 30 healthy male Sprague-Dawley (SD) rats were randomly divided into group A (Sham group, n=10), group B (AMI model group, n=10) and group C (AMI model + rosiglitazone group, n=10) using a random number table. It was observed through H&E staining that group A had myocardial cells with normal morphology and infiltration of few inflammatory factors, while group B had swollen myocardial cells with disorderly and irregular morphology, large and dark-colored nuclei, infiltration of massive inflammatory factors, large amounts of fibrous tissue hyperplasia in the intercellular space, disorderly arranged, thickened and lengthened myocardial fibers with widened gaps. Moreover, group C exhibited infiltration of fewer inflammatory factors and more normal myocardial tissue structure compared with group B. According to the sirius-red staining results, group A had normally arranged myocardial cells with a small amount of collagen hyperplasia, while group B had collagen interstitial hyperplasia and higher content of myocardial collagen than group A. Compared with that in group B, the myocardial collagen deposit was substantially reduced in group C. TUNEL staining results showed that the apoptosis rate of rat myocardial cells in group B was obviously higher than that in group A (40.37 vs. 5.23%), and it was notably lower in group C than that in group B (24.82 vs. 40.37%). According to the western blot results, the protein expression levels of the inflammatory factors TLR-4 and NF-κB in rat myocardial tissues were notably raised in group B compared with those in group A, and they were evidently lower in group C than those in group B. Rosiglitazone inhibits the TLR4/NF-κB signaling pathway to produce a myocardioprotective effect.

摘要

探讨罗格列酮通过Toll样受体4(TLR4)/核因子-κB(NF-κB)信号通路对急性心肌梗死(AMI)大鼠心肌细胞凋亡的影响。采用随机数字表法将30只健康雄性Sprague-Dawley(SD)大鼠随机分为A组(假手术组,n = 10)、B组(AMI模型组,n = 10)和C组(AMI模型+罗格列酮组,n = 10)。苏木精-伊红(H&E)染色观察显示,A组心肌细胞形态正常,炎症因子浸润少;B组心肌细胞肿胀,形态紊乱、不规则,细胞核大且颜色深,大量炎症因子浸润,细胞间隙大量纤维组织增生,心肌纤维排列紊乱、增粗、延长,间隙增宽。此外,与B组相比,C组炎症因子浸润较少,心肌组织结构更正常。天狼星红染色结果显示,A组心肌细胞排列正常,胶原增生少量;B组胶原间质增生,心肌胶原含量高于A组。与B组相比,C组心肌胶原沉积明显减少。TUNEL染色结果显示,B组大鼠心肌细胞凋亡率明显高于A组(40.37%对5.23%),C组明显低于B组(24.82%对40.37%)。蛋白质印迹法结果显示,与A组相比,B组大鼠心肌组织中炎症因子TLR-4和NF-κB的蛋白表达水平明显升高,C组明显低于B组。罗格列酮通过抑制TLR4/NF-κB信号通路发挥心肌保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/3292c087739e/etm-19-04-2491-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/bfb7bc246679/etm-19-04-2491-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/8ebb708414d6/etm-19-04-2491-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/6809090247db/etm-19-04-2491-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/5daef92200e6/etm-19-04-2491-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/3292c087739e/etm-19-04-2491-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/bfb7bc246679/etm-19-04-2491-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/8ebb708414d6/etm-19-04-2491-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/6809090247db/etm-19-04-2491-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/5daef92200e6/etm-19-04-2491-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c853/7086202/3292c087739e/etm-19-04-2491-g04.jpg

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