[Effects of telmisartan on inflammation and fibrosis after acute myocardial infarction in rats]

To explore the protection mechanisms of telmisartan on inflammation and fibrosis after myocardial infarction in rats.The model of acute myocardial infarction (AMI) was established by ligating left anterior descending coronary artery. The surviving rats were divided into AMI (AMI) and telmisartan treatment (telmisartan) groups. And another sham operation group (sham) was designated (n = 8). At the end of study, total heart weight (THW), left ventricular weight (LVW) and weight index were measured; myocardial infarction and inflammatory reactions detected by hematoxylin and eosin and Masson staining; the serum levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNFα), monocyte chemotactic protein-1 (MCP-1), interleukin-6 (IL-6) and interleukin-1 beta (IL-1β) by enzyme-linked immunosorbent assay (ELISA); the levels of transforming growth factor 1 (TGFβ1), collagen I, collagen III and MMP9 mRNA in myocardial tissue by reverse transcription-polymerase chain reaction (RT-PCR); the expressions of TGFβ1, collagen I, collagen III, matrix metallopeptidase 9 (MMP9) and nuclear factor-kappa B (NF-κB) by Western blot.Compared with sham group, significant pathological changes of myocardium occurred in AMI group. The serum levels of CRP [(472 ± 132) vs (104 ± 28) ng/ml], TNFα [(229 ± 41) vs (18 ± 5) pg/ml], MCP-1[(558 ± 116) vs (158 ± 20) pg/ml], IL-6 [(404 ± 63) vs (21 ± 4) pg/ml] and IL-1β [(625 ± 145) vs (189 ± 34) pg/ml] increased (P0.05). RT-PCR analysis showed that the expression levels of TGFβ1, collagen I, collagen III and MMP9 increased significantly. The results of Western blot were consistent and NF-κB was activated significantly (P0.05). Compared with AMI group, the above-mentioned indicators decreased obviously in telmisartan group (P0.05).Telmisartan may regulate inflammation and myocardial fibrosis after acute myocardial infarction by signaling pathways of NF-κB and TGFβ in rats.