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10.1111/j.1476-5381.2010.01070.x http://scihub22266oqcxt.onion/10.1111/j.1476-5381.2010.01070.x 20942814!3041257!20942814     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20942814&cmd=llinks): Failed to open stream: HTTP request failed! 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Scutellarin alleviates interstitial fibrosis and cardiac dysfunction of infarct rats by inhibiting TGFbeta1 expression and activation of p38-MAPK and ERK1/2 |pdf=|usr=}}{{20942814}} gab.com Text Scutellarin alleviates interstitial fibrosis and cardiac dysfunction of infarct rats by inhibiting TGFbeta1 expression and activation of p38-MAPK and ERK1/2 JO: Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=20942814 #FOAvip BACKGROUND AND PURPOSE: Interstitial fibrosis plays a causal role in the development of heart failure after chronic myocardial infarction (MI), and anti-fibrotic therapy represents a promising strategy to mitigate this pathological process. The purpose of this study was to investigate the effect of long-term administration of scutellarin (Scu) on cardiac interstitial fibrosis of myocardial infarct rats and the underlying mechanisms. EXPERIMENTAL APPROACH: Scu was administered to rats that were subjected to coronary artery ligation. Eight weeks later, its effects on cardiac fibrosis were assessed by examining cardiac function and histology. The number and collagen content of cultured cardiac fibroblasts exposed to angiotensin II (Ang II) were determined after the administration of Scu in vitro. Protein expression was detected by Western blot technique, and mRNA levels by quantitative reverse transcription-PCR. KEY RESULTS: The echocardiographic and haemodynamic measurements showed that Scu improved the impaired cardiac function of infarct rats and decreased interstitial fibrosis. Scu inhibited the expression of FN1 and TGFbeta1, but produced no effects on inflammatory cytokines (TNFalpha, IL-1beta and IL-6) in the 8 week infarct hearts. Scu inhibited the proliferation and collagen production of cardiac fibroblasts (CFs) and the up-regulation of FN1 and TGFbeta1 induced by Ang II. The enhanced phosphorylation of p38-MAPK and ERK1/2 in both infarct cardiac tissue and cultured CFs challenged by Ang II were suppressed by Scu. CONCLUSIONS AND IMPLICATIONS: Long-term administration of Scu improved the cardiac function of MI rats by inhibiting interstitial fibrosis, and the mechanisms may involve the suppression of pro-fibrotic cytokine TGFbeta1 expression and inhibition of p38 MAPK and ERK1/2 phosphorylation. Twit Text FOAVip Scutellarin alleviates interstitial fibrosis and cardiac dysfunction of infarct rats by inhibiting TGFbeta1 expression and activation of p38-MAPK and ERK1/2 ????Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=20942814 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20942814 #FOAvip English Wikipedia <ref>{{Cite pmid|20942814}}</ref> Scutellarin alleviates interstitial fibrosis and cardiac dysfunction of infarct rats by inhibiting TGFbeta1 expression and activation of p38-MAPK and ERK1/2 #MMPMID20942814 Pan Z; Zhao W; Zhang X; Wang B; Wang J; Sun X; Liu X; Feng S; Yang B; Lu Y Br J Pharmacol 2011[Feb]; 162 (3): 688-700 PMID20942814show ga BACKGROUND AND PURPOSE: Interstitial fibrosis plays a causal role in the development of heart failure after chronic myocardial infarction (MI), and anti-fibrotic therapy represents a promising strategy to mitigate this pathological process. The purpose of this study was to investigate the effect of long-term administration of scutellarin (Scu) on cardiac interstitial fibrosis of myocardial infarct rats and the underlying mechanisms. EXPERIMENTAL APPROACH: Scu was administered to rats that were subjected to coronary artery ligation. Eight weeks later, its effects on cardiac fibrosis were assessed by examining cardiac function and histology. The number and collagen content of cultured cardiac fibroblasts exposed to angiotensin II (Ang II) were determined after the administration of Scu in vitro. Protein expression was detected by Western blot technique, and mRNA levels by quantitative reverse transcription-PCR. KEY RESULTS: The echocardiographic and haemodynamic measurements showed that Scu improved the impaired cardiac function of infarct rats and decreased interstitial fibrosis. Scu inhibited the expression of FN1 and TGFbeta1, but produced no effects on inflammatory cytokines (TNFalpha, IL-1beta and IL-6) in the 8 week infarct hearts. Scu inhibited the proliferation and collagen production of cardiac fibroblasts (CFs) and the up-regulation of FN1 and TGFbeta1 induced by Ang II. The enhanced phosphorylation of p38-MAPK and ERK1/2 in both infarct cardiac tissue and cultured CFs challenged by Ang II were suppressed by Scu. CONCLUSIONS AND IMPLICATIONS: Long-term administration of Scu improved the cardiac function of MI rats by inhibiting interstitial fibrosis, and the mechanisms may involve the suppression of pro-fibrotic cytokine TGFbeta1 expression and inhibition of p38 MAPK and ERK1/2 phosphorylation. |*Erigeron[MESH] |Animals[MESH] |Apigenin/*therapeutic use[MESH] |Collagen/metabolism[MESH] |Cytokines/metabolism[MESH] |Drugs, Chinese Herbal/*therapeutic use[MESH] |Echocardiography[MESH] |Fibrosis[MESH] |Glucuronates/*therapeutic use[MESH] |Heart Failure/complications/*drug therapy/physiopathology[MESH] |Hemodynamics/drug effects/physiology[MESH] |Male[MESH] |Mitogen-Activated Protein Kinase 1/*metabolism[MESH] |Myocardial Infarction/complications/*drug therapy/pathology/physiopathology[MESH] |Phytotherapy[MESH] |Rats[MESH] |Rats, Wistar[MESH] |Transforming Growth Factor beta1/*metabolism[MESH] |Ventricular Dysfunction, Left/etiology/physiopathology[MESH] |Ventricular Remodeling/drug effects[MESH]Scutellarin alleviates interstitial fibrosis and cardiac dysfunction o(epmc).pdf DeepDyve Pubget Overpricing