Peroxisome proliferator-activated receptor delta agonists attenuated the C-reactive protein-induced pro-inflammation in cardiomyocytes and H9c2 cardiomyoblasts

Yao Jen Liang, Chao Yi Chen, Shiow Jen Juang, Ling Ping Lai, Kou Gi Shyu, Bao Wei Wang, Shannen Yuan Chun Liu, Jyh Gang Leu

研究成果: 雜誌貢獻文章

8 引文 斯高帕斯(Scopus)

摘要

C-reactive protein (CRP) has emerged as a new marker for cardiovascular diseases. Activation of peroxisome proliferator-activated receptor δ (PPARδ) plays beneficial roles in cardiac disorders. However, the relationship between CRP and PPARδ in cardiac cells remains unclear. This study focused on the underlying molecular mechanisms of CRP and PPARδagonists. Cardiomyocytes and cardiomyoblast cell line (H9c2) were used in different groups: Untreated; 15μg/ml CRP with or without 1μM PPARδ agonists (L-165041). CRP increased PPARδ and interleukin-6 expression in cardiomyocytes and H9c2 cardiomyoblasts. NF-κB inducing kinase (NIK) and NF-κB pathway also activated by CRP stimulation. These changes could be inhibited by L-165041 through p38MAPK and c-JNK pathways. However, transfection with siRNA of CD32 CRP receptor did not decrease CRP signaling or reverse the effects of L-165041 in CRP-treated cardiomyocytes and H9c2. Pretreatment with L-165041 attenuated apoptosis induced by hypoxia with or without CRP in H9c2 cardiomyoblasts. CRP up-regulated PPARδ expression in cardiomyocytes and H9c2. L-165041 attenuated CRP-induced pro-inflammatory signaling through p38MAPK and c-JNK in H9c2 cardiomyoblasts. However, PPARδ activation attenuated CRP-induced NF-κB pathway may be independent of CD32. These results may provide new evidence of PPARδ beneficial effects for inflammatory cardiomyopathy.
原文英語
頁(從 - 到)84-92
頁數9
期刊European Journal of Pharmacology
643
發行號1
DOIs
出版狀態已發佈 - 九月 2010

ASJC Scopus subject areas

  • Pharmacology

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