Pachymic acid protects H9c2 cardiomyocytes from lipopolysaccharide-induced inflammation and apoptosis by inhibiting the extracellular signal-regulated kinase 1/2 and p38 pathways.
Pachymic acid (PA), a lanostane-type triterpenoid and the major component of Poria cocos alcoholic extracts, has various pharmacological effects, including anti-inflammatory, anti-oxidative and anti-apoptotic. However, few studies have investigated the effects of PA on lipopolysaccharide (LPS)-induced H9c2 cell apoptosis and inflammation, or identified the possible mechanisms underlying these effects. In the present study, H9c2 cardiomyocytes were stimulated by LPS and treated with or without PA. The increased mRNA expression levels of tumor necrosis factor-α, interleukin (IL)-1 and IL-6 induced by LPS were attenuated following treatment with PA. PA also attenuated LPS-induced apoptosis, as determined by a terminal deoxynucleotidyl transferase dUTP nick end labeling assay, and regulated the LPS-induced protein expression levels of caspase 3, 8 and 9. Furthermore, the phosphorylations of extracellular-regulated kinase (Erk)1/2 and p38 in the LPS-treated H9c2 cells were inhibited by PA. These results suggested that treatment with PA prevented the LPS-induced inflammatory and apoptotic response in cardiomyocytes, which may be mediated by inhibition of the Erk1/2 and p38 pathways.
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hebei 430060, P.R. China.
Fang-Fang
FF
Li
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hebei 430060, P.R. China.
Yuan
Y
Yuan
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hebei 430060, P.R. China.
Yuan
Y
Liu
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hebei 430060, P.R. China.
Qing-Qing
QQ
Wu
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hebei 430060, P.R. China.
Rong
R
Jiao
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hebei 430060, P.R. China.
Zheng
Z
Yang
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hebei 430060, P.R. China.
Meng-Qiao
MQ
Zhou
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hebei 430060, P.R. China.
Qi-Zhu
QZ
Tang
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002460:Cell Line; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism; D007375:Interleukin-1 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism; D055441:Poria / Q000737:chemistry / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology*; D051381:Rats; D060888:Real-Time Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects; D014315:Triterpenes / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D020011:Protective Agents; D014315:Triterpenes; D014409:Tumor Necrosis Factor-alpha; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D048051:p38 Mitogen-Activated Protein Kinases; C102487:pachymic acid