Abstract | BACKGROUND: Endoplasmic reticulum (ER) stress-related apoptosis is involved in the pathophysiology of many cardiovascular diseases, and Panax quinquefolium saponin (PQS) is able to inhibit excessive ER stress-related apoptosis of cardiomyocytes following hypoxia/reoxygenation and myocardial infarction. However, the pathway by which PQS inhibits the ER stress-related apoptosis is not well understood. To further investigate the protective effect of PQS against ER stress-related apoptosis, primary cultured cardiomyocytes were stimulated with thapsigargin (TG), which is widely used to model cellular ER stress, and it could induce apoptotic cell death in sufficient concentration. METHODS: RESULTS: Both PQS pre-treatment and PERK knockdown remarkably inhibited the cardiomyocyte apoptosis induced by TG, increased cell viability, decreased phosphorylation of both PERK and eIF2α, and decreased protein levels of both ATF4 and CHOP. There was no statistically significant difference between PQS pre-treatment and PERK knockdown in the cardioprotective effect. CONCLUSIONS: Our data indicate that the PERK-eIF2α-ATF4-CHOP pathway of ER stress is involved in the apoptosis induced by TG, and PQS might prevent TG-induced cardiomyocyte apoptosis through a mechanism involving the suppression of this pathway. These findings provide novel data regarding the molecular mechanisms by which PQS inhibits cardiomyocyte apoptosis.
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Authors | Mi Liu, Mei Xue, Xiao-Reng Wang, Tian-Qi Tao, Fei-Fei Xu, Xiu-Hua Liu, Da-Zhuo Shi |
Journal | Journal of geriatric cardiology : JGC
(J Geriatr Cardiol)
Vol. 12
Issue 5
Pg. 540-6
(Sep 2015)
ISSN: 1671-5411 [Print] China |
PMID | 26512246
(Publication Type: Journal Article)
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