PMID- 26512246
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20151029
LR  - 20200930
IS  - 1671-5411 (Print)
IS  - 1671-5411 (Linking)
VI  - 12
IP  - 5
DP  - 2015 Sep
TI  - Panax quinquefolium saponin attenuates cardiomyocyte apoptosis induced by 
      thapsigargin through inhibition of endoplasmic reticulum stress.
PG  - 540-6
LID - 10.11909/j.issn.1671-5411.2015.05.009 [doi]
AB  - 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: Primary 
      cultured cardiomyocytes from neonatal rats were exposed to TG (1 micromol/L) 
      treatment for 24 h, following PQS pre-treatment (160 microg/mL) for 24 h or 
      pre-treatment with small interfering RNA directed against protein kinase-like 
      endoplasmic reticulum kinase (Si-PERK) for 6 h. The viability and apoptosis rate 
      of cardiomyocytes were detected by cell counting kit-8 and flow cytometry 
      respectively. ER stress-related protein expression, such as glucose-regulated 
      protein 78 (GRP78), calreticulin, PERK, eukaryotic translation initiation factor 
      2alpha (eIF2alpha), activating transcription factor 4 (ATF4), and C/EBP homologous 
      protein (CHOP) were assayed by western blotting. 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 eIF2alpha, 
      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-eIF2alpha-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.
FAU - Liu, Mi
AU  - Liu M
AD  - Department of Pathophysiology, Chinese PLA General Hospital, Beijing, China ; 
      Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
FAU - Xue, Mei
AU  - Xue M
AD  - Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
FAU - Wang, Xiao-Reng
AU  - Wang XR
AD  - Department of Pathophysiology, Chinese PLA General Hospital, Beijing, China.
FAU - Tao, Tian-Qi
AU  - Tao TQ
AD  - Department of Pathophysiology, Chinese PLA General Hospital, Beijing, China.
FAU - Xu, Fei-Fei
AU  - Xu FF
AD  - Department of Pathophysiology, Chinese PLA General Hospital, Beijing, China.
FAU - Liu, Xiu-Hua
AU  - Liu XH
AD  - Department of Pathophysiology, Chinese PLA General Hospital, Beijing, China.
FAU - Shi, Da-Zhuo
AU  - Shi DZ
AD  - Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
LA  - eng
PT  - Journal Article
PL  - China
TA  - J Geriatr Cardiol
JT  - Journal of geriatric cardiology : JGC
JID - 101237881
PMC - PMC4605950
OTO - NOTNLM
OT  - Cardiomyocyte apoptosis
OT  - Endoplasmic reticulum stress
OT  - Panax quinquefolium saponin
OT  - Thapsigargin
EDAT- 2015/10/30 06:00
MHDA- 2015/10/30 06:01
PMCR- 2015/09/01
CRDT- 2015/10/30 06:00
PHST- 2015/10/30 06:00 [entrez]
PHST- 2015/10/30 06:00 [pubmed]
PHST- 2015/10/30 06:01 [medline]
PHST- 2015/09/01 00:00 [pmc-release]
AID - jgc-12-05-540 [pii]
AID - 10.11909/j.issn.1671-5411.2015.05.009 [doi]
PST - ppublish
SO  - J Geriatr Cardiol. 2015 Sep;12(5):540-6. doi: 
      10.11909/j.issn.1671-5411.2015.05.009.