Panax quinquefolium saponin Optimizes Energy Homeostasis by Modulating AMPK-Activated Metabolic Pathways in Hypoxia-Reperfusion Induced Cardiomyocytes.
10.1007/s11655-020-3194-4
- Author:
Yong-Hui YU
1
;
Pei ZHANG
2
;
Cheng-Long WANG
3
,
4
;
Jian-Gang LIU
5
;
Peng LI
5
;
Da-Wu ZHANG
5
Author Information
1. Department of Traditional Chinese Medicine, China-Japan Friendship Hospital, Beijing, 100029, China.
2. Graduate Shcool, Beijing University of Chinese Medicine, Beijing, 100029, China.
3. Center for Cardiovascular Diseases, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China. wcl796@
4. com.
5. Center for Cardiovascular Diseases, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
- Publication Type:Journal Article
- Keywords:
Chinese medicine;
Panax quinquefolium saponin;
adenosine monophosphate-activated protein kinase α pathways;
energy metabolism;
hypoxia-reperfusion;
neonatal rat ventricular myocytes
- From:
Chinese journal of integrative medicine
2021;27(8):613-620
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To investigate the effects and underlying mechanisms of Panax quinquefolium saponin (PQS) on energy deficiency in hypoxia-reperfusion (H/R) induced cardiomyocytes.
METHODS:The H/R injury involved hypoxia for 3 h and then reperfusion for 2 h. Cardiomyocytes recruited from neonatal rat ventricular myocytes (NRVMs) were randomly divided into control, H/R, H/R+compound C (C.C), H/R+PQS, and H/R+C. C+PQS groups. BrdU assay, lactase dehydrogenase (LDH) leakage and early apoptosis rate were evaluated to assess cell damages. Contents of high energy phosphate compounds were conducted to detect the energy production. Protein expression levels of adenosine monophosphate-activated protein kinase a (AMPKα), glucose transporter 4 (GLUT4), phosphate fructose kinase 2 (PFK2), fatty acid translocase/cluster of differentiation 36 (FAT/CD36), and acetyl CoA carboxylase 2 (ACC2) in the regulatory pathways were measured by Western blotting. Immunofluorescence staining of GLUT4 and FAT/CD36 was used to observe the mobilization of metabolic transporters.
RESULTS:PQS (50 mg/L) pretreatment significantly alleviated H/R-induced inhibition of NRVMs viability, up-regulation of LDH leakage, acceleration of early apoptosis, and reduction of energy production (P<0.05). Compared with the H/R group, up-regulated expression of AMPKα, GLUT4, PFK2, FAT/CD36 and ACC2 were observed, and more GLUT4 and FAT/CD36 expressions were detected on the membrane in the H/R+PQS group (P<0.05). These effects of PQS on H/R-induced NRVMs were eliminated in the H/R+C.C+PQS group (P<0.05).
CONCLUSION:PQS has prominent advantages in protecting NRVMs from H/R-induced cell damages and energy metabolic disorders, by activation of AMPKα-mediated GLUT4-PFK2 and FAT/CD36-ACC2 pathways.
