Effects of Paeoniflorin on Cardiac Dysfunction and Myocardial Cell Injury Induced by Cisplatin in Rats Based on ERK/p38 MAPK Signaling Pathway
10.13748/j.cnki.issn1007-7693.20233001
- VernacularTitle:基于ERK/p38 MAPK信号通路探讨芍药苷对顺铂诱导大鼠心功能障碍及心肌细胞损伤的影响
- Author:
Shijie ZHANG
1
;
Ruiqi TIAN
1
;
Yinchuan DING
1
;
Qi WU
2
;
Yiran WANG
2
;
Lei LIU
2
;
Hong SUN
2
;
Min XUE
1
Author Information
1. Xuzhou Medical University Department of Physiology, College of Basic Medicine；Xuzhou Medical University National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou 221004, China
2. Xuzhou Medical University Department of Physiology, College of Basic Medicine
- Publication Type:Journal Article
- Keywords:
cardiac dysfunction ；paeoniflorin ； inflammation；apoptosis；ERK/p38 MAPK
- From:
Chinese Journal of Modern Applied Pharmacy
2024;41(11):1476-1483
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE :To investigate the protective effect of paeoniflorin(PF) on cardiac dysfunction and myocardial cell injury induced by cisplatin(CDDP) in rats.
METHODS
SD male rats were randomly divided into control group, CPPD group, and CDDP PF+low-dose, high-dose group. PowerLab multifunctional recorder was used to detect the related indexes of cardiac function: the changes of left ventricular peak pressure(LVSP), left ventricular end-diastolic pressure(LVEDP) and left ventricular pressure change rate(±dp/dt). Serum levels of inflammatory factors TNF-α, IL-1β and IL-6 were measured in each group. Myocardial tissue was stained to observe the changes of tissue structure. H9c2 cardiomyocytes were divided into control group, CDDP group, PF group and CDDP+PF group. The activity of H9c2 cardiomyocytes was measured by CCK-8. The apoptosis of cardiomyocytes in each group was detected by flow cytometry. The expressions of MAPK signaling pathway related proteins p38, ERK, JNK and their phosphorylated proteins and apoptosis-related proteins Bax, Bcl-2, Casp3, Cl-casp3 were detected in cardiomyocytes by Western blotting.
RESULTS
Compared with the control group, LVSP and ±dp/dt decreased, LVEDP increased in rats of CDDP group(P<0.01). Compared with CDDP group, both CDDP+low-dose and high-dose PF pretreatment increased LVSP and ±dp/dt value(P<0.05 or P<0.01), decreased LVEDP(P<0.01), and could decrease the serum inflammatory factor TNF-α, IL-1β and IL-6(P<0.01). Cell level results showed that compared with control group, in CDDP group, the cell activity decreased, the apoptosis-related protein Bax, Cl-casp3 increased(P<0.01), expression of anti-apoptotic protein Bcl-2 decreased(P<0.01), and the expression of p38 and ERK phosphorylation also increased(P<0.01). Compared with CDDP group, PF could restore cell activit, down-regulate apoptosis-related protein Bax, Cl-casp3(P<0.05 or P<0.01), and increase anti-apoptotic protein Bcl-2 expression(P<0.01), inhibit MAPK pathway p38 and ERK phosphorylation expression(P<0.01).
CONCLUSION
PF can restore cardiac dysfunction and myocardial cell injury induced by cisplatin in rats, which may be related to inhibiting inflammation and apoptosis by regulating ERK/p38 MAPK signal expression.
