Title:The Protective of Baicalin on Myocardial Ischemia-Reperfusion Injury
Volume: 21
Issue: 13
Author(s): Xiaoli Liu, Shanshan Zhang, Chaoyue Xu, Yongchao Sun, Shujian Sui, Zhaohua Zhang*Yun Luan*
Affiliation:
- Department of Pediatrics, The Second Hospital, Cheeloo College of Medicine, Shandong University,China
- Institute of Medical Sciences, The Second Hospital, Cheeloo College of Medicine, Shandong University, No. 247, Beiyuan Dajie, Jinan, 250033,China
Keywords:
Baicalin, cardiomyocytes, I/R, apoptosis, CaSR, myocardial apoptosis.
Abstract:
Background: The aim of this study was to explore the inhibitory effect of baicalin on myocardial
apoptosis induced by Ischemia-Reperfusion (I/R).
Methods: Sprague Dawley rats' heart and myocardial cells I/R model were established in vivo and
vitro, then 100 mg/kg and 10 μmol/l baicalin were administrated, respectively. The experiment was
randomly divided into 4 groups (n=10): Control; I/R; IR+DMEM; and I/R+baicalin groups. Postoperation,
the Left Ventricular (LV) End-Diastolic Pressure (LVEDP), the maximum velocity of LV
contraction (dP/dtmax) and the maximum velocity of LV diastole (dP/dtmin) were recorded by the
transthoracic echocardiography; the myocardial apoptosis percentage was analyzed by Annexin VFITC/
PI and TUNEL staining, and the apoptosis gene and protein were detected by RT-PCR and western
blot. Furthermore, the protein expression of the calcium-sensing receptor (CaSR) and ERK1/2
phosphorylation were observed by western blot and Fura-2-acetoxymethyl ester. Moreover, primary
rats’ cardiomyocytes were cultured and ERK1/2 specific inhibitor PD98059 was added to the culture
medium. The cell survival rate, vitality and apoptosis were detected by MTT, lactate dehydrogenase
(LDH) and TUNEL staining assay Kit, respectively.
Results: Our present study showed that baicalin significantly improved LV hemodynamic parameters
and myocardial apoptosis in myocardial I/R injury rats. Furthermore, we found that baicalin could
down-regulate the protein expression of CaSR, but up-regulate the protein expression of ERK1/2. Furthermore,
when the cells were pretreated with ERK1/2 inhibitor PD98059, the cells survival rate significantly
decreased, but LDH activity and apoptosis significantly increased. The results indicated that
the effect of baicalin on myocardial I/R injury could be inhibited by ERK1/2 inhibitor.
Conclusion: In conclusion, our data suggests that baicalin attenuates I/R-induced myocardial injury
maybe through the suppression of the CaSR/ERK1/2 signaling pathway.