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The Protective of Baicalin on Myocardial Ischemia-reperfusion Injury.

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 was administrated, respectively. The experiment was randomly divided into 4 groups (n=10): Control; I/R; IR+DMEM; and I/R+baicalin groups. Post-operation, 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 V-FITC/PI and tunel staining, and the apoptosis gene and protein was detected by RT-PCR and western blot. Furthermore, the protein expression of 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 culture medium. The cells survival rate, vitality and the 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-regulation the protein expression of CaSR, but up-regulation the protein expression of ERK1/2. Furthermore, when the cells were pretreatment with ERK1/2 inhibitor PD98059, the cells survival rate was significantly decreased, but LDH activity and apoptosis were significantly increased. The results indicated that the effect of baicalin on myocardial I/R injury could been inhibited by ERK1/2 inhibitor.


CONCLUSION
In conclusion, our data suggested that baicalin attenuate I/R-induced myocardial injury maybe through suppression CaSR/ERK1/2 signaling pathway.