Effect of pretreatment with diallyltrisulfide on cardiomyocyte apoptosis after coronary microembolization in rats
10.3969/j.issn.1006-5725.2018.03.008
- VernacularTitle:大蒜素对大鼠冠状动脉微栓塞后心肌凋亡的影响
- Author:
Jiabao LIANG
1
;
Lang LI
;
Wenkai HE
Author Information
1. 广西医科大学第一附属医院心脏病研究所 南宁530021
- Keywords:
diallyltrisulfide;
coronary microembolization;
myocardial injury;
apoptosis
- From:
The Journal of Practical Medicine
2018;34(3):371-375
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of diallyltrisulfide on rats with myocardial injury after coro-nary microembolization (CME). Methods 20 survival of SD rats were randomly divided into CME group (CME group)and diallyltrisulfide pretreatment group(DATSgroup),and these rats were injected with microspheres(42 μm in diameter)into the left ventricles to induce the model of CME, 10 rats for each group.DATS group was received diallyltrisulfide (DATS) 40 mg/(kg·d) for 7 days before operation. Another 10 survival of SD rats was selected as sham operation group(Sham group),and these rats were injected with the same dose of normal saline by left ventri-cles. Cardiac function was assessed by echocardiography and the expression of Akt and caspase-3 of myocardial tissue of rats in each group were detected by TUMEL staining,RT-PCR and Western Blot,while testing the level of cTnI after operation of 6 h. Results Compared with Sham group, the cardiac function of CME group and DATS group was significantly decreased (P<0.05), the expression of caspase3 mRNA and protein was significantly increased (P<0.05), the expression on Akt mRNA and protein was significantly decreased (P<0.05) (P<0.05). Com-pared with CME group, the cardiac function of DATS group was significantly improved (P<0.05), the expression of caspase3 mRNA and protein was significantly decreased (P<0.05), the expression of Akt mRNA and protein was significantly increased (P<0.05), cTnI level was significantly decreased (P<0.05). Conclusion Diallyltrisulfide pretreatment can significantly reduce the apoptosis of cardiomyocytes after CME and improve cardiac function.The mechanism may be through the inhibition of Akt to activate cardiomyocyte caspase3-mediated death receptor activa-tion pathway.
