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Effect of berberine on cardiomyocyte apoptosis in coronary heart disease rats based on ERK-Calpain2 pathway
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DOI   10.11656/j.issn.1672-1519.2019.01.20
Key Words   berberine;coronary heart disease;myocardium;apoptosis;ERK-Calpain 2 pathway;mechanism
Author NameAffiliationE-mail
ZHU Na Department of Health Management, Henan Provincial People's Hospital, Zhengzhou 450000, China  
CAO Xueming Department of Cardiology, Henan Provincial People's Hospital, Zhengzhou 450000, China caoxueming2007@163.com 
Abstract
    [Objective] To study the effects of berberine (BBR) on cardiomyocyte apoptosis in coronary heart disease rats and the role of ERK-Calpain2 signaling pathway.[Methods] A rat model of coronary heart disease was established by feeding on a high-fat diet and injection of pituitrin. The model animals were divided into test group and control group. Blank groups were established with normal SD rats. The test group was given intragastric administration of BBR 80 mg/(kg·d). The control group and blank group were given double distilled water. The treatment cycle is 12 weeks. TUNEL immunofluorescence was used to detect cardiomyocyte apoptosis. RT-qPCR was used to detect GRP78, CHOP and Calpain2 mRNA levels. Western blot method was used to detect GRP78, CHOP, p-ERK, ERK, Caspase-3, Caspase-12 and Calpain2 protein expression in myocardial tissue.[Results] After myocardial TUNEL staining, compared with the control group, the apoptosis of the test group significantly reduced (P<0.01). Compared with the control group, the expression of Caspase-12, Caspase-3, GRP78 and CHOP proteins were down-regulated in different degrees (P<0.01). The expression of p-ERK and Calpain2 protein was down-regulated and the expression of Capastatin Protein increased (P<0.01) in the test group. Compared with the control group, the expression of GRP78, CHOP and Calpain2 mRNA in the experimental group decreased (P<0.01).[Conclusion] BBR can inhibit endoplasmic reticulum stress-induced apoptosis of myocardial cells in CHD rats. This effect may be related to the inhibition of ERK-Calpain2 signaling pathway.

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