Beetroot juice alleviates isoproterenol-induced myocardial damage by reducing oxidative stress, inflammation, and apoptosis in rats

被引:0
|
作者
Mohammad Raish
Ajaz Ahmad
Mushtaq Ahmad Ansari
Khalid M. Alkharfy
Abdul Ahad
Altaf Khan
Naushad Ali
Majid A. Ganaie
Mohammed Abbas Ali Hamidaddin
机构
[1] College of Pharmacy,Department of Pharmaceutics
[2] King Saud University,Department Clinical Pharmacy, College of Pharmacy
[3] King Saud University,Department Pharmacology and Toxicology, College of Pharmacy
[4] King Saud University,Department Pharmacology and Toxicology, College of Pharmacy
[5] Prince Sattam Bin Abdulaziz University,Quality Assurance Unit, College of Pharmacy
[6] King Saud University,Department Pharmaceutical Chemistry, College of Pharmacy
[7] King Saud University,undefined
来源
3 Biotech | 2019年 / 9卷
关键词
Beetroot juice; Isoproterenol; Oxidative stress; Myocardial injury; Cardioprotection;
D O I
暂无
中图分类号
学科分类号
摘要
Beetroot (Beta vulgaris L.) juice (BRJ) is a good source of betalain (betacyanins and betaxanthin) pigments and exhibits antioxidant, anti-inflammatory, and chemo-preventive activities in vitro and in vivo. The current study was performed to determine the cardioprotective effect of BRJ on lipid peroxidation, antioxidant defense, functional impairment, and histopathology in rats with isoproterenol (ISP)-induced myocardial injury. Myocardial ischemia was induced by ISP (85 mg/kg) s.c. injection at 24 h intervals, followed by oral administration of BRJ for 28 days at doses of 150 and 300 mg/kg. ISP-induced myocardial damage was confirmed by an increase in heart weight to body weight ratio, % infarction size, serum cardiac indices (AST, ALT, GGT, ALP, LDH and CK-MB), and histological alterations in the myocardium. Pretreatment with BRJ (150 and 300 mg/kg) followed by ISP induction reduced oxidative/nitrosative stress and restored the cardiac endogenous antioxidants in rats. ISP augmented cardiac inflammatory cytokines (TNF-α, IL-6 and IL-10), myeloperoxidase activity, NF-κB DNA binding and protein expression of NF-κB (p65), and the hyperlipidemia level was significantly reduced by the BRJ pretreatment. Furthermore, the BRJ pretreatment significantly reduced caspase-3, Bax, and MMP-9 protein expression, enhanced the Bcl-2 antiapoptotic protein expression, alleviated the extent of histological damage, myonecrosis, and edema, and maintained the architecture of cardiomyocytes. These findings suggest that BRJ pretreatment mitigates cardiac dysfunction and structural damages by decreasing oxidative stress, inflammation, and apoptosis in cardiac tissues. These results further support the use of BRJ in traditional medicine against cardiovascular diseases.
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