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

Abstract

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.

Cardioprotective effect of thymol against adrenaline-induced myocardial injury in rats

“…In this work, NF-κB and IL1β were suppressed by thymol pre-treatment, indicating that thymol exerted its cardioprotective effect against adrenaline-induced MI via its anti-inflammatory effect mediated by its anti-oxidant effect. This was paralleled with improved cardiac function indices and further confirmed previous reports that showed the importance of inhibition of inflammatory cytokines in alleviation of cardiac injury ( Seropian et al., 2014 ; Raish et al., 2019 ). The anti-inflammatory effect of thymol was described also in acute lung injury model via inhibition of TNF-α, IL-6 releases and NF-κB activation ( Wan et al., 2018 ).…”

Phikud Navakot Modulates the Level of Pro-Inflammatory Mediators and the Protein Expression of SOD1 and 2 and the Nrf2/HO-1 Signaling Pathway in Rats with Acute Myocardial Infarction

“…TNF- α and IL-6 are crucial indicators of inflammation after MI in both mice and human [20] as well as in a rat model of IMI [1, 4, 7, 10, 14]. The observation that these mediators act as indicators of inflammation agreed with our IMI rat model in which a significant increase in the serum cytokine levels of TNF- α and IL-6 was observed.…”

“…ISO administration also causes an elevation in the ST segment in ECG readings. Furthermore, it caused an increase in the levels of cardiac injury biomarkers, including troponin I, troponin T, creatine kinase-MB, lactate dehydrogenase, alkaline phosphatase, serum glutamic oxaloacetic transaminase, aspartate transaminase, and alanine transaminase [1–4]. ISO-treated rats exhibited myocardial cell swelling, myocardial degeneration, loss of myofibrils, and diffuse infiltration of inflammatory cells [1, 2, 4].…”

“…Furthermore, it caused an increase in the levels of cardiac injury biomarkers, including troponin I, troponin T, creatine kinase-MB, lactate dehydrogenase, alkaline phosphatase, serum glutamic oxaloacetic transaminase, aspartate transaminase, and alanine transaminase [1–4]. ISO-treated rats exhibited myocardial cell swelling, myocardial degeneration, loss of myofibrils, and diffuse infiltration of inflammatory cells [1, 2, 4]. There was also an increase in cardiac tissues and serum levels of the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor- α (TNF- α ) [1, 4].…”

“…ISO-treated rats exhibited myocardial cell swelling, myocardial degeneration, loss of myofibrils, and diffuse infiltration of inflammatory cells [1, 2, 4]. There was also an increase in cardiac tissues and serum levels of the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor- α (TNF- α ) [1, 4]. Moreover, the ISO-induced myocardial changes were the result of an increase in oxidative stress through reductions of the components of the myocardial antioxidant system, including glutathione, glutathione reductase, glutathione-S-transferase, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase, in rat hearts [3, 5].…”