4.7 Article

Betulinic acid protects against cardiotoxicity of the organophosphorus pesticide chlorpyrifos by suppressing oxidative stress, inflammation, and apoptosis in rats

Journal

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 30, Issue 17, Pages 51180-51190

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s11356-023-25917-6

Keywords

Organophosphorus pesticides; Cardiotoxicity; Betulinic acid; Oxidative stress; Inflammation

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This study aimed to evaluate the protective activity of betulinic acid (BA) against chlorpyrifos (CPF) cardiotoxicity in rats by mitigating oxidative stress, inflammation, and apoptosis, and enhancing Nrf2 and antioxidants. The results showed that BA can ameliorate tissue injury, decrease oxidative stress, inflammation and apoptosis, and increase antioxidants.
The widespread application of organophosphorus (OP) pesticides can affect the environment as well as the animal and human health. Chlorpyrifos (CPF) is a broad-spectrum OP pesticide used in agriculture and can cause several toxic effects in which oxidative stresses and inflammation play a key role. This study aimed to evaluate the protective activity of betulinic acid (BA), an antioxidant and anti-inflammatory pentacyclic triterpene, against CPF cardiotoxicity in rats. The rats were divided into four groups. CPF (10 mg/kg) and BA (25 mg/kg) were orally administered for 28 days, and blood and heart samples were collected. CPF-administered rats showed an increase in serum cardiac troponin I (cTnI), creatine kinase (CK)-MB, and lactate dehydrogenase (LDH), accompanied with multiple myocardial tissue alterations. Lipid peroxidation (LPO), nitric oxide (NO), nuclear factor-kappaB (NF-kappa B), interleukin (IL)-6, IL-1 beta, and tumor necrosis factor (TNF)-alpha were increased, and antioxidant were decrease in CPF-administered rats. BA ameliorated cardiac function markers and tissue injury, decreased LPO, NO, NF-kappa B, and proinflammatory cytokines, and increased antioxidants. In addition, BA decreased proapoptosis markers, and increased B-cell lymphoma (Bcl)-2, IL-10, Nrf2, and HO-1 in the heart of CPF-treated rats. In conclusion, BA protected against cardiotoxicity in CPF-administered rats by mitigating oxidative stress, inflammation, and apoptosis, and enhanced Nrf2 and antioxidants.

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