Kolaviron attenuated arsenic acid induced-cardiorenal dysfunction via regulation of ROS, C-reactive proteins (CRP), cardiac troponin I (CTnI) and BCL2
Autor: | Momoh A. Yakubu, J.O. Abiola, Adeolu Alex Adedapo, Ebunoluwa Racheal Asenuga, Ademola Adetokunbo Oyagbemi, Temidayo Olutayo Omobowale |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Antioxidant Kolaviron medicine.medical_treatment lcsh:Medicine Pharmacology medicine.disease_cause Chemoprevention Arsenic acid QT interval Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Troponin I Medicine Cardiovascular dysfunction business.industry lcsh:R Malondialdehyde 030104 developmental biology Complementary and alternative medicine chemistry Oxidative stress Apoptosis 030220 oncology & carcinogenesis Original Article business |
Zdroj: | Journal of Traditional and Complementary Medicine, Vol 8, Iss 3, Pp 396-409 (2018) Journal of Traditional and Complementary Medicine |
ISSN: | 2225-4110 |
Popis: | Arsenic acid is one of the abundant environmental pollutants present in soil, water and the air. Undoubtedly, it has found its way to the food chain in which humans and animals are the final targets thereby causing arrays of disease conditions including cardiovascular and renal dysfunction. Hence, the use of phytochemicals present in medicinal plants has gained global acceptance as chemotherapeutic agents that can prevent, ameliorate, reverse or treat diseases. From our study, arsenic acid intoxication led to significant increase in heart rate (HR), QRS, together with prolonged QT and QTc interval. However, Kolaviron (KV) at the dosage of 100 and 200 mg/kg body weight reversed the aforementioned electrocardiographic (ECG) changes. KV pre-treatment also ameliorated cardiorenal dysfunction via significant reduction in cardiac and renal markers of oxidative stress such as malondialdehyde, hydrogen peroxide generation, myeloperoxidase activity and nitric oxide contents. Immunohistochemistry revealed expressions of renal C-reactive proteins (CRP) and expressions of anti-apoptotic protein BCL2 in KV treated rats. Furthermore, cardiac troponin I (CTnI) expressions were lower in KV treated rats. Taken together, KV mitigated arsenic-acid induced cardiovascular dysfunction via up-regulation of antioxidant defense system and down-regulation of inflammatory and apoptotic signaling pathways. Graphical abstract Image 1 |
Databáze: | OpenAIRE |
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