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Kolaviron attenuated arsenic acid‐induced cardiovascular dysfunction by enhancing antioxidant defense system and inhibiting inflammatory and apoptotic signaling pathways
Author(s) -
Oyagbemi Ademola Adetokunbo,
Omobowale Temidayo Olutayo,
Olowu Ebunoluwa Racheal,
Adedapo Adeolu Alex,
Yakubu Momoh A
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.939.5
Subject(s) - malondialdehyde , pharmacology , oxidative stress , nitric oxide , myeloperoxidase , antioxidant , medicine , superoxide dismutase , apoptosis , reactive oxygen species , chemistry , biochemistry , inflammation
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 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. However, Kolaviron (KV) at the dosage of 100 and 200mg/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 (MDA), hydrogen peroxide generation (H 2 O 2 ), myeloperoxidase (MPO) activity and nitric oxide (NO) contents. Similarly, antioxidant deference system was significant improved in rats pre‐treated with KV. Immunohistochemistry revealed reduction in the expression of renal C‐reactive proteins (CRP) and increase in anti‐apoptotic protein BCL2 expression in KV treated rats. Furthermore, cardiac troponin I (CTnI) expression was 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.