Amelioration of cardiotoxic impacts of diclofenac sodium by vitamin B complex

N.A. Abdulmajeed, H.S. Alnahdi, N.O. Ayas, A.M. Mohamed

Biochemistry Department, Faculty of Science for Girls, King Abdulaziz University, Jeddah, Kingdon of Saudi Arabia. azzamohamed99@yahoo.com

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• Pharmacology

OBJECTIVE: The safety of Non-steroidal anti-inflammatory drugs (NSAIDs) use in clinical practice has been questioned. Clinical studies indicate that these drugs cause adverse cardiovascular effects. The aim of this study was to investigate the protective role of vitamin B complex against the cardiotoxic potency of diclofenac sodium induced cardiac damage.

MATERIALS AND METHODS: Diclofenac sodium was administered intraperitoneally to rats at either 1.5 mg or 3 mg/kg body weight for 14 consecutive days. Vitamin B complex (1.6 mg B1, 1.6 mg B6 and 16.7 µg B12/kg body weight, i.p.) was co-administered daily for 3 weeks along with diclofenac administration to rats intoxicated by either of the two doses.

RESULTS: The results revealed that co-administration of vitamin B complex with diclofenac to rats intoxicated by either of the two doses, markedly ameliorated increases in serum markers of cardiac damage, including, (AST), creatine kinase-MB (CK-MB) as well as decreases in phosphoglucoisomerase (PGI) and lactate dehydrogenase (LDH) activities in cardiac tissue compared with intoxicated rats. The B complex also could markedly attenuate the decreases in cardiac antioxidant enzymes namely, glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G-6-PDH) and catalase (CAT) compared with diclofenac intoxicated rats. Beside, the vitamin B complex successfully modulated the increases in serum glucose, serum lipid profiles, triglycerides (TGs), total cholesterol (TCh) and low density lipoprotein (LDL-C) as well as the decrease in the high density lipoprotein (HDL-C) in response to diclofenac toxicity.

CONCLUSIONS: These results support the use of vitamin B complex along with diclofenac therapy as a protective agent against cardiac tissue damage induced by diclofenac toxicity.

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