Thymoquinone supplementation attenuates cyclophosphamide-induced cardiotoxicity in rats.
This study examined the possible protective effects of thymoquinone (TQ), the main constituent of the volatile oil of black seed (Nigella sativa), against cyclophosphamide (CP)-induced cardiotoxicity. Adult male Wistar albino rats were divided into four treatment groups. Rats in the first group were served as control. Rats in the second group received TQ (50 mg/L in drinking water) for 12 days. Animals in the third group were injected with a single dose of CP (200 mg/kg, IP) at day 5. Rats in the fourth group received TQ (50 mg/L in drinking water) for 5 days before a single dose of CP (200 mg/kg, IP) and continued thereafter throughout the experiment. On day 13, animals were sacrificed; serum and hearts were isolated and analyzed. Cyclophosphamide resulted in a significant increase in serum creatine kinase, lactate dehydrogenase, cholesterol, triglycerides, creatinine, urea, and tumor necrosis factor-α. In heart tissues, CP resulted in a significant increase in thiobarbituric acid reactive substances and total nitrate/nitrite and a significant decrease in reduced glutathione, glutathione peroxidase, catalase, and adenosine triphosphate levels. Interestingly, TQ supplementation resulted in a complete reversal of all the biochemical changes induced by CP to their control values. Data from this study suggest that TQ supplementation attenuates CP-induced cardiotoxicity by a mechanism related, at least in part, to its ability to decrease oxidative and nitrosative stress and to preserve the activity of antioxidant enzymes as well as its ability to improve the mitochondrial function and energy production. .
Nagi
Mahmoud N
MN
Department of Pharmacology, College of Pharmacy, King Saud University, Riyadh, Kingdom of Saudi Arabia. mnnagi@hotmail.com
Al-Shabanah
Othman A
OA
Hafez
Mohamed M
MM
Sayed-Ahmed
Mohamed M
MM
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D016227:Benzoquinones / Q000627:therapeutic use*; D002784:Cholesterol / Q000097:blood; D052279:Creatine Kinase, MB Form / Q000097:blood; D003404:Creatinine / Q000097:blood; D003520:Cyclophosphamide / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D019587:Dietary Supplements; D005978:Glutathione / Q000378:metabolism; D006331:Heart Diseases / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy* / Q000517:prevention & control*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D009566:Nitrates / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014508:Urea / Q000097:blood
D016227:Benzoquinones; D009566:Nitrates; D009573:Nitrites; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D000255:Adenosine Triphosphate; D003520:Cyclophosphamide; D014508:Urea; D002784:Cholesterol; D003404:Creatinine; D007770:L-Lactate Dehydrogenase; D052279:Creatine Kinase, MB Form; D005978:Glutathione; C003466:thymoquinone