Abstract
T o investigate the possible protective effect of thymoquinone (TQ) in cisplatin (CP) induced myocardial injury. A total of 28 adult male Wistar-Albino rats were randomly and equally divided into four groups as follows: Group 1 (control), Group 2 (CP at 15 mg/kg dose), Group 3 (TQ 40 mg/kg/day for two days prior to CP injection and on third day, CP at 15 mg/kg dose was intraperitoneally administered and TQ treatment continued until fifth day) and Group 4 (TQ at 40mg/kg/day dose for five days). There was a significant increment in CP group in terms of congestion, edema and pycnotic nuclei in myocardial fibers, comparing with other groups. TQ group exhibited significant increase in expression of antiapoptotic protein Bcl-2, comparing with CP group (p<0.05). In only CP administered group, expression of antiapoptotic protein Bcl-2 was lowest comparing with other groups. Established data indicate that cisplatin is cardiotoxic and thymoquinone may be useful in treating CP-induced cardiac injury.
Highlights
Cisplatin is an effective chemotherapeutic drug that belonging to platinum relating agents used in oncological applications
In only CP administered group, expression of antiapoptotic protein Bcl-2 was lowest comparing with other groups
Established data indicate that cisplatin is cardiotoxic and thymoquinone may be useful in treating CP-induced cardiac injury
Summary
Cisplatin is an effective chemotherapeutic drug that belonging to platinum relating agents used in oncological applications. The optimal efficacy of CP use is generally restricted by toxic effects such as nephrotoxicity, ototoxicity and cardiovascular complications[3,4]. CP-induced cardiotoxicity which is characterized by various findings including electrocardiographic changes, arrhythmia, cardiomyopathy and congestive heart failure has been reported in numerous studies. Huge efforts were made over many years to find out more powerful but less toxic agents, CP is still widely prescribed[5]. Mechanisms underlying anti-tumoral activity of CP is wellknown, cellular and molecular factors which cause CP-induced cardiotoxicity are still unclear. Several experimental and clinical studies support the idea that the enhancement of oxidative stress may involve in this insult[6]
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