EFFECT OF TERT-BUTYLHYDROQUINONE ON CARDIAC INFLAMMATION AND APOPTOTIC BIOMARKERS IN ALBINO WISTAR RATS TREATED WITH CISPLATIN

Cisplatin (CDDP) is an anti-neoplastic medication, which was approved for the treatment of cancer years ago. However, the continuous administration of the medication causes side effects that cannot be ignored. Oxidative stress, inflammation and apoptosis are the mechanisms through which CDDP induces intoxication in various organs of the body. Tert-butylhydroquinone (tBHQ) is a known food additive and a powerful antioxidant. Therefore, the present study was aimed at exploring the ameliorating role of tBHQ on cardiac inflammation and apoptosis triggered by CDDP. Twenty-four (24) male albino Wistar rats were randomly grouped in four cages (n = 6/cage), namely: normal control (NC), tBHQ, CDDP, and tBHQ+CDDP group. tBHQ was administered orally at a dose of 50 mg/kg body weight (b.w) for 14 days. CDDP (7mg/kg b.w) was administered on the 8th day, intraperitoneally, to their respective groups. The rats were sacrificed on the 15th day under pentobarbitone (60 mg/kg b.w.) anesthesia. The heart was harvested for analysis of inflammation and apoptosis biomarkers. The results showed significant increases (p < 0.05) in NF-κB and TNFαpro-inflammatory protein levels. Furthermore, significant increases (p < 0.05) in proapoptotic protein levels such as Bax and caspase-3, and a significant decrease (p < 0.05) in the level of the anti-apoptotic protein, Bcl2, were observed in the CDDP group when compared to the NC group. Following the intervention with tBHQ, these negative effects were significantly (p < 0.05) ameliorated. In conclusion, tBHQ reduced CDDP-induced cardiotoxicity by reducing pro-inflammatory and proapoptotic protein levels, thereby lowering cardiomyocyte inflammation and apoptosis. Therefore, tBHQ may preserve the heart of cancer patients undergoing CDDP chemotherapy.