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        Treatment with protocatechuic acid attenuates cisplatin-induced toxicity in the brain and liver of male Wistar rats

        Anne A. Adeyanju,Babatunde J. Oso,Olorunfemi R. Molehin,Joshua O. Fadero,Busayo B. Odulote 경희대학교 융합한의과학연구소 2023 Oriental Pharmacy and Experimental Medicine Vol.23 No.1

        This study investigated the ameliorative effect of protocatechuic acid (PCA) in oxidative stress induced by cisplatin (CPL) in the brain and liver of Wistar rats and its involvement in the activation of nuclear factor-kappaB (NF-κB) and p53 gene pathways in cisplatin-induced brain toxicity. Experimental animals were randomly assigned to five groups. Group A (control) received normal saline orally for five days. Group B received a single dose of CPL (7 mg/kg body weight) on the 5th day intraperitoneally. Group C was administered 10 mg/kg/day of PCA orally for 5 days and CPL (7 mg/kg body weight) on the 5th day intraperitoneally. Group D received 20 mg/kg/day of PCA orally for 5 days and CPL (7 mg/kg body weight) on the 5th day intraperitoneally. Group E received 20 mg/kg/day of PCA orally for 5 days to study the effect of PCA at a higher dose. The rats were sacrificed on the 6th day. The biochemical assessments carried out included liver function test, serum lipid profile, and hepatic and neuronal antioxidant status. Histoarchitecture of the liver and brain and neuronal expressions of NF-κB and p53 were assessed through staining techniques. PCA maintained the serum protein, albumin, lipid profile, and prevented lipid peroxidation and reduction in the activities of antioxidant enzymes induced by a single dose of CPL. Moreover, PCA alleviated the CPL-induced degeneration of the hepatocytes, neuronal injuries and reduced the expressions of the neuronal NF-κB and p53 gene. Our data showed that PCA might be exerting its antioxidant activities in the brain through NF-kB and p53-dependent pathways. Overall, our results indicated that PCA could attenuate oxidative stress induced by CPL in both organs and also modulate the expression of NF-kB and p53 in the brain.

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