Boswellic Acid and Carnosine Ameliorate Vanadyl-Sulfate-Induced Renal Damage via Regulating Nrf2/HO-1 and PI3K/AKT Pathways

Nephrotoxicity is a condition caused by the negative effects of several chemotherapy treatments on the kidneys. Our target was to determine how boswellic and carnosic acids protected rats against vanadyl sulfate (VOS)-induced nephrotoxicity. A total of 30 male Wistar albino rats were used in the investigation. They were divided into sex groups (five rats in each group) as follows: Rats in the control group were given carboxymethyl cellulose (CMC) at a concentration of 0.5%. VOS group was administered a weekly intraperitoneal injection of VOS 50 mg/kg for six consecutive weeks. For 6 weeks in a row, rats in the boswellic acid group were given injections of BA every day at a dose of 100 mg/kg orally. Group receiving carnosic acid received 100 mg/kg of CA orally daily for 6 consecutive weeks. For 6 weeks, rats in the boswellic acid plus VOS group were given 50 mg/kg of VOS intraperitoneally (i.p.) once a week and 100 mg/kg of BA orally daily. For 6 weeks, the carnosic acid plus VOS group received 50 mg/kg of VOS intraperitoneally once a week and 100 mg/kg of CA orally daily. In contrast to the control group, our results demonstrated that the injection of vanadyl sulfate to the VOS group contributed a significant increase in creatinine and blood urea as well as disordered kidney oxidative antioxidant interaction. The injection of vanadyl sulfate to the VOS group produced an increase in renal MDA concentration and a decrease in renal SOD activity, GSH content, GR, and CAT activities in comparison to the control group. When compared to the control group, our study on renal mRNA expression revealed that administering vanadyl sulfate to the VOS group increases renal iNOS, PI3K, and AKT mRNA expressions and modulates the mRNA expression of renal Nrf2 and HO-1. According to the current investigation, treating rats with BA or CA can reduce their nephrotoxicity from VOS; when the defective kidney oxidative antioxidant redox levels were returned to normal, the fibrosis in the Van-treated animals decreased. These findings are consistent with interactions between the Pi3k/Akt and Nrf2/Ho-1 pathways, as one of the human body's most vital organs.