Esculetin Attenuates Doxorubicin-Induced Kidney Damage By Reducing Heat Shock Proteins Expression Levels

The effectiveness of Doxorobucin (DOX), a commonly used anti-cancer and immunosuppressive medication, is hindered by its potential for organ toxicity. Prolonged use of DOX is associated with severe hepatocellular toxicity. This study reveals fresh insights into the therapeutic impact of esculetin (E) on DOX-induced kidney cell damage. Esculetin demonstrates its remedial effects by modulating heat shock protein signaling pathways. In our research, we explored the impact of DOX and E on the expression of the 70 kDa HSP gene family, including Hspa1a, Hspa4, and Hspa5, which are small stress proteins in Rattus norvegicus. The study involved the assignment of five different groups (Control, DOX, E50 mg/kg, E100 mg/kg, DOX+ E50 mg/kg, and DOX+ E100 mg/kg). Subsequently, kidney tissues were collected from rats, and cDNA libraries were generated at the conclusion of the application process. The Real-Time PCR method was employed using these libraries to detect HSP70 genes. Analyses conducted on Hspa1a, Hspa4 and Hspa5 expression revealed a statistically significant increase in the DOX group compared to the control group. Additionally, the combination of DOX and esculetin demonstrates a reduction in the increase caused by DOX alone. The study suggests that esculetin could serve as a potential protective agent for shielding kidney tissue from oxidative damage and apoptosis.