Taurine alleviates kidney injury in a thioacetamide rat model by mediating Nrf2/HO-1, NQO-1, and MAPK/NF-κB signaling pathways

Abstract

This study aimed to investigate the molecular mechanisms by which taurine exerts its reno-protective effects in thioacetamide (TAA)-induced kidney injury in rats. Rats received taurine (100 mg/kg daily, intraperitoneally) either from day 1 of TAA injection (250 mg/kg twice weekly for 6 weeks) or after 6 weeks of TAA administration. Taurine treatment, either concomitant or later as a therapy, restored kidney functions, reduced BUN, creatinine, MDA, and increased renal levels of SOD and reversed the increase of KIM-1 and NGAL caused by TAA. Taurine treatment also led to a significant rise in Nrf2, HO-1, and NQO-1 levels, with significant suppression of ERK 1/2, NF-κB, and TNFα gene expressions, and IL-18 and TNFα protein levels compared to those in TAA kidney-injured rats. Taurine exhibited reno-protective potential in TAA-induced kidney injury through its anti-oxidant and anti-inflammatory effects. Taurine anti-oxidant activity is accredited to its effect on Nrf-2 induction and subsequent activation of HO-1 and NQO-1. In addition, taurine exerts its anti-inflammatory effect via regulating NF-κB transcription and subsequent production of pro-inflammatory mediators via MAPK signaling regulation.