Tempol functions as a broad-spectrum mimetic of SOD, effectively counteracting ROS[1]. Tempol markedly reduces the decline in mitochondrial respiration and the surge in LDH release from rat PT cells caused by H2O2, suggesting a decrease in cellular damage and mortality. The protective effects of Tempol are akin to those seen with the Fe2+ chelator DEF. Nonetheless, the simultaneous administration of DEF and Tempol does not enhance the protective effects against kidney ischemia/reperfusion injury or oxidative stress-induced injury/death of PT cells[2].
Tempol 动物研究
Animal study
Tempol can replicate the cardiac effects of resveratrol. Administered via gavage on a daily basis, Tempol leads to reduced PR and QTc intervals and elevated heart rates in mice, in contrast to those given an oral vehicle. These outcomes parallel those achieved with RSV treatment. The profiles of mice before and after treatment are depicted[1]. Tempol, a radical scavenger that can permeate cell membranes, mitigates the renal dysfunction and damage in rats caused by oxidative stress. It significantly lowers the elevated levels of urea, creatinine, γGT, AST, NAG, and FENa that result from renal ischemia/reperfusion, indicating an enhancement in renal health and a reduction in injury. Furthermore, Tempol considerably decreases the activity of kidney MPO and the concentration of MDA, which suggests a decrease in PMN infiltration and lipid peroxidation, respectively. Additionally, Tempol lessens the histological signs of renal harm linked to ischemia/reperfusion and markedly diminishes the staining for nitrotyrosine and PARS, implying a decrease in nitrosative and oxidative stress[2].
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