Effect and its mechanism of FoxO3a activates FasL on renal tubular epithelial cell apoptosis induced by renal ischemia /reperfusion injury
Jia Xu
Abstract
Jia Xu
Abstract
Objective To explore the role and mechanism of forkhead box proteinO3 a activates Fas ligand on renal tubular epithelial cell( RTC) apoptosis induced by renal ischemia/reperfusion( I/R).Methods The model by clamping renal pedicles for 45 minutes following reperfusion was established. The protein expression of forkhead box proteinO3 a and Fas ligand were examined by western blotting. Apoptosis of RTC was assessed by TdT- mediated dUTP nick- end Labeling( TUNEL) method and transmission electron microscopic( TEM). Renal function was assessed by biochemical automatic analyzer. Results The protein expression level of forkhead box proteinO3 a and Fas ligand was increased significantly following renal I /R at 1 h. RTC nucleus was shrinking,crushing followed renal I /R,and a significant increase in the number of TUNEL- positive cells following renal I /R was displayed compared with the sham group. The level of blood urea nitrogen( BUN) and serum creatinine( Scr) was increased significantly compared with the sham group( P 0. 05,P 0. 01). Conclusion FoxO3 a could be activated during renal I /R,and then up- regulated FasL protein expression,facilitated renal tubular epithelial cell apoptosis,in turn,aggravated renal I /R injury in rats.
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Objective To explore the role and mechanism of forkhead box proteinO3 a activates Fas ligand on renal tubular epithelial cell( RTC) apoptosis induced by renal ischemia/reperfusion( I/R).Methods The model by clamping renal pedicles for 45 minutes following reperfusion was established. The protein expression of forkhead box proteinO3 a and Fas ligand were examined by western blotting. Apoptosis of RTC was assessed by TdT- mediated dUTP nick- end Labeling( TUNEL) method and transmission electron microscopic( TEM). Renal function was assessed by biochemical automatic analyzer. Results The protein expression level of forkhead box proteinO3 a and Fas ligand was increased significantly following renal I /R at 1 h. RTC nucleus was shrinking,crushing followed renal I /R,and a significant increase in the number of TUNEL- positive cells following renal I /R was displayed compared with the sham group. The level of blood urea nitrogen( BUN) and serum creatinine( Scr) was increased significantly compared with the sham group( P 0. 05,P 0. 01). Conclusion FoxO3 a could be activated during renal I /R,and then up- regulated FasL protein expression,facilitated renal tubular epithelial cell apoptosis,in turn,aggravated renal I /R injury in rats.
Key concepts: TUNEL assay, Fas ligand, Apoptosis, Blood urea nitrogen, Renal function, Creatinine, Kidney, Renal ischemia