NOX1 abet mesangial fibrogenesis via iNOS induction in diabetes.

摘要: Both NADPH oxidase (NOX) and inducible nitric oxide synthase (iNOS) are the main sources of reactive oxygen species in kidney. However, their interactions oxidative stress contributions to kidney fibrosis during diabetic nephropathy have not been studied. Human mesangial cells were treated with normal glucose (5.6 mmol/L), high (30 mmol/L) presence or absence AGE (200 mg/L). Protein expressions NOX1, NOX2, NOX4, iNOS examined by immunoblotting. NOX was genetically silenced specific RNAi study between milieu. Superoxide (O·−) peroxynitrite (ONOO·−) productions assessed dihydroethidium hydroxyphenyl fluorescein, respectively. Fibrotic factors determined biochemistry assay. Superoxide, peroxynitrite, TGF-β, fibronectin as well protein increased milieu (high 30 mmol/L plus 200 abolishment induction 1400W would restore completely basal level attenuate superoxide production. Moreover, NOX1 inhibition only prevented but also abrogated changes consequent such fibrogenesis.