TGFB1 and diabetic kidney disease: In immunohistological research, treatment of mice with PO (300 mg/kg/day, p.o., for ten weeks) revealed that it could reduce the expression levels of advanced glycation end products (AGE), TGF-β1, and intercellular adhesion molecule- (ICAM-) 1 in diabetic nephropathy through suppression of renal fibrosis and inflammation in diabetic db/db mice [50].