FFNT25 ameliorates unilateral ureteral obstruction-induced renal fibrosis. (1st January 2019)

• Record Type: Journal Article
• Authors: Li, Wen; Lu, Yue; Lou, Yan; Zhao, Shiyue; Cui, Wenpeng; Wang, Yangwei; Luo, Manyu; Sun, Jing; Miao, Lining
• Is Part Of: Renal failure. Volume 41:Number 1(2019)
• Page Start: 419
• Page End: 426
• Publication Date: 2019-01-01
• Subjects: FFNT25 -- UUO -- renal fibrosis -- α-SMA -- PAI-1; Chronic renal failure -- Periodicals; Acute renal failure -- Periodicals; Uremia -- Periodicals; 616.614005
• DOI: 10.1080/0886022X.2019.1612430
• Languages: English
• ISSNs: 0886-022X

Abstract

Abstract: Renal fibrosis is a common pathological feature of chronic kidney disease (CKD) patients who progress to end-stage renal disease (ESRD). With the increasing incidence of CKD, it is of importance to develop effective therapies that blunt development of renal fibrosis. FFNT25 is a newly developed molecular compound that could be used to prevent fibrosis. In this study, we administered FFNT25 to rats following unilateral ureteral obstruction (UUO) to investigate its anti-fibrosis mechanism. Thirty-two Sprague-Dawley rats were randomly divided into four groups: (1) control (normal rats), (2) sham-operated, (3) UUO-operated + vehicle, and (4) UUO-operated + FFNT25. Two weeks after UUO, the rats were gavaged with either FFNT25 (20.6 mg/kg/day) or vehicle for two weeks. Serum, urine, and kidney samples were collected at the end of the study. FFNT25 reduced levels of renal fibrosis and decreased mRNA and protein levels of extracellular matrix (ECM) markers α-smooth muscle actin (α-SMA) and plasminogen activator inhibitor-1 (PAI-1) following UUO compared to vehicle treatment ( n = 8, p <.05). The current results indicate that FFNT25 can affect both the production and degradation of collagen fibers to reduce fibrosis.