Abstract
JiaWeiDangGui (JWDG) decoction has anti-inflammatory and antifibrotic effects, which is used widely for the treatment of various kidney diseases. In previous studies, we have found that JWDG decoction can reduce the quantity of proteinuria, but the mechanism was unknown. Here, we studied the protective effect of JWDG decoction in adriamycin-induced nephropathy on rat. JWDG decoction, at 10 mL/kg/d, 20 mL/kg/d, and 40 mL/kg/d, was orally administered daily for 12 weeks. Therapeutic effects and mechanisms were further examined. The kidney function related biochemical indexes were measured by automatic biochemistry analyzer. The pathomorphological changes were observed using light and transmission electron microcopies. The proteins expressions of podocin, nephrin, collagen IV, and fibronectin (FN) were examined by immunohistochemical staining, and key proteins involved in TGF-β/Smad signaling were evaluated by RT-PCR and western blotting. Compared with vehicle-treated controls, JWDG decoction decreased the quantity of proteinuria; reduced glomerulosclerotic lesions induced by ADR; and preserved the expression of podocin and nephrin. JWDG decoction also inhibited the expression of the collagen IV, FN, and fibrogenic TGF-β. Further studies revealed that inhibition of renal fibrosis was associated with the blockade of TGF-β/Smad signaling and downregulation of snail expression dose dependently. JWDG decoction prevents proteinuria production, podocyte dysfunction, and kidney injury in adriamycin nephropathy by inhibiting TGF-β/Smad signaling.
Highlights
IntroductionChronic kidney diseases (CKD) is characterized by a progressive loss of renal function, associated with reduction of glomerular filtration rate and massive accumulation of proteinuria
Chronic kidney diseases (CKD) are emerging as a public health problem worldwide [1]
We investigated effects of JWDG in the ADR nephropathy, a model characterized by initial podocyte injury and albuminuria and subsequent renal inflammation and fibrosis
Summary
CKD is characterized by a progressive loss of renal function, associated with reduction of glomerular filtration rate and massive accumulation of proteinuria. Adriamycin-induced nephropathy is a classic rat model of chronic kidney disease which is considered to be an experimental analogue of human minimal lesion nephrotic syndrome, leading to chronic proteinuria and renal failure [2,3,4]. It has been shown that podocytes play an important role in maintaining the integrity of the glomerular filtration barrier. The podocyte injury is one of the major causes leading to defective glomerular filtration, which results in proteinuria. TGF-β initiates its fibrosis activity through the Smad protein signaling pathways, which play crucial roles in renal fibrosis [17, 18]. The restoration of podocyte and the inhibition of TGF-β/Smad signaling will be potential strategies for reversing progression of CKD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
