Abstract
Xiao-Chai-Hu-Tang (XCHT), a traditional Chinese medicine formula consisting of seven medicinal plants, is used in the treatment of various diseases. We show here that XCHT could protect type-1 diabetic mice against diabetic nephropathy, using streptozotocin (STZ)-induced diabetic mice and high-glucose (HG)-exposed rat mesangial cell (RMC) as models. Following 4 weeks of oral administration with XCHT, renal functions and renal hypertrophy significantly improved in the STZ-diabetic mice, while serum glucose was only moderately reduced compared to vehicle treatment. Treatment with XCHT in the STZ-diabetic mice and HG-exposed RMC resulted in a decrease in expression levels of TGF-β1, fibronectin, and collagen IV, with concomitant increase in BMP-7 expression. Data from DPPH assay, DHE stain, and CM-H2DCFDA analysis indicated that XCHT could scavenge free radicals and inhibit high-glucose-induced ROS in RMCs. Taken together, these results suggest that treatment with XCHT can improve renal functions in STZ-diabetic mice, an effect that is potentially mediated through decreasing oxidative stress and production of TGF-β1, fibronectin, and collagen IV in the kidney during development of diabetic nephropathy. XCHT, therefore merits further investigation for application to improve renal functions in diabetic disorders.
Highlights
Increasing prevalence of nephropathy and/or end-stage renal disease (ESRD) in diabetic patients is becoming a serious social and health problem worldwide [1, 2]
These results suggest that treatment with XCHT can improve renal functions in STZ-diabetic mice, an effect that is potentially mediated through decreasing oxidative stress and production of TGF-β1, fibronectin, and collagen IV in the kidney during development of diabetic nephropathy
We have previously shown that exposing rat mesangial cell (RMC) to high-glucose (HG) medium raises ROS production in these cells [12], and ROS induced by hyperglycemia can stimulate TGF-β1 and contribute to diabetes nephropathy [6]
Summary
Increasing prevalence of nephropathy and/or end-stage renal disease (ESRD) in diabetic patients is becoming a serious social and health problem worldwide [1, 2]. Hyperglycemia is considered as the main factor to induce diabetic nephropathy (DN), and clinical strategies for management of DN include glycemic control and blood pressure regulation [3, 4]. Pathological changes of DN are characterized by structural abnormalities including renal-cell hypertrophy, increase in thickness of glomerular basement membranes, and progressive accumulation of extracellular matrix components [6]. Hyperglycemia and oxidative stress during DN induce abnormal production and stimulation of TGF-β1-resident renal cells [4, 6, 8, 9]. TGF-β1 causes augmented deposition of extracellular matrix proteins, such as collagen IV and fibronectin, in the glomeruli, inducing mesangial expansion and glomerular basement membrane thickening [1].
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