ArticleEvidence-based complementary and alternative medicine : eCAM2013
Renal Protective Role of Xiexin Decoction with Multiple Active Ingredients Involves Inhibition of Inflammation through Downregulation of the Nuclear Factor-κB Pathway in Diabetic Rats.
Article in Evidence-based complementary and alternative medicine : eCAM, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 15 citations in OpenAlex.
- Xiexin Tang improves the symptom of type 2 diabetic rats by modulation of the gut microbiota.Scientific reports · 2018Article
- Review of Herbal Traditional Chinese Medicine for the Treatment of Diabetic Nephropathy.Journal of diabetes research · 2016Review
- Article
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Authors and funding
10 authors at 2 institutions in 1 country.
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Abstract
In Chinese medicine, Xiexin decoction (XXD) has been used for the clinical treatment of diabetes for at least 1700 years. The present study was conducted to investigate the effective ingredients of XXD and their molecular mechanisms of antidiabetic nephropathy in rats. Rats with diabetes induced by high-fat diet and streptozotocin were treated with XXD extract for 12 weeks. XXD significantly improved the glucolipid metabolism disorder, attenuated albuminuria and renal pathological changes, reduced renal advanced glycation end-products, inhibited receptor for advanced glycation end-product and inflammation factors expression, suppressed renal nuclear factor- κ B pathway activity, and downregulated renal transforming growth factor- β 1. The concentrations of multiple components in plasma from XXD were determined by liquid chromatography and tandem mass spectrometry. Pharmacokinetic/pharmacodynamic analysis using partial least square regression revealed that 8 ingredients of XXD were responsible for renal protective effects via actions on multiple molecular targets. Our study suggests that the renal protective role of XXD with multiple effective ingredients involves inhibition of inflammation through downregulation of the nuclear factor- κ B pathway, reducing renal advanced glycation end-products and receptor for advanced glycation end-product in diabetic rats.
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