Abstract Title:

Paeoniflorin ameliorates renal function in cyclophosphamide-induced mice via AMPK suppressed inflammation and apoptosis.

Abstract Source:

Biomed Pharmacother. 2016 Dec ;84:1899-1905. Epub 2016 Nov 6. PMID: 27829543

Abstract Author(s):

Qiang Liu, Xuemei Lin, Hong Li, Jia Yuan, Yuping Peng, Lei Dong, Shejiao Dai

Article Affiliation:

Qiang Liu


The study is to investigate the effects of paeoniflorin (PA) on renal function in cyclophosphamide-induced mice. Mice were injected with intraperitoneal cyclophosphamide (CYP, 200mg/kg) or saline respectively. Mice were treated with PA (15, 30mg/kg/day) or vehicle for the next 7 days. Then, mice were sacrificed to analyze the biochemical, histological parameters and mechanism research. Our results shown that PA significantly decreased the urine levels of uric acid and creatinine, serum and kidney levels of cytokines such as interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), PA also obviously attenuated the histological changes of the kidney tissues caused by CYP. Moreover, Western blot demonstrated that PA increased the AMPK levels and inhibited NF-κB signaling pathway and apoptosis in CYP-stimulated kidney tissues. In conclusion, PA might be considered as an effective agent in the amelioration of the kidney toxicity resulting from CYP treatment.

Print Options

Sayer Ji
Founder of GreenMedInfo.com

Subscribe to our informative Newsletter & get Nature's Evidence-Based Pharmacy

Our newsletter serves 500,000 with essential news, research & healthy tips, daily.

Download Now

500+ pages of Natural Medicine Alternatives and Information.

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2021 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.