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Findings from Nanjing University Broaden Understanding of

Nephrology (Silymarin protects against renal injury through
normalization of lipid metabolism and mitochondrial
biogenesis in high fat-fed mice)
Date: Aug. 19, 2017
From: Obesity, Fitness & Wellness Week
Publisher: NewsRX LLC
Document Type: Report
Length: 452 words

Full Text:
2017 AUG 19 (NewsRx) -- By a News Reporter-Staff News Editor at Obesity, Fitness & Wellness Week -- Research findings on
Nephrology are discussed in a new report. According to news reporting originating in Jiangsu, People's Republic of China, by
NewsRx journalists, research stated, "Obesity is associated with an increased risk of chronic kidney diseases and the conventional
treatment with renin-angiotensin-aldosterone system (RAAS) inhibitors is not enough to prevent renal injury and prolong the
progression of disease. Recently, silymarin has shown protective effects on renal tissue injury, but the underlying mechanisms
remain elusive."

Funders for this research include Key Project of the Medical Science and Technology Development Foundation, Nanjing Department
of Health, National Natural Science Foundation of China, Six Talent Peaks Project in Jiangsu Province, Jiangsu Provincial Medical
Youth Talent.

The news reporters obtained a quote from the research from Nanjing University, "The goal of this study was to investigate the
potential capacity of silymarin to prevent renal injury during obesity induced by high fat diet (HFD) in mice. In vivo, male C57BL/6
mice received HFD (60% of total calories) for 12 weeks, randomized and treated orally with vehicle saline or silymarin (30 mg/kg
body weight/d) for 4 weeks. In vitro, human proximal tubular epithelial cells (HK2) were exposed to 300 mu M palmitic acid (PA) for
36 h followed by silymarin administration at different concentrations. The administration of silymarin significantly ameliorated HFD
induced glucose metabolic disorders, oxidative stress and pathological alterations in the kidney. Silymarin significantly mitigated renal
lipid accumulation, fatty acid beta-oxidation and mitochondrial biogenesis in HFD mice and PA treated HK2 cells. Furthermore,
silymarin partly restored mitochondrial membrane potential of HK2 cells after PA exposure."

According to the news reporters, the research concluded: "Silymarin can improve oxidative stress and preserve mitochondrial
dysfunction in the kidney, potentially via preventing accumulation of renal lipids and fatty acid beta-oxidation."

For more information on this research see: Silymarin protects against renal injury through normalization of lipid metabolism and
mitochondrial biogenesis in high fat-fed mice. Free Radical Biology and Medicine, 2017;110():240-249. Free Radical Biology and
Medicine can be contacted at: Elsevier Science Inc, 360 Park Ave South, New York, NY 10010-1710, USA. (Elsevier -
www.elsevier.com; Free Radical Biology and Medicine - www.journals.elsevier.com/free-radical-biology-and-medicine/)

Our news correspondents report that additional information may be obtained by contacting D.L. Zhu, Nanjing University, Sch Med,
Nanjing Drum Tower Hosp, Dept. of Endocrinol, Nanjing 210008, Jiangsu, People's Republic of China. Additional authors for this
research include R. Meng, B. Huang, Y. Bi, S.M. Shen and B. Feng.

Keywords for this news article include: Jiangsu, People's Republic of China, Asia, Nephrology, Kidney, Nanjing University.

Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2017, NewsRx LLC

Copyright: COPYRIGHT 2017 NewsRX LLC

http://www.newsrx.com/newsletters/Obesity,-Fitness-and-Wellness-Week.html
Source Citation (MLA 9th Edition)
"Findings from Nanjing University Broaden Understanding of Nephrology (Silymarin protects against renal injury through
 normalization of lipid metabolism and mitochondrial biogenesis in high fat-fed mice)." Obesity, Fitness & Wellness Week, 19 Aug.
2017, p. 2800. Gale Academic OneFile, link.gale.com/apps/doc/A500451143/AONE?u=lyceumph&sid=bookmark-
AONE&xid=65efa8df. Accessed 22 Mar. 2022.
Gale Document Number: GALE|A500451143