The protective effect of baicalin against renal ischemia-reperfusion injury through inhibition of inflammation and apoptosis

BMC Complementary and Alternative Medicine

Research Article

Guisheng Qi¹  Miao Lin¹  Gaurab Pokhrel¹  Ruiming Rong¹  Liping Li²  Tongyu Zhu²  Long Li² 

[1] Department of Urology, Fudan University Zhongshan Hospital, Shanghai, China;Shanghai Key Laboratory of Organ Transplantation, Shanghai, China;

关键词: Baicalin;    Ischemia-reperfusion;    Kidney;    Inflammation;    Apoptosis;   

DOI  :  10.1186/1472-6882-14-19

 received in 2013-08-07, accepted in 2014-01-09,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundRenal ischemia-reperfusion injury (IRI) increases the rates of acute kidney failure, delayed graft function, and early mortality after kidney transplantation. The pathophysiology involved includes oxidative stress, mitochondrial dysfunction, and immune-mediated injury. The anti-oxidation, anti-apoptosis, and anti-inflammation properties of baicalin, a flavonoid glycoside isolated from Scutellaria baicalensis, have been verified. This study therefore assessed the effects of baicalin against renal IRI in rats.MethodsBaicalin was intraperitoneally injected 30 min before renal ischemia. Serum and kidneys were harvested 24 h after reperfusion. Renal function and histological changes were assessed. Markers of oxidative stress, the Toll-like receptor (TLR)2 and TLR4 signaling pathway, mitochondrial stress, and cell apoptosis were also evaluated.ResultsBaicalin treatment decreased oxidative stress and histological injury, and improved kidney function, as well as inhibiting proinflammatory responses and tubular apoptosis. Baicalin pretreatment also reduced the expression of TLR2, TLR4, MyD88, p-NF-κB, and p-IκB proteins, as well as decreasing caspase-3 activity and increasing the Bcl-2/Bax ratio.ConclusionsBaicalin may attenuate renal ischemia-reperfusion injury by inhibiting proinflammatory responses and mitochondria-mediated apoptosis. These effects are associated with the TLR2/4 signaling pathway and mitochondrial stress.

【 授权许可】

Unknown   
© Lin et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.