期刊论文详细信息
BMC Complementary and Alternative Medicine
The protective effect of baicalin against renal ischemia-reperfusion injury through inhibition of inflammation and apoptosis
Tongyu Zhu1  Ruiming Rong2  Guisheng Qi2  Gaurab Pokhrel2  Liping Li1  Long Li1  Miao Lin2 
[1] Shanghai Key Laboratory of Organ Transplantation, Shanghai, China;Department of Urology, Fudan University Zhongshan Hospital, Shanghai, China
关键词: Apoptosis;    Inflammation;    Kidney;    Ischemia-reperfusion;    Baicalin;   
Others  :  1220342
DOI  :  10.1186/1472-6882-14-19
 received in 2013-08-07, accepted in 2014-01-09,  发布年份 2014
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【 摘 要 】

Background

Renal 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.

Methods

Baicalin 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.

Results

Baicalin 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.

Conclusions

Baicalin 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】

   
2014 Lin et al.; licensee BioMed Central Ltd.

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