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Open Access Research article

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

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

Author Affiliations

1 Department of Urology, Fudan University Zhongshan Hospital, Shanghai, China

2 Shanghai Key Laboratory of Organ Transplantation, Shanghai, China

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BMC Complementary and Alternative Medicine 2014, 14:19  doi:10.1186/1472-6882-14-19

Published: 13 January 2014

Abstract

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.

Keywords:
Baicalin; Ischemia-reperfusion; Kidney; Inflammation; Apoptosis