Green tea polyphenols alleviate early BBB damage during experimental focal cerebral ischemia through regulating tight junctions and PKCalpha signaling

BMC Complementary and Alternative Medicine

Yixue Xue²  Yunhui Liu³  Bo Yu³  Ping Wang²  Zhenhua Wang¹  Xiaobai Liu² 

[1] Department of Physiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning Province, 110001, People’s Republic of China;Institute of Pathology and Pathophysiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning Province, 110001, People’s Republic of China;Department of Neurosurgery, Shengjing Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, 110004, People’s Republic of China

关键词: Protein kinase Cα;    Tight junction;    Blood–brain barrier;    Cerebral ischemia;    Green tea polyphenols;   

Others  :  1221059
DOI  :  10.1186/1472-6882-13-187

 received in 2012-12-06, accepted in 2013-07-17,  发布年份 2013

【 摘 要 】

Background

It has been supposed that green tea polyphenols (GTPs) have neuroprotective effects on brain damage after brain ischemia in animal experiments. Little is known regarding GTPs’ protective effects against the blood-brain barrier (BBB) disruption after ischemic stroke. We investigated the effects of GTPs on the expression of claudin-5, occludin, and ZO-1, and the corresponding cellular mechanisms involved in the early stage of cerebral ischemia.

Methods

Male Wistar rats were subjected to a middle cerebral artery occlusion (MCAO) for 0, 30, 60, and 120 min. GTPs (400 mg/kg/day) or vehicle was administered by intragastric gavage twice a day for 30 days prior to MCAO. At different time points, the expression of claudin-5, occludin, ZO-1, and PKCα signaling pathway in microvessel fragments of cerebral ischemic tissue were evaluated.

Results

GTPs reduced BBB permeability at 60 min and 120 min after ischemia as compared with the vehicle group. Transmission electron microscopy also revealed that GTPs could reverse the opening of tight junction (TJ) barrier at 60 min and 120 min after MACO. The decreased mRNA and protein expression levels of claudin-5, occludin, and ZO-1 in microvessel fragments of cerebral ischemic tissue were significantly prevented by treatment with GTPs at the same time points after ischemia in rats. Furthermore, GTPs could attenuate the increase in the expression levels of PKCα mRNA and protein caused by cerebral ischemia.

Conclusions

These results demonstrate that GTPs may act as a potential neuroprotective agent against BBB damage at the early stage of focal cerebral ischemia through the regulation of TJ and PKCα signaling.

【 授权许可】

   
2013 Liu et al.; licensee BioMed Central Ltd.

【 图 表 】

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