Journal
BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
Volume 13, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1472-6882-13-187
Keywords
Green tea polyphenols; Cerebral ischemia; Blood-brain barrier; Tight junction; Protein kinase C alpha
Categories
Funding
- Natural Science Foundation, China [30901781, 81171131, 81172197, 81272564, 30973079, 81072056]
- Special fund for Scientific Research of Doctor-degree Subjects in Colleges and Universities, China [20092104110015, 20102104110009]
- Natural Science Foundation of Liaoning Province, China [201102300]
- Liaoning Science and Technology Plan Projects, China [2011225020]
- Shenyang Science and Technology Plan Projects, China [F11-264-1-153, F12-277-1-05]
- Outstanding Scientific Fund of Shengjing Hospital, China
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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 PKC alpha 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 PKC alpha 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 PKC alpha signaling.
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