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Lycium Barbarum Extracts Protect the Brain From Blood-Brain Barrier Disruption and Cerebral Edema in Experimental Stroke
Posted by Admin, Senior Editor in Gogi Berry (Wolfberry)
Authored by PubMed
Topics: Gogi Berry Wolfberry Lycium Barbarum

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Goji berries (Lycium barbarum, wolfberry) grow on an evergreen shrub found in temperate and subtropical regions in China, Mongolia and in the Himalayas in Tibet. They are in the nightshade (Solonaceae) family. Goji berries are usually found dried. They are shriveled red berries that look like red raisins. Goji berries are rich in antioxidants, particularly carotenoids such as Beta-carotene and zeaxanthin. One of zeaxanthin's key roles is to protect the retina of the eye by absorbing blue light and acting as an antioxidant. Goji berries have been used for 6,000 years by herbalists in China, Tibet and India to: protect the liver, help eyesight, improve sexual function and fertility, strengthen the legs, boost immune function, improve circulation, and to promote longevity.

Yang D, Li SY, Yeung CM, Chang RC, So KF, Wong D, Lo AC. Lycium barbarum extracts protect the brain from blood-brain barrier disruption and cerebral edema in experimental stroke. 1. PLoS One. 2012;7(3):e33596. Epub 2012 Mar 16.
BACKGROUND AND PURPOSE: Ischemic stroke is a destructive cerebrovascular disease and a leading cause of death. Yet, no ideal neuroprotective agents are available, leaving prevention an attractive alternative. The extracts from the fruits of Lycium barbarum (LBP), a Chinese anti-aging medicine and food supplement, showed neuroprotective function in the retina when given prophylactically. We aim to evaluate the protective effects of LBP pre-treatment in an experimental stroke model. METHODS: C57BL/6N male mice were first fed with either vehicle (PBS) or LBP (1 or 10 mg/kg) daily for 7 days. Mice were then subjected to 2-hour transient middle cerebral artery occlusion (MCAO) by the intraluminal method followed by 22-hour reperfusion upon filament removal. Mice were evaluated for neurological deficits just before sacrifice. Brains were harvested for infarct size estimation, water content measurement, immunohistochemical analysis, and Western blot experiments. Evans blue (EB) extravasation was determined to assess blood-brain barrier (BBB) disruption after MCAO. RESULTS: LBP pre-treatment significantly improved neurological deficits as well as decreased infarct size, hemispheric swelling, and water content. Fewer apoptotic cells were identified in LBP-treated brains by TUNEL assay. Reduced EB extravasation, fewer IgG-leaky vessels, and up-regulation of occludin expression were also observed in LBP-treated brains. Moreover, immunoreactivity for aquaporin-4 and glial fibrillary acidic protein were significantly decreased in LBP-treated brains. CONCLUSIONS: Seven-day oral LBP pre-treatment effectively improved neurological deficits, decreased infarct size and cerebral edema as well as protected the brain from BBB disruption, aquaporin-4 up-regulation, and glial activation. The present study suggests that LBP may be used as a prophylactic neuroprotectant in patients at high risk for ischemic stroke.


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