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Neuroprotective Effects of Polysaccharides From Wolfberry, the Fruits of Lycium Barbarum, Against Homocysteine-Induced Toxicity in Rat Cortical Neurons

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.

Ho YS, Yu MS, Yang XF, So KF, Yuen WH, Chang RC. Neuroprotective effects of polysaccharides from wolfberry, the fruits of Lycium barbarum, against homocysteine-induced toxicity in rat cortical neurons. 1. J Alzheimers Dis. 2010;19(3):813-27.

Previous clinical and epidemiological studies have suggested that elevated plasma homocysteine (Hcy) levels increased the risk of Alzheime's disease (AD). Although the underlying mechanisms of its toxicity are elusive, it has been shown that Hcy damages neurons by inducing apoptosis, DNA fragmentation, and tau hyperphosphorylation. Wolfberry (Lycium barbarum) is a fruit that is known for its eye-protective and anti-aging properties in Asian countries. Previous studies from our laboratory have demonstrated that polysaccharides derived from wolfberry (LBA) have the ability to protect neurons from amyloid-beta (Abeta) peptide neurotoxicity. We hypothesize that the neuroprotective effects of wolfberry is not limited to Abeta and can also provide protection against other AD risk factors. In this study, we aim to elucidate the neuroprotective effects of wolfberry against Hcy-induced neuronal damage. Our data showed that LBA treatment significantly attenuated Hcy-induced neuronal cell death and apoptosis in primary cortical neurons as demonstrated by LDH and caspase-3 like activity assay. LBA also significantly reduced Hcy-induced tau phosphorylation at tau-1 (Ser198/199/202), pS396 (Ser396), and pS214 (Ser214) epitopes as well as cleavage of tau. At the same time, we also found that the phosphorylation level of p-GSK3beta (Ser9/Tyr 216) remained unchanged among different treatment groups at all detected time points. LBA treatment suppressed elevation of both p-ERK and p-JNK. In summary, our data demonstrated that LBA exerted neuroprotective effects on cortical neurons exposed to Hcy. Therefore, LBA has the potential to be a diseasemodifying agent for the prevention of AD.