Taurine has potent protective function against glutamate-induced neuronal injury presumably through its function in regulation of intracellular free calcium level, [Ca2+]i. In this communication, we report that taurine exerts its protective function through one or more of the following mechanisms: 1. Inhibition of glutamate-induced calcium influx through L-, N- and P/Q-type voltage-gated calcium channels and NMDA receptor calcium channel; 2. Attenuation of glutamate-induced membrane depolarization; 3. Prevention of glutamate-induced apoptosis via preventing glutamate-mediated down-regulation of Bcl-2; 4. Prevention of cleavage of Bcl-2 by calpain. This action of taurine is due to its inhibition on glutamate induced calpain activation. Based on these observations, we propose that taurine protects neurons against glutamate-induced neurotoxicity in part, by preventing glutamate-induced membrane depolarization, elevation of [Ca2+]i, activation of calpain, reduction of Bcl-2 and apoptosis.

The ethanol extract of dried flowers Osmanthus fragrans (OFE) was assessed for free radical scavenging effects measured by the bleaching of the 1,1-diphenyl-2-picryl-hydrazyl (DPPH) radical, scavenging of the hydroxyl anion, investigation of the ferric reducing/antioxidant power (FRAP) and lipid-peroxidation inhibition in rat tissues. OFE contained a high amount of total flavonoid and polyphenol. OFE presented the effects in the metal reducing power, FRAP assay with IC50 values of 0.23 µg/ml, and 7.74 µg/ml, respectively. OFE presented similar activities toward the DPPH and hydroxyl anion scavenging ability with IC50 values of 10 µg/ml. OFE with IC50 values between 46 and 97 µg/ml inhibited lipid peroxidation initiated by ferrous chloride in rat brain, liver, heart and kidney mitochodrias. Moreover, the neuroprotective activity of OFE was investigated under different insults (glutamate, arachidonic acid, and 6-hydroxydopamine) in Wistar rat primary cortical neurons. OFE with EC50 values between 66 and 165 µg/ml attenuated the neurotoxicity on MTT and LDH assays. In addition, the AKT protein expression of excitotoxicity and oxidative stress was displayed by western blotting analysis. OFE could up-regulate the glutamate and 6-OHDA decreased AKT expression. This is the first demonstration of the neuroprotective, free radical scavenging and anti-oxidative effects of O. fragrans.

Recently the herbal medicine was widely used to treat the neurodegenerative diseases. Neuroinflammation is a characteristic of pathologically affected tissue in several neurodegenerative disorders. These changes are particularly observed in affected brain areas of Alzheimer's disease (AD) and neuronal injury. In the central nervous system, ischemic insult-induced neuronal injury is believed to result from glutamate toxicity and glucose deprivation. Rhubarb– the root of Rheum officinale is one of the famous Chinese herbs as astringent bitters in gastric constipation and in diarrhea. It is used to treat blood stasis and cathartic by traditional medicine. Rhubarb has a very broad spectrum of biological activities and pharmacological functions, such as laxative, antiphlogistic, and homeostatic in the treatment of constipation, diarrhea, jaundice, and gastro-intestinal hemorrhage, etc. In this study, five natural anthraquionones of R. officinale were investigated the neuroprotective effects against glutamate/NMDA (Glu/NMDA) stimulation in primary cultured rat brain cortical neurons. Cell death was accessed by lactate dehydrogenase (LDH) release assay for necrosis, and mitochondrial activity was accessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) reduction activity assay. Among the five anthraquionones tested, it was found aloin, emodin and aloe-emodin decreased MTT reduction activity, whereas sennoside A and B significantly reduced Glu/NMDA-increased LDH release in cultured neurons. These results suggest that Rhubarb extract contain both neuroprotective and neurotoxic anthraquionones