Protective and therapeutic role of Ginkgo biloba extract through TRPV1 channels in an in vitro Alzheimer's disease model.

Alzheimer's disease (AD) is a common cause of dementia that classified as neurodegenerative disorder.Based on the number of AD patients and related societal costs, certain clinical studies focused on the potential benefits of natural drugs (1).Researchers employed various synthetic or herbal compounds to determine their potential effects in AD (2).It is believed that Ginkgo biloba originated on the remote mountainous valleys at Zhejiang province in eastern China (3).Standardized Ginkgo biloba extract (GBE) is derived from the dried Ginkgo leaves and could be therapeutic in the management of dementia and memory disorders, as well as the Alzheimer's disease (AD).The medicinal use of Ginkgo biloba has been documented in China for nearly 5,000 years, namely to treat asthma (4,5).Crucial effects for AD have been reported primarily on the apoptotic pathway and mitochondrial functions, such as energy metabolism improvements, mitochondrial membrane stabilization, cytochrome C inhibition, anti-apoptotic Bcl-2 protein upregulation, and pro-apoptotic Bax protein downregulation, the reduction of caspase 9 and 3 levels and apoptotic necrosis in oxidative stress.Several basic and preclinical researches demonstrated that standardized Ginkgo biloba extract could groups than in the control (p<0.001).The apoptosis and intracellular ROS values were higher in AD group than in the GB+AD and AD+GB group (p<0.001) and the apoptosis level was higher in AD+GB group than GB+AD group (p<0.001) and the mitochondrial depolarization, caspase 3 and caspase 9 levels were higher in the GB+AD, AD and AD+GB groups when compared to the control group (p<0.001).Also, the values were lower in the GB+AD group, AD group and AD+GB groups when compared with the GB+AD+capsazepine group, AD+capsazepine group and AD+GB+capsazepine respectively (p<0.001).Conclusion: These results show us that GB has a protective effect besides its therapeutic effect in Alzheimer's disease via TRPV1 channel.