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Celastrol attenuates cadmium-induced neuronal apoptosis

Recently, Professor Long Chen’s research team published a series of papers revealing the important molecular mechanism which celastrol prevent Cadmium -induced neurotoxicity.
Cadmium (Cd), a well-known heavy metal pollutant which can easily traverses the blood-brain barrier and accumulates in the brain is a potential pathogenic factor leading to neuronal cell dysfunction/apoptosis or neurodegeneration and related diseases. Celastrol, a pentacyclic triterpene extracted from the roots of Tripterygium wilfordi [thunder god vine (TGV)] plant, is known to possess antioxidant and anti-inflammatory properties.

Three findings are as follows: 1) Celastrol prevents the inactivation of AMPK by mitochondrial ROS, thus attenuating Cd-induced mTOR activation and neuronal apoptosis; 2) Celastrol attenuates cadmium-induced neuronal apoptosis via inhibiting Ca2+-CaMKII-Dependent Akt/mTOR Pathway; 3) Celastrol ameliorates Cd-induced neuronal apoptosis by targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. The series of research findings provide important scientific evidence and guidance for taking celastrol as the promising agent for prevention of Cd-induced neuronal apoptosis or neurodegenerative diseases.

The above-mentioned research findings entitled as “Celastrol prevents cadmium-induced neuronal cell death by blocking reactive oxygen species-mediated mammalian target of rapamycin pathway”, “Celastrol attenuates cadmium-induced neuronal apoptosis via inhibiting Ca2+-CaMKII-dependent Akt/mTOR pathway” and “Celastrol ameliorates Cd-induced neuronal apoptosis by targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway” are published on the international-famous journals BritishJournal of Pharmacology (2017;174:82-100. SCI IF=5.259), Journal of Cellular Physiology (2017;doi:10.1002/jcp.25703. SCI IF= 4.155) and Journal of Neurochemistry (2017;doi:10.1002/jcp.25703. SCI IF= 3.842) respectively. The first authors of the three papers are doctoral candidate Ruijie Zhang and Chong Xu.

This research was supported by the National Natural Science Foundation of China (NSFC), the Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD), US National Institutes of Health (NIH) and the Research Innovation Program for University Graduates of Jiangsu Province.

 

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