Celastrol treatment attenuates the inflammatory response in Alzheimer's disease model mice.

OBJECTIVE

Alzheimer's disease (AD) is the most common neurodegenerative disease. Unfortunately, current effective therapeutics for AD are limited, and thus, the discovery of novel anti-AD agents is urgently needed. Celastrol, a plant-derived triterpene, has both antioxidant and anti-inflammatory activities.

METHODS AND

RESULTS

Here, we found that celastrol treatment promoted microglial M2 polarization and inhibited inflammatory factor expression in both in vivo and in vitro experiments. Celastrol treatment significantly improved cognitive function in AD mice by regulation the TLR4/NFκB pathway, overexpression TLR4 reversed the protective effect of CEL to cognitive function in AD model mice. Suggesting that TLR4/NFκB plays a crucial role in regulating the inflammatory response.

CONCLUSION

Taken together, the results indicate that celastrol treatment attenuated the inflammatory response in AD mice by promoting microglial M2 polarization via the TLR4/NFκB pathway.