Neuroprotective effects of Coptis chinensis Franch polysaccharide on amyloid-beta (Aβ)-induced toxicity in a transgenic Caenorhabditis elegans model of Alzheimer's disease (AD).

This study aims to investigate the neuroprotective effects of Coptis chinensis Franch polysaccharide (CCP) on Aβ transgenic CL4176 Caenorhabditis elegans, as well as its mechanism of action. The results in life span experiment showed that CCP could significantly increase the lifespan of C. elegans and the effect is in the descending order of 100mg/L>500mg/L>200mg/L. The behavioral experiments also demonstrated that CCP at the concentration of 100mg/L could delay the paralysis rate of C. elegans, which was significantly different from the control group. In terms of Aβ toxicity in C. elegans, morphological observation using Thioflavin S staining method indicated that the deposition of Aβ protein in the head area of the untreated C. elegans was much more than those in the CCP (100mg/L)-treated CL4176. In line with this finding, fluorogenic quantitative real-time PCR confirmed that the transcriptional levels of HSP16.2 (Y46H3A.D) and HSP16.41 (Y46H3A.E) in C. elegans was 21 times and 79 times higher than those in untreated control. Thus, these data demonstrate that CCP could reduce Aβ-induced toxicity by delaying the aging, decreasing the rate of paralysis, inhibiting the deposition of Aβ, and increasing the expression levels of HSP genes in transgenic C. elegans.