LAUSR

In this study, we investigated the protective effect and possible mechanism of a polysaccharide (CCP) from Coptis chinensis against Amyloid-β protein (Aβ)-induced toxicity in PC12 cells. The results showed pretreatment with CCP significantly protected PC12 cells from Aβ25-35 induced cell death, lactate dehydrogenase (LDH) release, nuclear fragmentation, mitochondrial dysfunction and cytochrome c release from mitochondria. Furthermore, CCP (100 μg/ml) significantly inhibited Aβ25-35 induced c-Jun N-terminal kinase (JNK) phosphorylation, but not influence signal-regulated kinase (ERK) and P38 mitogen-activated protein kinase (p38MAPK) pathway, and interestingly, the promoting effect of CCP on PC12 cell survival was only blocked by pre-treatment with a SP600125 (JNK inhibitor). In addition, Aβ25-35-induced increase of Bax and cleaved caspase-3, as well as decrease of Bcl-2 protein expression was markedly reversed by CCP or SP600125. Thus, our results indicate that the neuroprotective effect of CCP is associated with JNK-dependent apoptotic pathway.