The Regulating Mechanism of Chrysophanol on Protein Level of CaM-CaMKIV to Protect PC12 Cells Against Aβ25-35-Induced Damage

Objective: To investigate the neuroprotective effect of chrysophanol (CHR) on PC12 treated with A beta(25-35), and the involved mechanism. Methods: After the establishment of an AD cell model induced by A beta(25-35), the cell survival rate was detected by MTT, cell apoptosis was assayed by Hoechst 33 342 staining, mRNA expressions of calmodulin (CaM), calcium/calmodulin-dependent protein kinase kinase (CaMKK), calcium/calmodulin-dependent protein kinase IV (CaMKIV) and tau (MAPT; commonly known as tau) were determined by qRT-PCR, and protein levels of CaM, CaMKK, CaMKIV, phospho-CaMKIV (p-CaMKIV), tau and phospho-tau (p-tau) were detected by Western blot analysis. Results: When pretreated with CHR before exposure to A beta(25-35), PC12 cells showed that increased cell viability and reduced apoptosis. The qRT-PCR results indicated that the deposition of A beta(25-35) triggers a decrease in levels of CaM, CaMKK, CaMKIV, and tau in PC12 cells. In addition, Western blot results also suggested that A beta(25-35) decreases the protein expression of CaM, CaMKK, CaMKIV, p-CaMKIV, and the ratio of p-tau to tau in PC12 cells. However, the above effects were significantly alleviated after the treatment of CHR. Conclusion: CHR plays a neuroprotective role in AD though decreasing the protein level of CaM-CaMKK-CaMKIV and the expression of p-tau downstream.