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The Regulating Mechanism of Chrysophanol on Protein Level of CaM-CaMKIV to Protect PC12 Cells Against Aβ(25-35)-Induced Damage

OBJECTIVE: To investigate the neuroprotective effect of chrysophanol (CHR) on PC12 treated with Aβ(25-35), and the involved mechanism. METHODS: After the establishment of an AD cell model induced by Aβ(25-35), the cell survival rate was detected by MTT, cell apoptosis was assayed by Hoechst 33342 st...

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Detalles Bibliográficos
Autores principales: Ye, Ting, Gao, Hua-Wu, Xuan, Wei-Ting, Ye, Shu, Zhou, Peng, Li, Xin-Quan, Wang, Yan, Song, Hang, Liu, Yan-Yan, Cai, Biao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7381772/
https://www.ncbi.nlm.nih.gov/pubmed/32764873
http://dx.doi.org/10.2147/DDDT.S245128
Descripción
Sumario:OBJECTIVE: To investigate the neuroprotective effect of chrysophanol (CHR) on PC12 treated with Aβ(25-35), and the involved mechanism. METHODS: After the establishment of an AD cell model induced by Aβ(25-35), the cell survival rate was detected by MTT, cell apoptosis was assayed by Hoechst 33342 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 Aβ(25-35), PC12 cells showed that increased cell viability and reduced apoptosis. The qRT-PCR results indicated that the deposition of Aβ(25-35) triggers a decrease in levels of CaM, CaMKK, CaMKIV, and tau in PC12 cells. In addition, Western blot results also suggested that Aβ(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.