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Please use this identifier to cite or link to this item: http://142.54.178.187:9060/xmlui/handle/123456789/12931
Title: Effects of velvet antler polypeptides on Alzheimer's disease cell model via miR-613 / HDAC6 pathway
Authors: Guo, Jindong
Lu, Meng
Zhou, Yuhui
Wu, Bowen
Wu, Mishan
Keywords: Velvet antler polypeptides
Alzheimer's disease
miR-613
HDAC6
apoptosis
oxidative stress
Issue Date: 12-May-2020
Publisher: Karachi:Pakistan Journal of Pharmaceutical Sciences, university of Karachi.
Citation: Guo, J., Lu, M., Zhou, Y., Wu, B., & Wu, M. (2020). Effects of velvet antler polypeptides on Alzheimer's disease cell model via miR-613 HDAC6 pathway. Pakistan Journal of Pharmaceutical Sciences, 33(3 (Special)), 1427-1433.
Abstract: To study the effect of velvet antler polypeptides (VAP) on Alzheimer's disease (AD) cell model, Aβ25-35 was used to induce SK-N-SH cells to obtain AD cell model. The MDA, SOD, GSH-Px levels were determined using relevant kits. Flow cytometry was conducted to detect apoptosis, Western blot was employed to measure Bcl-2, Bax, HDAC6 protein expression, and qPCR was used to assay microRNA (miR)-613 and HDAC6 mRNA levels. TargetScan prediction combined with dual luciferase reporting experiments was conducted to analyze the targeting relationship between miR-613 and HDAC6. miR-613 was transfected in SK-N-SH cells; Alternatively, anti-miR-613 was transfected, followed by Aβ25-35 and 80 mg/L of VAP. The AD model cells showed increased MDA content, apoptosis rate, Bax protein expression, HDAC6 mRNA and protein expression, but lower SOD, GSH-Px activities, Bcl-2 protein level, and miR-613 expression (p<0.05). VAP reduced MDA content, apoptosis rate, Bax protein expression, HDAC6 mRNA and protein expression, but enhanced SOD, GSH-Px activities, Bcl-2 protein level, and miR-613 expression (p<0.05). Over-expression of miR-613 increased SOD, GSH-Px activities, and Bcl-2 protein expression in AD model cells, but reduced HDAC6 protein levels, MDA content, apoptosis rate, and Bax protein levels (p<0.05). VAP may regulate Aβ25-35-induced apoptosis so as to treat Alzheimer's disease.
URI: http://142.54.178.187:9060/xmlui/handle/123456789/12931
ISSN: 1011-601X
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