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《China Journal of Traditional Chinese Medicine and Pharmacy》 2017-05
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Study on neuroprotective effect of schisandrin B by regulating the Aβ and its downstream NF-κB/TNF-α pathway

YANG Qing;LI Na;SUI Xin;LI Xiao-hua;SHI Xiao-zheng;LIU Ying-na;LIN Jia-nan;ZHANG Hui-yuan;KAN Mo;XIU Zhi-ru;QU Xiao-bo;Changchun University of Chinese Medicine;  
Objective: To study on neuroprotective effect of schisandrin B by regulating the Aβ and its downstream NF-κB/TNF-α pathway. Methods: The binding constants, dissociation constants and dissociation equilibrium constants of Sch B in vitro were determined by Open SPR. The effect of Sch B on depolymerization of Aβ oligomers was determined by SDS-PAGE. The effects of Sch B on the proliferation of SH-SY5 Y cells were detected, and the apoptosis of damaged neurons was detected by FACS at the cellular level. Western blot was used to detect the protein expressions involving the mitochondrial apoptosisrelated factors including Bcl-XL and Caspase-3, Alzheimer's disease pathological biomarkers including Aβ1-42, p-Tau and its downstream NF-κB/TNF-α signalling pathway. Results: Sch B can promote the depolymerization of Aβ oligomers, increase the cell proliferation rates of SH-SY5 Y induced by Aβ, inhibit apoptosis of SH-SY5 Y after injuried by Aβ, it can increase expression of Bcl-XL and reduce expression of Caspase-3, inhibit expression of Aβ1-42 and p-Tau, down-regulated expression of NF-κB/TNF-α signaling pathway. Conclusion: Sch B could target the affinity of Aβ ligands and promote the depolymerization of Aβ oligomers, and inhibit the apoptosis of neurons. The mechanism might be related to the depolymerization and downregulation of oligomers neuron Aβ expression, inhibition of Tau hyperphosphorylation, and further down-regulation of NF-κB/TNF-α pathway.
【Fund】: 2016年吉林省科技厅自然科学基金项目(No.20160101229JC)~~
【CateGory Index】: R285
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