The influence of B55γ on the neuroprotective effect of W026B in t-MCAO mice

doi:10.5246/jcps.2020.10.066

Abstract

Abstract:

As a newly synthesized lignan derivative, W026B has been proved to be a neuroprotective agent, and it can significantly reduce cerebral infarct volume, improve behavioral scores and protect blood brain barrier in different models. However, its exact mechanism is still unclear. In the present study, a protein named B55γ, one of candidate targets of W026B screened by proteomic study, was investigated to explore its influence on the effect of W026B in t-MCAO mice. siRNA PPP2R2C was used to knockdown the expression of protein B55γ in t-MCAO mice. The results showed that the knockdown of B55γ significantly suppressed the neuroprotective effect of W026B. Further results showed that the knockdown of PPP2R2C, B55γ gene, abolished the effect of W026B on reducing the level of NF-κB p65 in ischemic brain tissue, and knockdownof PPP2R2C also reversed the effect of W026B on decreasing the activity of caspase-3 in ischemic brain tissue.In conclusion, protein B55γ might be an important mediator of the protective effect of W026B. B55γ actively participated in the brain protective effect of W026B by affecting the inflammatory response and apoptotic pathway during ischemia reperfusion. These results revealed a new mechanism underlying the neuroprotective effect of W026B.

Key words: Ischemia reperfusion, W026B, B55γ, siRNA, Inflammation, Apoptosis

CLC Number:

R963

Supporting:

Kexiang Gao, Xiaoyan Liu, Yuanjun Zhu, Ye Liu, Yinye Wang. The influence of B55γ on the neuroprotective effect of W026B in t-MCAO mice[J]. Journal of Chinese Pharmaceutical Sciences, 2020, 29(10): 711-718.

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