Journal of Chinese Pharmaceutical Sciences ›› 2020, Vol. 29 ›› Issue (10): 711-718.DOI: 10.5246/jcps.2020.10.066

• Original articles • Previous Articles     Next Articles

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

Kexiang Gao1, Xiaoyan Liu1, Yuanjun Zhu1, Ye Liu2, Yinye Wang1*   

  1. 1. Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100191, China
    2. Beijing Honghui New Medical Technology Co. Ltd., Beijing Daxing Biological Medicine Industry Base, Beijing 102600, China
  • Received:2020-06-24 Revised:2020-08-15 Online:2020-10-31 Published:2020-08-30
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  • Supported by:
    National Natural Science Foundation of China (Grant No. 81503060, 81573333).


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

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