The Journal of Practical Medicine ›› 2024, Vol. 40 ›› Issue (14): 1935-1940.doi: 10.3969/j.issn.1006-5725.2024.14.006

• Basic Research • Previous Articles     Next Articles

The neuroprotective mechanism of RKIP signaling pathway expression on microglial polarization in cerebral hemorrhage rat

Ruxue SUN1,Mengli ZHU1(),Jingjing LIU2,Fei. CHEN1   

  1. *.Department of Emergency medicine,Wuhan Integrated Traditional Chinese and Western Medicine Hospital (Wuhan No. 1 Hospital),Wuhan 430030,China
  • Received:2024-02-21 Online:2024-07-25 Published:2024-07-15
  • Contact: Mengli ZHU E-mail:rnb8976@163.com

Abstract:

Objective This study aimed to investigate the neuroprotective effect of microglia polarization mediated by Raf kinase inhibitor protein (RKIP) intracerebral hemorrhage (ICH) model. Methods Forty-eight adult male Sprague-Dawley (SD) rats were randomly divided into three groups:the Sham + Vector group,the ICH + Vector group, and the ICH + RKIP group, with 16 rats in each group. The collagenase ICH model was established in ICH+Vector group and ICH + RKIP group. Before operation and 1, 3, 5,and 7 days after operation, 8 animals in each group were tested for behavior. Apoptosis of neurons was detected by flow cytometry. Seven days after ICH, the expressions of RKIP, p-p65, and TRAF6 around hematoma were analyzed by protein blot. Results Compared with ICH + Vector group, rats in ICH + RKIP group need less time to find the platform, spend longer time in the target quadrant, and significantly reduce the times of crossing the platform (P < 0.05). The number of Nissl corpuscles in ICH + RKIP group was significantly higher than that in ICH + Vector group (P < 0.05). In addition, the number of neuronal apoptosis in ICH + RKIP group was significantly lower than that in ICH + Vector group (P < 0.05). Compared with Sham group, rats receiving ICH showed a gradual decrease in RKIP expression, and reached the lowest value on the 7th day (P < 0.05). Seven days after ICH, the expression of RKIP protein in hematoma of rats in ICH + RKIP group was significantly higher than that in ICH + Vector group (P < 0.05), and the expression of p-p65 and TRAF6 protein was significantly lower than that in ICH + Vector group (P < 0.05). Compared with ICH + Vector group, the number of iNOS + Ibal1+ cells in ICH + RKIP group decreased significantly (P < 0.05), while the number of Arg-1 + Ibal1+ cells increased significantly (P < 0.05). Conclusion Up-regulation of RKIP promotes functional recovery after ICH, and its mechanism involves inhibiting TRAF6/NF-κB signaling pathway.

Key words: Raf kinase inhibitor protein, microglial cells, polarization, cerebral hemorrhage

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