Effects of long-term administration of nicotiflorin on neurological function in rats with cerebral ischemia-reperfusion injury
10.12206/j.issn.2097-2024.202407038
- VernacularTitle:菸花苷长期给药对脑缺血再灌注损伤大鼠神经功能的影响
- Author:
Yifan FENG
1
;
Xiaodong YAN
1
;
Wenbin ZHANG
2
;
Bingfeng LI
1
;
Meili GUO
1
Author Information
1. School of Pharmacy, Naval Medical University, Shanghai 200433, China.
2. School of Pharmacy, Naval Medical University, Shanghai 200433, China;Mobile Ninth Detachment of Armed Police Force, Pingliang 744000, China.
- Publication Type:Originalarticles
- Keywords:
nicotiflorin;
cerebral ischemia-reperfusion;
transcriptomics;
pyroptosis;
long-term functional recovery
- From:
Journal of Pharmaceutical Practice and Service
2025;43(5):228-234
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the promoting effect of long-term administration of nicotiflorin on the recovery of neurological function in rats with cerebral ischemia-reperfusion injury （CIRI）. Methods The CIRI model was established and nicotiflorin was injected intraperitoneally after 1 hour of obstruction for 8 weeks. Tail suspension deflection experiment, balance beam experiment and water maze test were performed in the 2nd, 4th and 8th weeks. After 8 weeks, TTC staining was used to observe the volume of infarct atrophy, transcriptome sequencing was employed to screen differential expressed genes （DEGs） and highly enriched pathways were analyzed, Western-bloting and Elisa were used to assess proteins expression related to the pyroptosis pathway and inflammatory cytokines IL-1β and IL-18. Results By long-term administration of nicotiflorin, the contralateral deflection rate was significantly reduced and beam experiment score of CIRI rats was balanced, the number of crossing the platform in water maze test was increased （P<0.05）, the volume of cerebral infarction atrophy was decreased （P<0.01）, which significantly promoted the recovery of neurological function in rats. Transcriptome sequencing found that the expression of genes in the pyroptosis-related signaling pathways in the brain tissue of rats in the nicotiflorin group was significantly down-regulated （P<0.05）. Western-blot and Elisa experiments showed that nicotiflorin reduced the expression levels of Caspase-1 and GSDMD-N and other pyroptosis-related proteins, and at the same time, the release of inflammatory factors IL-1β and IL-18 was significantly reduced （P<0.05）, indicating that nicotiflorin could inhibit the inflammatory process of pyroptosis. Conclusion Nicotiflorin exhibited a significant long-term promotion effect on the recovery of neurological function in CIRI rats, which potentially attributed from its ability to inhibit pyroptosis.
