Role of curcumin-mediated inhibition of inflammation in alleviating brain ischemia-reperfusion synaptic injury
10.3969/j.issn.1006-2483.2024.01.017
- VernacularTitle:姜黄素抑制炎症在缓解脑缺血再灌注突触损伤中的作用
- Author:
Minghui ZHAO
1
;
Honghong SHANG
1
;
Fengqin LI
1
;
Bingmei XYU
1
;
Xiaolu CAO
2
Author Information
1. Institute of Pharmaceutical Process , Hubei Province Key Laboratory of Occupational Hazard Identification and Control , School of Medicine , Wuhan University of Science and Technology , Wuhan , Hubei 430065, China
2. Environmental Toxicology Laboratory , Hubei Province Key Laboratory of Occupational Hazard Identification and Control , School of Medicine , Wuhan University of Science and Technology , Wuhan , Hubei 430065 , China
- Publication Type:Journal Article
- Keywords:
Cerebral ischemia-reperfusion;
Curcumin;
NLRP3;
Synapsin1;
CAMKⅡ
- From:
Journal of Public Health and Preventive Medicine
2024;35(1):74-78
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the potential effect and mechanism of curcumin in inhibiting synaptic injury in the cortex of rats with cerebral ischemia-reperfusion. Methods Sprague-Dawley rats were divided into sham-operated group, model group, low-dose curcumin (50 mg/kg) group, and high-dose curcumin (100 mg/kg) group. A model of middle cerebral artery occlusion for 2 hours and reperfusion for 24 hours was constructed, and curcumin was administered. Based on the neurological function score, the effects of curcumin on cerebral infarct volume, synaptic ultrastructure changes, inflammatory cell infiltration, and the expression of NLRP3, Caspase-1, Synapsin1, and CAMKⅡ were observed after the end of the animal treatment. Results The neurological function scores were 0, 3.25±0.43, 2.50±0.50, and 1.50±0.50 for the sham-operated group, model group, low-dose curcumin group, and high-dose curcumin group, respectively. The percentage of cerebral infarct volume was 0, (38.89±2.21)%, (33.48±1.77)%, and (23.69±2.19)%, respectively. Compared with the sham operation group, the model group had severe synaptic ultrastructure damage, extensive inflammatory cell infiltration, significantly increased expression of Caspase-1 and NLRP3 (P < 0.5), and significantly decreased expression of Synapsin1 and CAMKⅡ (P < 0.5). Curcumin treatment significantly inhibited synaptic damage, reduced inflammatory cell infiltration, decreased the expression of Caspase-1 and NLRP3 (P < 0.5), and increased the expression of Synapsin1 and CAMKII (P < 0.5), when compared with the model group. Conclusion Ischemia-reperfusion-mediated synaptic injury in rat brain triggers an inflammatory response in cortical nerve cells, and curcumin alleviates synaptic damage and reduces brain injury by inhibiting inflammatory factor levels.
