Effects of astaxanthin on the expression of NF-κB inflammatory signaling pathway related proteins in hippocampus of rats after acute carbon monoxide poisoning
10.3760/cma.j.issn.1674-6554.2019.12.002
- VernacularTitle: 虾青素对急性一氧化碳中毒大鼠海马NF-κB炎症信号通路相关蛋白表达的影响
- Author:
Ruiqi LEI
1
;
Li JIANG
;
Gangfeng GU
;
Hongyan PENG
;
Ye GAO
;
Qin HAN
;
Jinglun LI
Author Information
1. Department of Neurology, Southwest Medical University Affiliated Hospital, Luzhou 646000, China
- Publication Type:Journal Article
- Keywords:
Carbon monoxide poisoning;
NF-κ
B;
Astaxanthin;
Hippocampal;
Inflammatory;
Rat
- From:
Chinese Journal of Behavioral Medicine and Brain Science
2019;28(12):1064-1069
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of astaxanthin on neuronal injury in hippocampus of rats after acute carbon monoxide poisoning(ACMP) and the relationship with NF-κB inflammatory signaling pathway.
Methods:Male SD rats screened by water maze were randomly divided into three group(n=50): control group (NC group), CO poisoning group (COP group), CO poisoning+ astaxanthin group (AST group) . ACMP rat model was established by static inhaled exposure method. Meanwhile, rats in AST group were further given astaxanthin twice a day by gavage.At 1 day, 7 days, 14 days, 21 days and 28 days after CO poisoning (10 rats in each group were selected), the learning and memory abilities were evaluated by Morris water maze test. The pathological changes of the neurons in hippocampal CA1 region were observed by hematoxylin-eosin(HE) staining.The expression and activation of NF-κB in hippocampus were detected by immunoblotting and immunofluorescence, and the expression of TNF-α and IL-6 protein in hippocampus were examined by ELISA.
Results:Morris water maze test showed that there were no significant difference in escape latency and crossing platform times between the three groups (P>0.05). Compared with NC group, the escape latency of COP group was prolonged at 14, 21 and 28 days after CO poisoning (t=-6.04, -6.28, -8.18, all P<0.05), and the number of crossing platform was decreased (t= 5.96, 7.85, 6.51, all P<0.05). Compared with the COP group, the escape latency of the rats in AST group at the 14, 21 and 28 days was shortened (t=4.74, 4.82, 5.98, all P<0.05), and the number of crossing platform was increased (t=-3.72, -4.45, -6.53, all P<0.05). Compared with NC group, the number of NF-κ B positive cells in CA1 area of hippocampus in COP group increased at every time point (t=-8.62, -18.00, -16.67, -11.15, -6.22, all P<0.05); the number of NF-κ B positive cells in CA1 area in AST group decreased at 7 d, 14 d, 21 d and 28 d after CO poisoning, the difference was statistically significant (t= 6.55, 6.96, 4.40, 4.17; all P<0.05). Western blot showed that the changes of NF-κB protein was similar to that of immunofluorescence. After 7 days of CO poisoning, the level of NF-κB protein in hippocampus of COP group was (1.44±0.08), it was higher than that of NC group (t=-20.07, P<0.05), while that of AST group was (0.68±0.10), it was lower than that of COP group (t=10.23, P<0.05). The results of Elisa showed that TNF-α and IL-6 in the hippocampus of COP group were higher than those of NC group at every time point(all P<0.05), while compared with COP group, TNF-α and IL-6 in AST group were lower (all P<0.05). After 7 days of CO poisoning, TNF -α in COP group ((39.04±5.29) pg/ml)was higher than that in NC group ((14.13±2.12) pg/ml) (t=-7.58, P<0.05); TNF -α in AST group ((25.77±3.31) pg/ml) was lower than that in COP group (t=3.69, P<0.05). After 7 days of CO poisoning, the level of IL-6 in COP group ((181.79±9.12) pg/ml)was higher than that in NC group ((73.12±11.04) pg/ml) (t=-8.24, P<0.05), and the level of IL-6 in AST group ((121.47±9.80) pg/ml) was lower than that in COP group (t=7.80, P<0.05).
Conclusion:The excessive inflammatory response which mediated by NF-κB signaling pathway is involved in ACMP-induced neuronal damage in hippocampus.Astaxanthin can down-regulate the expression of NF-κB inflammatory signaling pathway related proteins, and pave a way for the treatment of ACMP brain damage and cognitive dysfunction.
