Effect of madecassoside on hippocampal NR2B expression and cognitive function in rat traumatic brain injury model
10.3760/cma.j.cn115396-20201004-00303
- VernacularTitle:羟基积雪草苷对创伤性脑损伤后海马区NR2B表达与认知功能的影响
- Author:
Yanfeng JIA
1
;
Shiwen GUO
Author Information
1. 西安交通大学第一附属医院神经外科 710061
- Keywords:
Brain injuries;
Hippocampus;
Madecassoside;
Traumatic brain injury;
Cognitive function
- From:
International Journal of Surgery
2021;48(7):466-472,F3
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the Effect of madecassoside (MC) on hippocampal NR2B expression and cognitive function following traumatic brain injury (TBI).Methods:One hundred and sixteen SD rats were provided by the experimental animal center of Medical College in Xi′an Jiao Tong University. Rats were randomly divided into four groups ( n=29) as following: Control group (Con group), TBI group, MC treated TBI rats group (TBI+ MC group) and MC treated control rats group (Con+ MC group). NR2B protein levels in hippocampus were detected by Western-blot at 12 h, 1 d, 3 d, 7 d, 14 d and 21 d post trauma. Hippocampal NR2B positive cells were studied by immunohistochemical (IHC) staining at 21 d post trauma. Cognitive functions of rats were evaluated by Morris water maze (MWM) test from 21 d to 25 d post trauma. Results:Expression of hippocampal NR2B in TBI group at 12 h, 1 d and 3 d post injury were 3.31±0.28, 2.17±0.31 and 1.96±0.31, which presented statistical difference among the three time-points ( P<0.05) and were significantly increased compared to Con group ( P<0.05). However, there was no difference of NR2B level between TBI group (0.93±0.13) and Con group ( P>0.05) at 7 d post injury. In addition, NR2B expression in TBI group at 14 d and 21 d post injury were 0.45±0.04 and 0.21±0.04, which were much lower than that in Con group. IHC staining revealed that the number of hippocampal NR2B positive cells in TBI group (33.26±9.71) were lesser than that of Con group (86.62±17.05). Increased Escape latency, decreased platform crossing times and target quadrant duration were found in TBI group compared with Con group ( P<0.05). Hippocampal NR2B expression in TBI+ MC group at 12 h, 1 d and 3 d post injury were 2.37±0.34, 1.38±0.22 and 1.14±0.16. Difference among the three time-points exhibited statistical significance ( P<0.05). In addition, they were much lower than that in TBI group at the same time-points ( P<0.05), but no difference was found between TBI+ MC group (0.97±0.06) and TBI group at 7 d post injury ( P>0.05). Moreover, NR2B expression in TBI+ MC group at 14 d and 21 d post injury were 0.86±0.08 and 0.52±0.06, which were much higher than that in TBI group ( P<0.05). IHC staining showed the number of hippocampal NR2B positive cells in TBI+ MC group (69.08±12.24) were much more than that of TBI group (33.26±9.71). A decrease of escape latency, an increase of platform crossing times and target quadrant duration were found in TBI+ MC group compared to TBI group ( P<0.05). Conclusion:MC treatment could inhibit the up-regulation of NR2B in hippocampus at early period of TBI and prevent the down-regulation of NR2B at advanced stage of TBI, which led to a remarkable improvement for the cognitive dysfunction caused by TBI.
