Regulation of Naoxin'an Capsule on Glial Cell Activation and Inflammatory Response in Rats with Chronic Cerebral Hypoperfusion-induced Vascular Cognitive Impairment
10.13422/j.cnki.syfjx.20211806
- VernacularTitle:脑心安胶囊对慢性脑缺血致血管性认知障碍大鼠胶质细胞激活及炎性反应的调节作用
- Author:
Guang-hui HAN
1
;
Dong-yue LI
2
;
Hong-ni YU
1
;
Wei-zhe ZHEN
1
;
Tao MA
1
Author Information
1. Dongfang Hospital， Beijing University of Chinese Medicine，Beijing 100078，China
2. School of Traditional Chinese Medicine， Beijing University of Chinese Medicine，Beijing 100029，China
- Publication Type:Research Article
- Keywords:
chronic cerebral hypoperfusion;
vascular cognitive impairment （VCI）;
Naoxin'an capsule;
glial cells;
inflammatory response
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2021;27(19):46-55
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the protective effect of Naoxin'an capsule （NC） against glial cell activation and inflammatory damage in brain of rats with chronic cerebral hypoperfusion-induced vascular cognitive impairment （VCI）. Method:One hundred and fifty rats were randomly divided into a sham operation group （n=20） and a modeling group （n=130）. Following the modeling with the two vessels occlusion （2-VO） technique， 87 successfully modeled rats were randomly divided into the model group， positive drug group （aricept， 0.5 mg·kg-1）， and low-， medium-， and high-dose （0.18， 0.36， 0.72 g·kg-1） NC groups， with 17-18 rats in each group. After intragastric administration of NC for eight weeks， the Morris water maze test and passive avoidance test were conducted to detect the effects of NC on learning and memory ability of VCI rats. Changes in neuronal structure of rat hippocampal CA1 area were observed by hematoxylin-eosin （HE） staining， and the neuronal apoptosis in hippocampus by terminal deoxynucleotidyl transferase （TdT）-mediated dUTP nick end labeling （TUNEL） staining. Western blot assay was used to detect the expression levels of glial fibrillary acidic protein （GFAP）， ionized calcium-binding adapter molecule 1 （Iba-1）， phosphorylated p38 mitogen-activated protein kinase （p38 MAPK）， and phosphorylated nuclear factor κB （NF-κB）， followed by the measurement of interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） in the brain by enzyme-linked immunosorbent assay （ELISA）. Result:Compared with the sham operation group， the model group displayed obviously decreased spatial learning and memory ability and memory retention ability （P<0.05， P<0.01）， neuronal damage in hippocampal CA1 area， enhanced neuronal apoptosis （P<0.01）， up-regulated GFAP and Iba-1 （P<0.01）， elevated phosphorylation of p38 MAPK and NF-κB （P<0.01）， and increased IL-1β and TNF-α （P<0.01）. Compared with the model group， NC at each dose significantly improved the spatial learning and memory ability and memory retention ability of VCI rats （P<0.05， P<0.01）， ameliorated the neuronal damage in hippocampus CA1 area， reduced the apoptosis rate of nerve cells （P<0.05， P<0.01）， down-regulated the expression of GFAP and Iba-1 （P<0.01）， decreased the phosphorylation levels of p38 MAPK and NF-κB （P<0.05， P<0.01）， and lowered TNF-α and IL-1β levels （P<0.01）. Conclusion:NC alleviates the inflammatory damage of the central nervous system caused by activated p38 MAPK and NF-κB and improves chronic cerebral hypoperfusion-induced VCI in rats by inhibiting the activation of microglia and astrocytes.
