Protective Effect of Xiaochaihutang on Ammonia-Induced Astrocyte Edema in Rats by Inhibition of NF-κB Signaling Pathway
- VernacularTitle:小柴胡汤抑制NF-κB信号通路对氨诱导大鼠星形胶质细胞水肿的保护作用研究
- Author:
Jin LI
1
,
2
;
Qinxing FENG
;
Weiyi JIA
;
Zhengyun LIU
;
Jiajia LIU
;
Shangfu XU
Author Information
- Keywords: Xiaochaihutang; Astrocytes; Edema; Ammonia; NF-κB P65 signaling pathway
- From: World Science and Technology-Modernization of Traditional Chinese Medicine 2023;25(6):2044-2051
- CountryChina
- Language:Chinese
- Abstract: Objective To observe the effect of Xiaochaihutang on ammonia-induced edema of astrocytes in rats and explore the mechanism of Xiaochaihutang in the treatment of cerebral edema based on NF-κB signaling pathway.Methods Astrocytes were isolated from the cerebral cortex of SD rats 1-2 days old.When the cell content was more than 95%,the cells could be subcultured and divided into three groups:Vehicle group(10%blank control group serum,Vehicle),Model group(10%blank control group serum+5 mmol·L-1 ammonium chloride,Model),and Xiaochaihutang group(10%serum+5 mmol·L-1 ammonium chloride,XCHT).The expression of AQP4 was detected by immunofluorescence.The levels of AQP4,GFAP,and TNF-α were detected by RT-PCR and Western blot.NF-κB P65 was measured by Western blot.Results ① Ammonium chloride increased the expression of AQP4 in astrocytes(P<0.01)and decreased the expression of GFAP(P<0.05,P<0.01),however,the expression of AQP4 in astrocytes decreased(P<0.01)while GFAP increased(P<0.05)after the intervention of serum containing Xiaochaihutang.② Compared with the Vehicle group,the expression level of TNF-α and phosphorylation of NF-κB P65 in the Model group was significantly increased(P<0.05),while after Xiaochaihutang serum medicated treatment,TNF-α and phosphorylation of NF-κB P65 content lower(P<0.05).Conclusion Xiaochaihutang can improve the edema of astrocytes induced by ammonia and enhance the activity of astrocytes.Its mechanism may be related to inhibition of NF-κB signaling pathways,and reduce inflammation medium(especially TNF-α)produced and released.
