Improvement effect and mechanism of N-butylphthalide on inflammatory injury of bone marrow mesenchymal stem cells in rats
- VernacularTitle:丁苯酞对大鼠骨髓间充质干细胞炎性损伤的改善作用及机制
- Author:
Eryi ZHAO
1
;
Zhongyan ZHAO
1
;
Daimei WANG
2
;
Peijian HUANG
1
;
Shixiong HUANG
1
;
Shijun HU
1
;
Ling XIE
1
;
Zhengping CHEN
3
Author Information
1. Dept. of Neurology，Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University，Haikou 570311，China
2. Dept. of Pharmacy，Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University，Haikou 570311，China
3. Dept. of Pharmacy，Qianjiang Central Hospital of Chongqing，Chongqing 409099，China
- Publication Type:Journal Article
- Keywords:
N-butylphthalide;
bone marrow mesenchymal stem cell;
lipopolysaccharide;
inflammatory injury;
rat
- From:
China Pharmacy
2023;34(8):946-949
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To study the improvement effect and possible mechanism of N-butylphthalide on inflammatory injury of bone marrow mesenchymal stem cells （BMSCs） in rats. METHODS BMSCs of rats were divided into control group， model group， N-butylphthalide low-concentration， medium-concentration and high-concentration groups （10， 20， 50 μmol/L）. BMSCs were cultured in vitro and lipopolysaccharide （the final concentration of 10 mg/L） was used to establish the inflammatory injury model. After the intervention of N-butylphthalide， the survival rate， apoptotic rate， the contents of tumor necrosis factor α （TNF- α）， interleukin 1β （IL-1β） and IL-6 in cell culture medium， the mRNA expression of nuclear factor-κB（NF-κB） p65， and the protein expressions of caspase-3， B-cell lymphoma 2 （Bcl-2）， Bcl-2 related X protein （Bax） and NF-κB p65 in cells were detected. RESULTS Compared with control group， the survival rate and protein expression of Bcl-2 were decreased significantly in model group （P＜0.05）； the apoptotic rate， contents of TNF-α， IL-1β and IL-6， the mRNA expression of NF-κB p65， and the protein expressions of caspase-3， Bax and NF-κB p65 were increased significantly （P＜0.05）. Compared with model group， above indexes were significantly reversed in all concentration groups of N-butylphthalide （P＜0.05）， in concentration-dependent manner. CONCLUSIONS N-butylphthalide can ameliorate the inflammatory injury of BMSCs induced by lipopolysaccharide， and its mechanism may be related to the inhibition of NF-κB signaling pathway.
