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1.海南省人民医院/海南医学院附属海南医院神经内科,海口 570311
2.海南省人民医院/海南医学院附属海南医院药学部,海口 570311
3.重庆市黔江中心医院药学部,重庆 409099
副主任医师,硕士。研究方向:脑血管病基础与临床、干细胞神经元分化。电话:0898-68622179。E-mail:zhaoguanduo@126.com
副主任药师。研究方向:临床药学。电话:023-79245775。E-mail:chenzhengping1974@163.com
纸质出版日期:2023-04-30,
收稿日期:2022-10-13,
修回日期:2023-03-26,
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赵二义,赵仲艳,王带媚等.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 Δ[J].中国药房,2023,34(08):946-949.
ZHAO Eryi,ZHAO Zhongyan,WANG Daimei,et al.Improvement effect and mechanism of N-butylphthalide on inflammatory injury of bone marrow mesenchymal stem cells in rats[J].ZHONGGUO YAOFANG,2023,34(08):946-949.
赵二义,赵仲艳,王带媚等.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 Δ[J].中国药房,2023,34(08):946-949. DOI: 10.6039/j.issn.1001-0408.2023.08.10.
ZHAO Eryi,ZHAO Zhongyan,WANG Daimei,et al.Improvement effect and mechanism of N-butylphthalide on inflammatory injury of bone marrow mesenchymal stem cells in rats[J].ZHONGGUO YAOFANG,2023,34(08):946-949. DOI: 10.6039/j.issn.1001-0408.2023.08.10.
目的
2
研究丁苯酞对大鼠骨髓间充质干细胞(BMSCs)炎性损伤的改善作用及其可能机制。
方法
2
将大鼠BMSCs分为对照组、模型组和丁苯酞低、中、高浓度组(10、20、50 μmol/L)。体外培养BMSCs并采用脂多糖(终浓度为10 mg/L)建立炎性损伤模型,经丁苯酞干预后检测细胞存活率、凋亡率和细胞培养液中肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)、白细胞介素6(IL-6)含量以及细胞中核因子κB(NF-κB)p65 mRNA和胱天蛋白酶3(caspase-3)、B细胞淋巴瘤2(Bcl-2)、Bcl-2相关X蛋白(Bax)和NF-κB p65蛋白表达。
结果
2
与对照组比较,模型组细胞存活率和Bcl-2蛋白表达水平均显著降低(
P
<0.05);细胞凋亡率,TNF-α、IL-1β、IL-6含量,NF-κB p65 mRNA以及caspase-3、Bax、NF-κB p65蛋白表达水平均显著升高(
P
<0.05)。与模型组比较,丁苯酞各浓度组上述指标均显著逆转(
P
<0.05),且呈浓度依赖性。
结论
2
丁苯酞对脂多糖诱导的BMSCs炎性损伤具有改善作用,其机制可能与抑制NF-κB信号通路有关。
OBJECTIVE
2
To study the improvement effect and possible mechanism of
N
-butylphthalide on inflammatory injury of bone marrow mesenchymal stem cells (BMSCs) in rats.
METHODS
2
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
2
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
2
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.
丁苯酞骨髓间充质干细胞脂多糖炎性损伤大鼠
bone marrow mesenchymal stem celllipopolysaccharideinflammatory injuryrat
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