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  被引量:2

Improvement effect and mechanism of N-butylphthalide on inflammatory injury of bone marrow mesenchymal stem cells in rats

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作  者:赵二义[1] 赵仲艳[1] 王带媚[2] 黄培坚[1] 黄仕雄[1] 胡诗俊 谢凌 陈正萍 ZHAO Eryi;ZHAO Zhongyan;WANG Daimei;HUANG Peijian;HUANG Shixiong;HU Shijun;XIE Ling;CHEN Zhengping(Dept.of Neurology,Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University,Haikou 570311,China;Dept.of Pharmacy,Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University,Haikou 570311,China;Dept.of Pharmacy,Qianjiang Central Hospital of Chongqing,Chongqing 409099,China)

机构地区:[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

出  处:《中国药房》2023年第8期946-949,960,共5页China Pharmacy

基  金:海南省重点研发计划科研项目(No.ZDYF2021SHFZ112);海南省卫生健康行业科研项目(No.20A200223)。

摘  要:目的 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 将大鼠BMSCs分为对照组、模型组和丁苯酞低、中、高浓度组(10、20、50μmol/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 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 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 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(10,20,50μmol/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 factorα(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-1βand 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.

关 键 词:丁苯酞 骨髓间充质干细胞 脂多糖 炎性损伤 大鼠 

分 类 号:R965[医药卫生—药理学] R743[医药卫生—药学]

 

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