基础医学与临床 ›› 2022, Vol. 42 ›› Issue (6): 908-912.doi: 10.16352/j.issn.1001-6325.2022.06.024

• 研究论文 • 上一篇    下一篇

绞股蓝皂苷减轻脂多糖诱导大鼠肾上腺嗜铬细胞瘤细胞系PC12损伤

姜秀芳1, 耿亚楠1, 阳盛洪2, 魏平2, 赵名1*, 朱玲玲1*   

  1. 1.军事科学院军事医学研究院 军事认知与脑科学研究所, 北京 100850;
    2.中国人民解放军陆军第957医院,西藏自治区 阿里地区 859000
  • 收稿日期:2021-04-06 修回日期:2021-10-15 出版日期:2022-06-05 发布日期:2022-06-02
  • 通讯作者: * zhaoming1981@hotmail.com;linglingzhuamms@126.com
  • 基金资助:
    国家自然科学基金(81430044,82072104)

Gypenoside alleviates injury of rat adrenal pheochromocytoma cell line PC12 induced by lipopolysaccharide

JIANG Xiu-fang1, GENG Ya-nan1, YANG Sheng-hong2, WEI Ping2, ZHAO Ming1*, ZHU Ling-ling1*   

  1. 1. Institute of Military Cognition and Brain Sciences, Academy of Military Medical Sciences, Academy of Military Sciences, Beijing 100850;
    2. the 957th Hospital of PLA, Ali 859000, China
  • Received:2021-04-06 Revised:2021-10-15 Online:2022-06-05 Published:2022-06-02
  • Contact: * zhaoming1981@hotmail.com;linglingzhuamms@126.com

摘要: 目的 探讨绞股蓝皂苷对脂多糖(LPS)诱导的大鼠肾上腺嗜铬细胞瘤(PC12)细胞损伤的保护作用及其机制。方法 LPS处理PC12细胞建立神经元炎性损伤模型;实时定量PCR检测炎性因子表达,CCK-8法检测细胞活力,蛋白印迹检测NF-κB蛋白。结果 不同剂量(0、100、300和1 000 ng/mL)的LPS刺激PC12细胞12 h后,TNF-α、IL-6和IL-1β mRNA水平随剂量的增加而逐渐升高。LPS导致细胞活力下降到85.7%,不同浓度绞股蓝皂苷(30, 100 μg/mL)预处理细胞6 h后,30和100 μg/mL绞股蓝皂苷能够使细胞活力分别恢复至96.2%和97.9%。绞股蓝皂苷预处理后,LPS诱导的TNF-α、IL-6和IL-1β的mRNA水平升高都受到不同程度的抑制。LPS刺激导致NF-κB通路信号蛋白p65的磷酸化(p-p65)水平上调,但绞股蓝皂苷预处理能够使升高的p-p65下调。结论 绞股蓝皂苷通过抑制NF-κB信号通路减轻LPS诱导的PC12细胞炎性反应,从而起到保护神经元损伤的作用。

关键词: 绞股蓝皂苷, 炎性反应, 脂多糖, PC12细胞

Abstract: Objective LPS-treated PC12 cells were used to establish neuron inflammation model. RT-PCR was used to detect the mRNA of cytokines. CCK-8 assay was used to check determine cell viability. Western blot was used to detect NF-κB pathway. Methods LPS-treated PC12 cells were used to establish neuron inflammation model. RT-PCR was used to detect the mRNA of cytokines. CCK-8 assay was used to check determine cell viability. Western blot was used to detect NF-κB pathway. Results After 12 hrs treatment of PC12 cells with different doses of LPS (0, 100, 300 and 1 000 ng/mL), the mRNA level of TNF-α,IL-6 and IL-1β all increased. The cells pre-treated with different doses of gypenoside (30, 100 μg/mL) and then treated with LPS for 24 h, cell viability decreased to 85.7%. However, 30 and 100 μg/mL gypenoside pre-treatment resulted in cell viability increased to 96.2% and 97.9% respectively. Gypenoside also inhibited LPS-induced cell inflammation as indicated by increased mRNA level of TNF-α, IL-6 and IL-1β caused by LPS stimulation. LPS increased the phosphorylation of p65 (p-p65) and the phosporylation was also inhibited by gypenoside treatment. Conclusions Gypenoside alleviates LPS-induced inflammation and then protects PC12 cells from injury induced by LPS through inhibiting NF-κB pathway.

Key words: gypenoside, inflammation, lipopolysaccharide (LPS), PC12 cells

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