静脉麻醉药对脂多糖诱导的神经星形胶质细胞增殖的影响及其机制

董闯 王昊*

doi:10.16098/j.issn.0529-1356.2018.03.005

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解剖学报 ›› 2018, Vol. 49 ›› Issue (3) : 299-302. DOI: 10.16098/j.issn.0529-1356.2018.03.005

神经生物学

静脉麻醉药对脂多糖诱导的神经星形胶质细胞增殖的影响及其机制

董闯王昊*

作者信息 +

Effects of intravenous anesthetics on lipopolysaccharide-induced proliferation of glial cells and its mechanisms

DONG Chuang WANG Hao*

Author information +

文章历史 +

摘要

目的检测静脉麻醉药对脂多糖诱导的神经星形胶质细胞的影响及其机制。方法利用MTT实验、集落形成实验和Annexin V-FITC/PI双染色法检测静脉麻醉药对脂多糖作用后的神经星形胶质细胞增殖和凋亡的影响。Western blotting技术检测相关机制。结果静脉麻醉药可以逆转脂多糖诱导的神经星形胶质细胞增殖。经麻醉药处理后的神经星形胶质细胞p-Akt和p-mTOR蛋白表达下降，Caspase-3和Caspase-9表达水平升高。结论静脉麻醉药可以通过抑制mTOR通路逆转脂多糖诱导的神经星形胶质细胞增殖。

Abstract

Objective To detect the effect and mechanism of intravenous anesthetics on lipopolysaccharide (LPS) treated glial cells. Methods The proliferative ratio and the apoptotic ratio of glial cells after treated with LPS were detected by MTT assay, colony formation assay, and Annexin V-FITC/PI double staining, respectively. The protein related to the mechanisms was analyzed by Western blotting. Results Intravenous anesthetics reversed the LPS-induced proliferation of glial cells. The levels of p-Akt and p-mTOR were downregulated, while the levels of Caspase-3 and Caspase-9 were upregulated in intravenous anesthetics treated cells than untreated ones. Conclusion Intravenous anesthetics may reverse LPS-induced proliferation of glial cells by suppressing mTOR signaling pathway.

导出引用

董闯王昊. 静脉麻醉药对脂多糖诱导的神经星形胶质细胞增殖的影响及其机制[J]. 解剖学报. 2018, 49(3): 299-302 https://doi.org/10.16098/j.issn.0529-1356.2018.03.005

DONG Chuang WANG Hao. Effects of intravenous anesthetics on lipopolysaccharide-induced proliferation of glial cells and its mechanisms[J]. Acta Anatomica Sinica. 2018, 49(3): 299-302 https://doi.org/10.16098/j.issn.0529-1356.2018.03.005

参考文献

［1］Lin L, Desai R, Wang X, et al. Characteristics of primary rat microglia isolated from mixed cultures using two different methods［J］. J Neuroinflammation, 2017, 14(1):101-110.

[2］Ding Y, Zhang J, Wang R. Inhibition of tissue transglutaminase attenuates lipopolysaccharide-induced inflammation in glial cells through AKT/mTOR signal pathway［J］. Biomed Pharmacother, 2017, 89:1310-1319.

［3］You LH, Yan CZ, Zheng BJ, et al. Astrocyte hepcidin is a key factor in LPS-induced neuronal apoptosis［J］. Cell Death Dis, 2017, 8(3):e2676-e2683.

［4］Luo ZhZh, Zhou ZhD, Hu YH, et al. Effects of lornoxican or morphine PCIA on plasma levels of TNF-α and IL-10 in the patients with cancer ［J］. Practical Clinical Medicine, 2006, 7(12):80-82. (in Chinese)

罗振中，周志东，胡衍辉，等. 氯诺昔康或吗啡行术后镇痛对癌症患者TNF-α和IL-10的影响［J］。实用临床医学，2006，7(12)：80-82

［5］Wu ShJ, Fang XM. Anaesthesia and immunoimmunoinflammatory response［J］. China Continuing Medical Education, 2010, 2(4): 30-34. (in Chinese)

吴水晶，方向明.麻醉与免疫炎症反应［J］.中国继续医学教育，2010， 2(4)：30-34.

［6］Ko WK, Lee SH, Kim SJ, et al. Anti-inflammatory effects of ursodeoxycholic acid by lipopolysaccharide-stimulated inflammatory responses in RAW 264.7 macrophages［J］. PLoS One, 2017, 12(6):e0180673-e0180684.

［7］Liu SQ, Zhang ML, Zhang HJ, et al. Matrine promotes oligodendrocyte development in CNS autoimmunity through the PI3K/Akt signaling pathway［J］. Life Sci, 2017, 180:36-41.［8］Yang Z, Zeng B, Pan Y, et al. Autophagy participates in isoliquiritigenin-induced melanin degradation in human epidermal keratinocytes through PI3K/AKT/mTOR signaling［J］. Biomed Pharmacother, 2017, 97:248-254.

［9］Houssaini A, Adnot S. mTOR: a key to both pulmonary vessel remodeling and right ventricular function in pulmonary arterial hypertension ［J］ ? Am J Respir Cell Mol Biol, 2017, 57(5):509-511.

［10］Chen X, Zhang Z, Bi Y, et al. mTOR signaling disruption from myeloid-derived suppressive cells protects against immune-mediated hepatic injury through the HIF1α-dependent glycolytic pathway［J］. J Leukoc Biol, 2016, 100(6):1349-1362.