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作 者:陈崇利 陈金鑫 朱月 徐曼如 何小静 伍文彬[1] Chen Chongli;Chen Jinxin;Zhu Yue;Xu Manru;He Xiaojing;Wu Wenbin(Hospital of Chengdu University of Traditional Chinese Medicine,Chengdu 610072;Dazhou integrated TCM&Western Medicine Hospital,Dazhou 635002)
机构地区:[1]成都中医药大学附属医院,成都610072 [2]达州市中西医结合医院,达州635002
出 处:《中药药理与临床》2022年第5期7-11,共5页Pharmacology and Clinics of Chinese Materia Medica
基 金:国家自然科学基金(编号:82174358);四川省科技计划重点项目(编号:2018JY0060)。
摘 要:目的:探究黄连解毒汤含药脑脊液对Aβ_(1-42)致小鼠BV2小胶质细胞神经炎症及α7烟碱型乙酰胆碱受体(α7 nicotinic acetylcholine receptor,α7nAChR)表达的影响。方法:小鼠BV2细胞随机分为空白对照组、模型对照组、石杉碱甲10%含药脑脊液组及5%、10%、20%黄连解毒汤含药脑脊液组,使用Aβ_(1-42)复制BV2细胞炎症模型。24 h后,采用MTT法检测BV2吸光度值及细胞存活率,采用ELISA法检测肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白介素-6(Interleukin-6,IL-6)、IL-8含量;采用RT-PCR法和Western blot法分别检测A7nachr mRNA和蛋白表达。结果:与空白对照组比较,Aβ_(1-42)干预后,BV2细胞促炎因子TNF-α、IL-6、IL-8含量显著升高(P<0.01),A7nachr mRNA及蛋白表达显著下调(P<0.01);与模型对照组比较,黄连解毒汤含药脑脊液各组均能降低BV2细胞促炎因子TNF-α、IL-6、IL-8含量,上调α7nachr mRNA和蛋白的表达(P<0.01)。结论:黄连解毒汤含药脑脊液可能通过激活胆碱能抗炎通路中α7nAChR表达,改善Aβ_(1-42)诱导BV2细胞炎症反应。Objective:To observe the effect of cerebrospinal fluid containing Huanglian Jiedu Decoction(黄连解毒汤,HLJDT-CFS)on the Aβ_(1-42)-induced inflammation andα7 nicotinic acetylcholine receptor(α7 nAChR)level of BV2 cells.Methods:BV2 microglia of mice were randomized into blank control group,model group,huperzine A group,and 5%,10%,and 20%HLJDT-CFS groups.Oligomer Aβ_(1-42) was used to induce AD neuroinflammation in BV2 cells.After 24 hours of incubation,the absorbance and survival of BV2 cells were detected by methyl thiazolyl tetrazolium(MTT)assay,and content of tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),and interleukin-8(IL-8)was measured by enzyme-linked immunosorbent assay(ELISA).The level ofα7nAChR mRNA was detected by RT-PCR,while theα7 nAChR protein level was measured by Western blotting.Results:Compared with the blank control group,Aβ_(1-42) significantly decreased the cell viability and increased the expression of inflammatory factors TNF-a,IL-6,and IL-8.HLJDT-CFS reduced the levels of TNF-α,IL-6,and IL-8 and up-regulated theα7nAChR mRNA and protein levels.Conclusion:HLJDD-CSF can alleviate the Aβ_(1-42)-induced inflammation in BV2 cells by activatingα7 nAChR in the cholinergic anti-inflammatory pathway.
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