1.湖北中医药大学药学院(湖北 武汉 430065)
2.湖北中医药大学基础医学院(湖北 武汉 430065)
艾文琪,女,在读硕士生,主要从事中医药防治老年性痴呆的物质基础及机制研究
兰洲,教授,硕士生导师;E-mail:lzlz_84@163.com
纸质出版日期:2024-03-25,
收稿日期:2023-04-27,
修回日期:2023-05-27,
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艾文琪,张学松,郑军佐等.仙茅⁃淫羊藿水提物入血成分的抗炎作用研究[J].上海中医药大学学报,2024,38(02):29-35.
AI Wenqi,ZHANG Xuesong,ZHENG Junzuo,et al.Study on anti⁃inflammatory effect of components absorbed into blood of aqueous extract of "Curculiginis Rhizoma and Epimedii Folium"[J].Academic Journal of Shanghai University of Traditional Chinese Medicine,2024,38(02):29-35.
艾文琪,张学松,郑军佐等.仙茅⁃淫羊藿水提物入血成分的抗炎作用研究[J].上海中医药大学学报,2024,38(02):29-35. DOI: 10.16306/j.1008-861x.2024.02.005.
AI Wenqi,ZHANG Xuesong,ZHENG Junzuo,et al.Study on anti⁃inflammatory effect of components absorbed into blood of aqueous extract of "Curculiginis Rhizoma and Epimedii Folium"[J].Academic Journal of Shanghai University of Traditional Chinese Medicine,2024,38(02):29-35. DOI: 10.16306/j.1008-861x.2024.02.005.
目的
2
探究仙茅-淫羊藿水提物(EX)中入血成分的抗炎作用。
方法
2
采用AutoDockTools软件将EX中5种入血成分(仙茅苷、淫羊藿苷、宝藿苷I、苔黑酚葡萄糖苷和朝藿定A)与靶蛋白髓细胞触发受体2(TREM2)进行分子对接;采用细胞计数试剂盒(CCK8)检测EX中5种入血成分在不同浓度下对小胶质细胞(BV2)细胞活力的影响;采用LPS刺激BV2或小鼠骨髓来源的巨噬细胞(BMDMs)及尼日利亚菌素(nigericin)刺激LPS预处理的BMDMs细胞建立炎症模型,并用酶联免疫吸附测定法(ELISA)检测5种入血成分对细胞上清液中肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)水平的影响。
结果
2
EX的入血成分仙茅苷、淫羊藿苷、宝藿苷I和朝藿定A与TREM2结合十分稳定,苔黑酚葡萄糖苷与TREM2结合较为稳定;仙茅苷、淫羊藿苷、宝藿苷I、朝藿定A和苔黑酚葡萄糖苷均可在一定浓度下减少BMDMs细胞产生的IL-1β水平,而仅高浓度的仙茅苷和淫羊藿苷可减少BMDMs细胞产生的TNF-α水平。
结论
2
EX的5种入血成分均可与TREM2结合,抑制下游NF-κB、NLRP3炎症通路改善炎症,可能是EX调控TREM2改善学习记忆能力和神经炎症的有效物质基础,在EX中起到协同增效的作用。
Objective: To explore the anti-inflammatory effect of the components absorbed into serum of the aqueous extract of "Curculiginis Rhizoma and Epimedii Folium" (EX).
Methods
2
AutoDockTools software was used to dock the five components absorbed into serum of EX (Curculigoside, Icariin, Baohuoside I, Oricinol glucoside and Epimedin A) with target protein TREM2. CCK8 method was used to detect the effects of the five components on BV2 cell viability at different concentrations. LPS was used to stimulate BV2 or mouse bone marrow-derived BMDMs cells and Nigericin to stimulate LPS pretreated BMDMs cells to establish inflammatory models, and the effects of the five components on TNF-α and IL-1β levels in the cell supernatant were detected by ELISA.
Results
2
The components absorbed into serum of EX including Curculigoside, Icariin, Baohuoside I and Epimedin A, bound very stably to TREM2, while the binding of Orcinol glucoside to TREM2 was relatively stable. Curculigoside, Icariin, Baohuoside I, Orcinol glucoside and Epimedin A all reduced the level of IL-1β produced by BMDMs at certain concentrations, while only high concentrations of Curculigoside and Icariin reduced the level of TNF-α produced by BMDMs.
Conclusion
2
5 components absorbed into serum of EX could all bind to TREM2 and inhibit downstream NF-κB or NLRP3 inflammatory pathways to improve inflammation, which might be an effective material basis for EX to regulate TREM2 to improve learning and memory ability and neuroinflammation, and work synergistically in EX.
仙茅-淫羊藿水提物TREM2分子对接炎症
Curculiginis Rhizoma and Epimedii Foliumaqueous extractTREM2molecular dockinginflammation
SCHELTENS P, BLENNOW K, BRETELER M M, et al. Alzheimer's disease[J]. Lancet, 2016, 388(10043): 505-517.
HENEKA M T, CARSON M J, EI KOURY J, et al. Neuroinflammation in Alzheimer's disease[J]. Lancet Neurol, 2015, 14(4): 388-405.
HICKMAN S E, KINGERY N D, OHSUMI T K, et al. The microglial sensome revealed by direct RNA sequencing[J]. Nat Neurosci, 2013, 16(12): 1896-1905.
YEH F L, HANSEN D V, SHENG M. TREM2, Microglia, and Neurodegenerative Diseases[J]. Trends Mol Med, 2017, 23(6): 512-533.
ULRICH J D, ULLAND T K, COLONNA M, et al. Elucidating the Role of TREM2 in Alzheimer' s Disease[J]. Neuron, 2017, 94(2): 237-248.
KRASEMANN S, MADORE C, CIALIC R, et al. The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases[J]. Immunity, 2017, 47(3): 566-581.
MAZAHERI F, SNAIDERO N, KLEINBERGER G, et al. TREM2 deficiency impairs chemotaxis and microglial responses to neuronal injury[J]. EMBO Rep, 2017, 18(7): 1186-1198.
闫涛. 治疗阿尔茨海默病的药物研究进展[J]. 天津药学, 2016, 28(3): 46-49.
YAN T. Research progress of drugs for the treatment of Alzheimer's disease[J]. Tianjin Pharmacy, 2016, 28(3): 46-49.
SHI K, CHEN L, CHEN L, et al. Epimedii Folium and Curculiginis Rhizoma ameliorate lipopolysaccharides-induced cognitive impairment by regulating the TREM2 signaling pathway[J]. J Ethnopharmacol, 2022, 284: 114766.
袁德培,邱幸凡,王平,等. 肾虚髓衰、脑络痹阻是老年性痴呆的基本病机[J]. 中华中医药杂志, 2008, 23(8): 732-734.
YUAN D P, QIU X F, WANG P, et al. Kidney deficiency and pulp failure and cerebral obstruction are the basic pathogenesis of senile dementia[J]. China Journal of Traditional Chinese Medicine and Pharmacy, 2008, 23(8): 732-734.
崔远武,张玉莲. 中医对老年性痴呆的认识和辨证思路分析[J]. 中国老年学杂志, 2015, 35(5): 1419-1422.
CUI Y W, ZHANG Y L. Understanding of Senile dementia and analysis of Syndrome differentiation in Traditional Chinese Medicine[J]. Chinese Journal of Gerontology, 2015, 35(5): 1419-1422.
MATCOVITCH-NATAN O, WINTER D R, GILADI A, et al. Microglia development follows a stepwise program to regulate brain homeostasis[J]. Science, 2016, 353(6301): aaad8670.
D'MELLO C, LE T, SWAIN M G. Cerebral microglia recruit monocytes into the brain in response to tumor necrosis factoralpha signaling during peripheral organ inflammation[J]. J Neurosci, 2009, 29(7): 2089-2102.
SHARMA S, YANG B, STRONG R, et al. Bone marrow mononuclear cells protect neurons and modulate microglia in cell culture models of ischemic stroke[J]. J Neurosci Res, 2010, 88(13): 2869-2876.
KLEINBERGER G, YAMANISHI Y, SUAREZ-CALVET M, et al. TREM2 mutations implicated in neurodegeneration impair cell surface transport and phagocytosis[J]. Sci Transl Med, 2014, 6(243): 243ra86.
FORD J W, MCVICAR D W. TREM and TREM-like receptors in inflammation and disease[J]. Curr Opin Immunol, 2009, 21(1): 38-46.
COLONNA M, WANG Y. TREM2 variants: new keys to decipher Alzheimer disease pathogenesis[J]. Nat Rev Neurosci, 2016, 17(4): 201-207.
JIN J J, KIM H D, MAXWELL J A, et al. Toll-like receptor 4-dependent upregulation of cytokines in a transgenic mouse model of Alzheimer's disease[J]. J Neuroinflammation, 2008, 5: 23.
KIGERL K A, DE RIVERO V J, DIETRICH W D, et al. Pattern recognition receptors and central nervous system repair[J]. Exp Neurol, 2014, 258: 5-16.
BUTOVSKY O, JEDRYCHOWSKI M P, MOORE C S, et al. Identification of a unique TGF-beta-dependent molecular and functional signature in microglia[J]. Nat Neurosci, 2014, 17(1): 131-143.
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