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-  2018 

在慢阻肺炎症反应中黄芪多糖的抗炎作用及抑制TLR4/NF-κB通路的机制
Anti-inflammatory effect of astragalus polysaccharides and the mechanism of inhibiting TRL4/ NF-κB pathway in COPD inflammatory response

DOI: 10.7652/jdyxb201805029

Keywords: 慢性阻塞性肺疾病(COPD),黄芪多糖,TLR4/NF-κB通路,炎症反应,巨噬细胞
chronic obstructive pulmonary disease (COPD)
,astragalus,astragalus polysaccharide (APS),TLR4/NF-κB pathway,inflammatory reaction,macrophage

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Abstract:

摘要:目的 探讨黄芪多糖(astragalus polysaccharides, APS)治疗慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)炎症反应的作用机制。方法 收集长沙民政职业技术学院医学院校企合作医院呼吸科门诊就诊稳定期COPD患者19例,健康体检者20例,分离培养外周血单核细胞源性巨噬细胞。随机将COPD患者细胞分为COPD组、脂多糖组(LPS组)、APS高浓度组、APS低浓度组,并与健康体检者细胞(健康组)进行比较。酶联免疫吸附测定法(enzyme-linked immunosorbent assay, ELISA)检测各组细胞上清液中炎症相关因子的含量,荧光定量PCR检测巨噬细胞中Toll样受体4(TLR4)、NF-κB mRNA表达。结果 与健康组比较,COPD组TLR4、NF-κB mRNA表达、肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)、基质金属蛋白酶-9(MMP-9)、前列腺素E2(PGE2)含量显著升高(P<0.05);与COPD组比较,LPS组TLR4、NF-κB mRNA表达、TNF-α、IL-6、MMP-9、PGE2含量显著升高(P<0.05);与LPS组比较,APS组TLR4、NF-κB mRNA表达、TNF-α、IL-6、MMP-9、PGE2含量显著下降(P<0.05),且APS高浓度组下降明显(P<0.05)。结论 APS降低细胞TLR4、NF-κB mRNA表达,且下游炎症因子含量降低,一定程度缓解了LPS引起的细胞损伤,说明APS可能通过抑制TLR4/NF-κB通路,调节炎症反应而发挥抗炎作用。
ABSTRACT: Objective To study the mechanism of astragalus polysaccharide (APS) in treatment of inflammatory response in chronic obstructive pulmonary disease (COPD). Methods We recruited 19 patients with stable COPD and 20 healthy persons for physical check-up from the Department of Respiration of School-Enterprise Cooperation Hospital of Changsha Social Work College Medical School. Monocyte-derived macrophages from peripheral blood were isolated and cultured. The cells were randomly divided into COPD group, LPS group, high-concentration APS group, and low-concentration APS group. They were compared with healthy persons (healthy group). The content of inflammatory factors in supernatant was detected by enzyme linked immunosorbent assay (ELISA) and the expressions of TLR4 and NF-κB mRNA in macrophages were detected by q-PCR. Results The levels of TNF-α, IL-6, MMP-9, PGE2 and the expressions of TLR4 and NF-κB mRNA were significantly higher in COPD group than in healthy group (P<0.05). Levels of TNF-α, MMP-9, PGE2, and IL-6 and the expressions of TLR4 and NF-κB mRNA were significantly higher in LPS group than in COPD group (P<0.05). Compared with LPS group, they were significantly decreased in APS group (P<0.05). Conclusion APS can significantly decrease the levels of TNF-α, IL-6, MMP-9, and PGE2 in macrophages. The decrease of inflammatory factors in the downstream can alleviate LPS-induced cell injury to some extent, suggesting that APS may regulate the inflammatory response and exert anti-inflammatory effects by inhibiting the TLR4/NF-κB pathway

References

[1]  梁志科,刘朝晖,赵子文,等. MAPK在介导人肺泡巨噬细胞模型噬菌中的作用[J]. 国际呼吸杂志, 2016, 36(4):277-282.
[2]  于红红,吴玛莉,张智伟,等. 四妙勇安汤含药血清对巨噬细胞TLR4/MyD88信号通路及其下游炎症因子的影响[J]. 免疫学杂志, 2016, 32(6):519-522.
[3]  ROGIER R, EDERVEEN T, BOEKHORST J, et al. A1.01 Activation of TLR4 by dysbiotic intestinal microbiota following IL-1 receptor antagonist deficiency triggers TH17-mediated arthritis[J]. Ann Rheum Dis, 2016, 75(Suppl 1):A1.1-A1.
[4]  ZHANG X, SUN CY, ZHANG YB, et al. Kegan Liyan oral liquid ameliorates lipopolysaccharide-induced acute lung injury through inhibition of TLR4-mediated NF-κB signaling pathway and MMP-9 expression[J]. J Ethnopharmacol, 2016, 186(4):91-102.
[5]  CIANCIULLI A, SALVATORE R, PORRO C, et al. Folic acid is able to polarize the inflammatory response in LPS activated microglia by regulating multiple signaling pathways[J]. Mediat Inflamm, 2016, 2016(6636):1-10.
[6]  闫香桂,吴国芳,黄芬,等. 中医药治疗稳定期慢性阻塞性肺疾病研究进展[J]. 中医学报, 2016, 31(9):1284-1288.
[7]  黄进,张晨,詹菲,等. 黄芪多糖对肝纤维化大鼠TGF-β1/Smads信号通路的影响[J]. 中华中医药杂志, 2015, 30(6):2184-2186.
[8]  徐海军,陶文众,彭欢欢,等. 黄芪多糖和葡萄籽提取物对衰老模型小鼠负重游泳时间和血常规参数的影响[J]. 天然产物研究与开发, 2015, 27(1):158-162.
[9]  常晓,李惠林,楚淑芳,等. 黄芪多糖介导NRG-1/ErbB信号通路对糖尿病心肌细胞凋亡的作用[J]. 中国中医基础医学杂志, 2016, 22(9):1192-1195.
[10]  FU J, WANG Z, HUANG L, et al. Review of the botanical characteristics, phytochemistry, and pharmacology of astragalus membranaceus (Huangqi)[J]. Phytother Res, 2014, 28(9):1275-1283.
[11]  李飞,牛田,刘志刚,等. MMP-2及MMP-9与主动脉疾病相关性的研究进展[J]. 现代生物医学进展, 2015, 15(18):3577-3580.
[12]  EDATT L, HARITHA K, SRUTHI TV, et al. 2-Deoxy glucose regulate MMP-9 in a SIRT-1 dependent and NFkB independent mechanism[J]. Mol Cell Biochem, 2016, 423(1-2):197.
[13]  郝伟欣. 慢性阻塞性肺疾病[J]. 中国全科医学, 2006, 14(3):172-174.
[14]  黄丽,何建国. 慢性阻塞性肺疾病合并肺栓塞研究进展[J]. 中国循环杂志, 2016, 31(1):113-113.
[15]  李亭亭,张雪,柯越海,等. 肺泡巨噬细胞的研究进展[J]. 中国细胞生物学学报, 2017,39(2):232-237.
[16]  孙雪芳,王洪新,梁灵君,等. 黄芪多糖通过TLR4/NF-κB信号通路抑制脂多糖诱导的大鼠心肌细胞肥大[J]. 中国药理学通报, 2013, 29(2):208-212.
[17]  黄能,詹剑华,罗锦花,等. 黄芪多糖对严重烫伤大鼠血清炎症因子的影响[J]. 中华烧伤杂志, 2015, 31(4):274.
[18]  王蕾,杨汀,王辰. 2017年版慢性阻塞性肺疾病诊断、处理和预防全球策略解读[J]. 中国临床医生杂志, 2017, 45(1):104-108.
[19]  林炜明,戴爱玲,尹会方,等. 人外周血巨噬细胞培养及功能鉴定[J]. 中国免疫学杂志, 2015, 31(1):86-89.
[20]  李晶,周伟,袁伟明,等. 不同浓度脂多糖对大鼠肠上皮细胞增殖和白细胞介素-6、白细胞介素-1β及肿瘤坏死因子-α分泌的影响[J]. 中华实用儿科临床杂志, 2015, 30(7):490-493.
[21]  陶静秋,吴晓梅. Toll样受体4在慢性阻塞性肺疾病中作用的研究进展[J]. 国际免疫学杂志, 2015, 38(4):392-394.
[22]  王鹏雁,蒋明,王昌明,等. 脂多糖诱导下慢性阻塞性肺疾病大鼠模型远端肺动脉平滑肌细胞中Toll样受体4表达情况研究[J]. 中国全科医学, 2017, 20(21):2603-2608.
[23]  朱雪坤,杨日芳,孟艳秋. Toll样受体4配体的研究进展[J]. 中国药理学与毒理学杂志, 2016, 30(4):389-396.
[24]  PADWAL MK, SARMA U, SAHA B. Comprehensive logic based analyses of Toll-like receptor 4 signal transduction pathway[J]. PLoS One, 2014, 9(4):e92481.
[25]  BOERSEMA AGS, UTOMO L, BAYON Y, et al. Monocyte subsets in blood correlate with obesity related response of macrophages to biomaterials in vitro[J]. Biomaterials, 2016, 109(2):32-39.
[26]  张秀梅,李成华. 脂多糖诱导的肿瘤坏死因子(LITAF)生物学功能研究进展[J]. 中国细胞生物学学报, 2015, 37(4):553-559.
[27]  刘萍,秦兴国. 慢性阻塞性肺疾病肺康复综合治疗的研究进展[J]. 医学临床研究, 2015, 10(5):983-985.
[28]  殷鹏,王黎君,刘世炜,等. 1990年与2010年中国15岁以上人群慢性阻塞性肺疾病的疾病负担分析[J]. 中华预防医学杂志, 2015, 9(4):364-368.
[29]  熊金梦,毛科稀,叶旭军. 辅助性T细胞与慢性阻塞性肺疾病的研究进展[J]. 临床内科杂志, 2016, 33(8):574-576.
[30]  张雪,费霞,张?F. COPD患者糖皮质激素不敏感的发生机制和应对策略研究进展[J]. 国际呼吸杂志, 2016, 36(21):1643-1647.
[31]  朱国民,殷放宙,邓旭坤. NF-κB在马钱子碱抑制非小细胞肺癌细胞环氧化酶2生成中的作用研究[J]. 中国中药杂志, 2012, 37(9):1269-1273.

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