原花青素B1对脂多糖介导的炎症反应的抑制作用及其机制探讨

发布时间：2018-04-13 09:46

本文选题：原花青素B + 脂多糖类　；参考：《中华危重症医学杂志(电子版)》2015年05期

【摘要】：目的探索原花青素B1的抗炎活性及其抗炎机制。方法以人急性单核细胞白血病细胞系(THP-1)为模型,设立不含脂多糖(LPS)的磷酸盐缓冲溶液(PBS)处理THP-1细胞为对照组,检测不同浓度原花青素B1(50、100、150、200 mg/L)对THP-1细胞活力的影响。分别应用1 mg/L的LPS(LPS组)、1 mg/L的LPS联合原花青素B1 50 mg/L(处理A组)、1 mg/L的LPS联合原花青素B1 100 mg/L(处理B组)预处理THP-1细胞,收集各组THP-1细胞上清液,应用双抗体夹心亲和素-生物素-过氧化物酶复合物-酶联免疫吸附法测定各组THP-1细胞中TNF-α的释放水平。应用实时定量PCR法测定各组THP-1细胞My D88 m RNA和髓样分化蛋白2(MD-2)m RNA的表达情况。结果不同浓度原花青素的THP-1细胞活力与对照组比较,差异有统计学意义(F=31.35,P0.001),进一步比较发现,50、100 mg/L原花青素的THP-1细胞活力与对照组比较差异均无统计学意义(P均0.05),而150、200 mg/L原花青素的THP-1细胞活力均明显低于对照组(P均0.05)。处理A、B组的TNF-α水平较LPS组均显著减低(P均0.05),且处理B较处理A组下降更为明显(P0.05)。对照组、LPS组及处理A组间My D88 m RNA和MD-2m RNA的表达差异均有统计学意义(F=62.500、46.700,P均0.001),且LPS组的My D88 m RNA和MD-2 m RNA表达均较对照组及处理A组明显升高(P均0.05),处理A组的My D88 m RNA和MD-2 m RNA表达高于对照组(P均0.05)。结论原花青素B1可明显抑制LPS介导的炎症反应,负性调节Toll样受体-My D88信号通路,可能是其抑制炎症反应的潜在机制。
[Abstract]:Objective to explore the anti-inflammatory activity and anti-inflammatory mechanism of proanthocyanidin B1.Methods Human acute monocytic leukemia cell line (THP-1) was used as a model. THP-1 cells were treated with phosphate buffer without lipopolysaccharide (LPS). The effects of different concentrations of proanthocyanidin B150100150mg / L on the viability of THP-1 cells were detected.THP-1 cells were pretreated with 1 mg/L LPS(LPS group with 1 mg/L LPS combined with proanthocyanidin B15 50 mg / L (group A treated with 1 mg/L LPS combined with procyanidin B100 mg / L (treatment group B)), and the supernatant of THP-1 cells in each group was collected.The release of TNF- 伪 in THP-1 cells was determined by double antibody sandwich affinity biotin peroxidase complex and enzyme linked immunosorbent assay (Elisa).The expression of my D 88 m RNA and myeloid differentiation protein (2(MD-2)m RNA) in THP-1 cells were measured by real time quantitative PCR assay.Results the activity of THP-1 cells at different concentrations of proanthocyanidins was compared with that of the control group.The difference was statistically significant (P 0.001). It was found that the THP-1 cell viability of P0 0100 mg/L proanthocyanidins was not significantly different from that of the control group (P < 0 05), while the THP-1 cell activity of 150200 mg/L proanthocyanidins was significantly lower than that of the control group (P < 0 05).The level of TNF- 伪 in group A was significantly lower than that in group LPS (P 0.05), and the level of TNF- 伪 in group B was significantly lower than that in group A (P 0.05).The expression of D 88 m RNA and MD-2 m RNA was higher than that of control group (P 0.05).Conclusion proanthocyanidin B1 can inhibit the inflammatory response mediated by LPS and negatively regulate the signaling pathway of Toll like receptor -My D88, which may be the underlying mechanism of its inhibition of inflammatory response.
【作者单位】：大连医科大学附属第一医院急诊科;
【基金】：辽宁省教育厅高等学校科研项目(L2013348)
【分类号】：R392

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