紫檀芪对棕榈酸诱导巨噬细胞炎症因子分泌的影响
| 作者: |
1陈卓,
1李子铭,
2杨永玉
1 中南大学湘雅三医院老年医学科，长沙 410013 2 中南大学湘雅二医院药学部，长沙 410011 |
| 通讯: |
杨永玉
Email: yongyuyang@126.com |
| DOI: | 10.3978/j.issn.2095-6959.2021.08.002 |
| 基金: | 湖南省自然科学基金(2019JJ50923)；湖南省中医药管理局科研计划项目(2020039)。 |
摘要
目的：研究紫檀芪(pterostilbene，PTE)对棕榈酸(palmitic acid，PA)诱导巨噬细胞炎症因子分泌的影响及可能机制。方法：采用MTT法检测PTE对巨噬细胞RAW264.7活性的影响；先用不同浓度的PTE预处理RAW264.7，后用PA处理，ELISA法检测巨噬细胞培养上清液中炎症因子IL-18、IL-1β和TNF-α水平，采用蛋白质印迹法检测巨噬细胞中NLRP3、凋亡相关斑点样蛋白(apoptosis-associated speck-like protein containing CARD，ASC)、半胱天冬酶1(caspase-1)、核转录因子-κB p65(NF-κB p65)、p-NF-κB p65的表达。结果：与对照组比较，0~200 μmol/L浓度的PTE对巨噬细胞的活力无影响。50 μmol/L和100 μmol/L的PTE可显著抑制PA诱导的巨噬细胞炎症因子IL-18、IL-1β和TNF-α水平的升高，降低PA诱导巨噬细胞中NLRP3、ASC、caspase-1蛋白表达的升高。PTE可减少PA诱导胞质中p-IKK和p-NF-κB p65表达的升高，以及IκBα表达的降低。PTE还可降低PA诱导的p-NF-κB p65的核转位。结论：PTE可抑制PA诱导巨噬细胞炎症因子表达的升高，其机制可能与其抑制炎症小体活化的通路有关。
关键词：
紫檀芪；巨噬细胞；炎症小体；核转录因子-κB
Effect of pterostilbene on palmitic acid-induced secretion of inflammatory factors in macrophages
CorrespondingAuthor: YANG Yongyu Email: yongyuyang@126.com
DOI: 10.3978/j.issn.2095-6959.2021.08.002
Foundation: This work was supported by the Natural Science Foundation of Hunan Province (2019JJ50923) and Hunan Provincial Administration of Traditional Chinese Medicine Scientific Research Project (2020039), China.
Abstract
Objective: To study the effect of pterostilbene (PTE) on palmitic acid (PA)-induced inflammatory factor secretion in macrophages and its possible mechanism. Methods: MTT method was used to detect the effect of pterostilbene on the activity of RAW264.7 cells. RAW264.7 cells were pretreated with different concentrations of pterostilbene and then treated by PA. ELISA kit was used to detect the levels of IL-18, IL-1β and TNF-α in the supernatant of macrophages, and Western blotting was used to detect the expression of NLRP3, apoptosis-associated speck-like protein containing CARD (ASC), caspase-1, Nuclear factor of κB p65 (NF-κB p65), p-NF-κB p65 in macrophages. Results: Compared with the control group, MTT test results showed that PTE at a concentration of 0–200 μmol/L had no effect on the activity of macrophages. PTE at 50 and 100 μmol/L could significantly inhibit the PA-induced the expression of IL-18, IL-1β and TNF-α, and reduce PA-induced the expression of NLRP3, ASC, caspase-1 in macrophages. Meanwhile, PTE inhibited the expression of p-IKK and p-NF-κB p65, and reduced the decrease of the expression of IκBα in cytoplasm of PA-induced RAW264.7 cells. PTE can also reduce the nuclear translocation of p-NF-κB p65 induced by PA. Conclusion: Pterostilbene can inhibit PA-induced increase of inflammatory factor expression in macrophages, and its mechanism may be related to its inhibition of the pathway of inflammasomes.
Keywords：
pterostilbene; macrophages; inflammasome; nuclear factor of κB