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绿原酸通过与 TLR4 介导的下游通路相互作用缓解 LPS 诱导的 BV2 细胞炎症应激。

Chlorogenic Acid Alleviates the Inflammatory Stress of LPS-Induced BV2 Cell via Interacting with TLR4-Mediated Downstream Pathway.

机构信息

Department of Neurology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, China.

Department of Neurology, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430077 Hubei, China.

出版信息

Comput Math Methods Med. 2022 May 18;2022:6282167. doi: 10.1155/2022/6282167. eCollection 2022.

Abstract

BACKGROUND

Neuroinflammation is related with the inflammatory stress of brain tissue induced by the activation of microglial in the central nervous system (CNS), which is still an intractable disease for modern clinical system. Chlorogenic acid has multiple biological activities such as antivirus and anti-inflammation, while few researches have revealed its therapeutic functions in neuroinflammation.

METHODS

BV2 cells were treated with lipopolysaccharide (LPS) to establish neuroinflammation cell models, and the effects and mechanism of chlorogenic acid in improving the inflammatory progression were investigated. In brief, the toxicity of chlorogenic acid on BV2 cells was detected with MTT assay. The levels of the inflammatory factors including TNF-, IL-6, IL-1, and IFN- were measured with ELISA, and the abundances of TLR4, MyD88, TRIF, and NF-B were observed by qRT-PCR and western blot.

RESULTS

Chlorogenic acid did not exhibit obvious toxic and side effects on BV2 cells. The levels of TNF-, IL-6, IL-1, and IFN- were observably upregulated in BV2 cells after treating with LPS. Chlorogenic acid significantly reduced the levels of TNF-, IL-6, IL-1, and IFN-. Moreover, the abundances of TLR4, MyD88, TRIF, and NF-B were increased in LPS-induced BV2 cells, while chlorogenic acid could obviously reduce their expressions.

CONCLUSION

This study suggests that chlorogenic acid can improve the inflammatory stress of LPS-induced BV2 cell via interacting with the TLR4-mediated downstream pathway, which is a potential drug for neuroinflammation treatment.

摘要

背景

神经炎症与中枢神经系统(CNS)中小胶质细胞的激活引起的脑组织炎症应激有关,这仍然是现代临床系统的一种难治性疾病。绿原酸具有抗病毒和抗炎等多种生物学活性,而很少有研究表明其在神经炎症中的治疗作用。

方法

用脂多糖(LPS)处理 BV2 细胞建立神经炎症细胞模型,研究绿原酸改善炎症进展的作用及其机制。简而言之,用 MTT 法检测绿原酸对 BV2 细胞的毒性。用 ELISA 法测定 TNF-α、IL-6、IL-1 和 IFN-等炎症因子的水平,并用 qRT-PCR 和 Western blot 观察 TLR4、MyD88、TRIF 和 NF-B 的丰度。

结果

绿原酸对 BV2 细胞无明显毒性和副作用。用 LPS 处理 BV2 细胞后,TNF-α、IL-6、IL-1 和 IFN-的水平明显上调。绿原酸显著降低了 TNF-α、IL-6、IL-1 和 IFN-的水平。此外,LPS 诱导的 BV2 细胞中 TLR4、MyD88、TRIF 和 NF-B 的丰度增加,而绿原酸能明显降低其表达。

结论

本研究表明,绿原酸可通过与 TLR4 介导的下游通路相互作用改善 LPS 诱导的 BV2 细胞的炎症应激,这是一种治疗神经炎症的潜在药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2179/9132620/50d2df490a81/CMMM2022-6282167.001.jpg

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