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朝藿定 C 减轻脂多糖诱导的炎症,抑制 TLR4-NF-κB/NLRP3 信号通路。

Tectoridin alleviates lipopolysaccharide-induced inflammation inhibiting TLR4-NF-κB/NLRP3 signaling and .

机构信息

School of Pharmacy, Xi'an Jiaotong University, Xi'an, Shaanxi, China.

Shaanxi Panlong Pharmaceutical Group Limited by Share LTD, Xi'an, Shaanxi, China.

出版信息

Immunopharmacol Immunotoxicol. 2022 Oct;44(5):641-655. doi: 10.1080/08923973.2022.2073890. Epub 2022 Jun 3.

DOI:10.1080/08923973.2022.2073890
PMID:35506641
Abstract

BACKGROUND

Tectoridin, widely extracted and separated from the rhizome of Maxim, is extensively reported to have affluent bioactivity, but rarely reported to have anti-inflammatory effects. In this study, we aim to investigate the anti-inflammatory effects and the underlying mechanisms of tectoridin.

METHODS

Here, RAW264.7 macrophages were stimulated with Lipopolysaccharide (LPS) for the inflammation model . Experimental animals received tectoridin and Dexamethasone (DEX) before LPS injection for endotoxic shock mouse model . The pro-inflammatory mediators and cytokines in the cell supernatant and serum were detected by ELISA kits. The tissue damages were assessed by biochemical indexes and H&E staining. Immunohistochemistry and Western blot were performed for the detection of proteins.

RESULTS

Our data showed that tectoridin attenuated the LPS-up-regulated nitric oxide (NO), interleukin-6 (IL-6), and interleukin-18 (IL-18) from macrophages and tumor necrosis factor-α (TNF-α); (IL-6) and (IL-1β) in the serum levels. Besides, our histopathological study showed that the damages caused by LPS in the lung, liver, and kidney tissues were decreased. Furthermore, our results demonstrated that tectoridin inhibited the activation of TLR4-NF-κB/NLRP3 signaling proved by immunohistochemistry assay and Western blot.

CONCLUSION

Taken all together, tectoridin might have the potential ability of anti-inflammatory effects and the possible mechanism may be relevant to its inhibition of TLR4-NF-κB/NLRP3 signaling.

摘要

背景

水飞蓟宾广泛存在于续随子属植物的根茎中,具有丰富的生物活性,但其抗炎作用鲜有报道。本研究旨在探讨水飞蓟宾的抗炎作用及其机制。

方法

采用脂多糖(LPS)刺激 RAW264.7 巨噬细胞构建炎症模型,给予水飞蓟宾和地塞米松(DEX)预处理建立内毒素休克小鼠模型。采用 ELISA 试剂盒检测细胞上清液和血清中促炎介质和细胞因子的变化,采用生化指标和 H&E 染色评估组织损伤,采用免疫组化和 Western blot 检测蛋白表达。

结果

水飞蓟宾可降低 LPS 诱导的巨噬细胞和血清中一氧化氮(NO)、白细胞介素-6(IL-6)、白细胞介素-18(IL-18)和肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-1β(IL-1β)的水平。此外,组织病理学研究表明,水飞蓟宾可减轻 LPS 引起的肺、肝、肾组织损伤。进一步研究表明,水飞蓟宾通过抑制 TLR4-NF-κB/NLRP3 信号通路的激活发挥抗炎作用。

结论

水飞蓟宾可能具有抗炎作用,其机制可能与抑制 TLR4-NF-κB/NLRP3 信号通路有关。

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