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木犀草素通过 HMGB1-TLR-NF-κB 信号通路缓解 DSS 诱导的小鼠结肠炎。

Luteolin Relieved DSS-Induced Colitis in Mice via HMGB1-TLR-NF-κB Signaling Pathway.

机构信息

Henan University of Chinese Medicine, Zhengzhou, 450046, Henan, China.

Department of General Surgery, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, 215009, Jiangsu, China.

出版信息

Inflammation. 2021 Apr;44(2):570-579. doi: 10.1007/s10753-020-01354-2. Epub 2020 Oct 5.

DOI:10.1007/s10753-020-01354-2
PMID:33015735
Abstract

The aim of this study was to investigate the effect of luteolin (Lu) on dextran sodium sulfate (DSS)-induced colitis in mice. Mice spleen was weighed. The length of colon was measured. H&E staining was used to observe the pathological changes of colon in mice. Superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and intestine of mice were detected by commercial kits. Serum and intestinal cytokines were detected by ELISA kits. The expression of HMGB1 mRNA was detected by real-time PCR. The expression of HMGB1-TLR-NF-κB pathway was detected by Western blot. The level of HMGB1 was detected by immunohistochemistry. The results showed that Lu significantly increased the colon length/body weight ratio and significantly decreased the spleen weight/body weight ratio. Lu significantly increased serum and intestinal SOD levels and decreased MDA levels. Lu significantly increased serum and intestinal cytokine levels in mice. qPCR and immunohistochemistry results showed that Lu significantly reduced HMGB1 mRNA level and protein level. In addition, Lu significantly reduced the expression of HMGB1-TLR-NF-κB signaling pathway protein of intestine in mice. In conclusion, Lu significantly reduced and alleviated DSS-induced colitis in mice, and the mechanism was related to the regulation of intestinal HMGB1-TLR-NF-κB signaling pathway in mice.

摘要

本研究旨在探讨木犀草素(Lu)对葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎的影响。称取小鼠脾脏重量。测量结肠长度。H&E 染色用于观察小鼠结肠的病理变化。通过商业试剂盒检测血清和肠道中小鼠超氧化物歧化酶(SOD)和丙二醛(MDA)的含量。通过 ELISA 试剂盒检测血清和肠道细胞因子。通过实时 PCR 检测 HMGB1 mRNA 的表达。通过 Western blot 检测 HMGB1-TLR-NF-κB 通路的表达。通过免疫组化检测 HMGB1 水平。结果表明,Lu 显著增加了结肠长度/体重比,显著降低了脾脏重量/体重比。Lu 显著提高了血清和肠道 SOD 水平,降低了 MDA 水平。Lu 显著增加了小鼠血清和肠道细胞因子水平。qPCR 和免疫组化结果表明,Lu 显著降低了 HMGB1 mRNA 水平和蛋白水平。此外,Lu 显著降低了小鼠肠道中 HMGB1-TLR-NF-κB 信号通路蛋白的表达。总之,Lu 显著减轻和缓解了 DSS 诱导的小鼠结肠炎,其机制与调节肠道 HMGB1-TLR-NF-κB 信号通路有关。

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