Protective effect of hydrangenol on lipopolysaccharide-induced endotoxemia by suppressing intestinal inflammation

被引:6
|
作者
Jang, Seo-Yun [1 ,2 ]
Kim, Su-Yeon [1 ,3 ,4 ]
Song, Hyeon-A [1 ,2 ]
Kim, Hyeyun [1 ,2 ]
Chung, Kyung-Sook [1 ]
Lee, Jong Kil [2 ,3 ,4 ]
Lee, Kyung-Tae [1 ,2 ,3 ,4 ,5 ]
机构
[1] Kyung Hee Univ, Coll Pharm, Dept Pharmaceut Biochem, Seoul 02447, South Korea
[2] Kyung Hee Univ, Grad Sch, Dept Fundamental Pharmaceut Sci, Seoul 02447, South Korea
[3] Kyung Hee Univ, Grad Sch, Dept Life & Nanopharmaceut Sci, Seoul 02447, South Korea
[4] Kyung Hee Univ, Coll Pharm, Neurobiota Res Ctr, Seoul 02447, South Korea
[5] Kyung Hee Univ, Coll Pharm, Dept Pharmaceut Biochem, 26 Kyungheedae to, Seoul 02447, South Korea
基金
新加坡国家研究基金会;
关键词
Hydrangenol; Sepsis; Immune cells; Inflammation; Tight junction; Gut microbiota; SEPSIS; CELLS; DEFINITIONS; DISRUPTION; EXPRESSION; BERBERINE; PATHWAY; SERRATA; LEAVES; RAT;
D O I
10.1016/j.intimp.2023.111083
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Hydrangenol, a dihydroisocoumarin, isolated from the leaves of Hydrangea serrata, possesses anti-inflammatory, anti-obesity, and anti-photoaging activities. In this study, we investigated the protective effects of hydrangenol (HG) against lipopolysaccharide (LPS)-induced endotoxemia and elucidated the underlying molecular mechanisms of action in C57BL/6 mice. Oral administration of HG (20 or 40 mg/kg) significantly restored the survival rate and population of macrophages, T helper cells (CD3+/CD4+), and Th17 cells (CD3+/CD4+/CCR6+) in the spleens of mice with LPS-induced endotoxemia. HG suppressed the expression of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-1 beta, and Interferon (IFN)-gamma and the mRNA and protein expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in the intestine and lung of LPStreated mice. Molecular data showed that HG ameliorated the activation of nuclear factor kappa B (NF-KB) p65, signal transducers and activators of transcription 3 (STAT3), and c-Fos and c-Jun (AP-1 subunits) via the myeloid differentiation primary response 88 (MyD88) dependent toll-like receptor 4 (TLR4) signaling pathway in the LPS-treated mouse intestines. HG treatment caused the recovery of LPS-induced impaired tight junction (occludin and claudin-2) protein and mRNA expressions. Furthermore, HG improved LPS-induced gut dysbiosis in mice. Taken together, our results suggest that HG protects against LPS-induced endotoxemia by restoring immune cells and the capacity of the intestinal barrier, reducing intestinal inflammation, and improving the composition of the gut microbiota.
引用
收藏
页数:9
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