n-butanol extract from Folium isatidis inhibits the lipopolysaccharide-induced downregulation of CXCR1 and CXCR2 on human neutrophils

Wu,Beibei; Wang,Liyin; Jiang,Lili; Dong,Lili; Xu,Fengli; Lu,Yili; Jin,Jiahui; Wang,Zhanyue; Liang,Guang; Shan,Xiaoou

doi:10.3892/mmr.2017.7870

n-butanol extract from Folium isatidis inhibits the lipopolysaccharide-induced downregulation of CXCR1 and CXCR2 on human neutrophils

Authors:
- Beibei Wu
- Liyin Wang
- Lili Jiang
- Lili Dong
- Fengli Xu
- Yili Lu
- Jiahui Jin
- Zhanyue Wang
- Guang Liang
- Xiaoou Shan
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Affiliations: Department of Pediatrics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, P.R. China, College of Basic Medical Sciences, Capital Medical University, Beijing 100050, P.R. China, Chemical Biology Research Center, School of Pharmacy, Wenzhou Medical University, Wenzhou, Zhejiang 325035, P.R. China
Published online on: October 25, 2017 https://doi.org/10.3892/mmr.2017.7870
Pages: 179-185
Copyright: © Wu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Neutrophils, immune cells crucial for protecting against invading pathogens, are important in sepsis. Neutrophil migration is regulated by chemokine receptors and their cognate ligands. Our previous study investigated the effect of n‑butanol extract from Folium isatidis on lipopolysaccharide (LPS)‑induced septic shock. The present study stimulated neutrophils with LPS to explore the influence of LPS on cell. Neutrophils were then pretreated with n‑butanol extract from Folium isatidis followed by LPS to examine the effect of this extract on neutrophil chemotaxis. The results showed that LPS decreased the expression levels of CXC‑chemokine receptor (CXCR)1, CXCR2 and L‑selectin (CD62L), and increased the expression of interleukin‑8 (IL‑8) by neutrophils. The addition of n‑butanol extract from Folium isatidis inhibited this LPS‑induced downregulation of CXCR1, CXCR2 and CD62L, and decreased the expression of IL‑8 on neutrophils. In addition, n‑butanol extract promoted myeloperoxidase activity in neutrophils. Taken together, LPS downregulated the expression of chemokine receptors, leading to the failure of neutrophils to migrate to sites of infection. The addition of n‑butanol extract, which promoted the ability of neutrophils to migrate, is a natural product and potential therapeutic agent with which to target neutrophil chemotaxis during LPS stimulation.

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