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Chitosan oligosaccharides inhibit the expression of interleukin-6 in lipopolysaccharide-induced human umbilical vein endothelial cells through p38 and ERK1/2 protein kinases.
Basic Clin Pharmacol Toxicol. 2010 May; 106(5):362-71.BC

Abstract

Chitosan oligosaccharides (COS) have been reported to exert anti-fungal activities, antitumour activities and immuno-enhancing effects. However, the potential roles of COS in the treatment of vascular inflammations remain unknown. In the present study, we examined the effects of COS on interleukin-6 (IL-6) production in human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS). Induction of HUVECs with LPS (100 ng/ml) increased the mRNA expression and protein secretion of IL-6 (versus the vehicle-treated group, p < 0.01), which were significantly reverted by the pre-treatment with COS (50-200 microg/ml) for 24 hr before LPS exposure (versus the LPS-treated group, p < 0.05 or 0.01). Signal transduction studies showed that the pre-treatment of HUVECs with COS (50-200 microg/ml) for 24 hr markedly inhibited the LPS-induced over-expression of phosphorylated p38 mitogen-activated protein kinase (MAPK), phosphorylated ERK1/2 and nuclear factor kappaB (NF-kappaB). Moreover, the LPS-induced NF-kappaB activation was suppressed by the specific ERK1/2 inhibitor PD98059 (30 microM) (versus the LPS-treated group, p < 0.01), but not by the specific p38 MAPK inhibitor SB203580 (25 microM). Additionally, both MAPK inhibitors markedly suppressed LPS-induced IL-6 mRNA expression in HUVECs (versus the LPS-treated group, p < 0.01). In conclusion, our results suggest that COS inhibit LPS-induced up-regulation of IL-6 in HUVECs, and this can be regulated by at least two parallel signalling pathways: one via p38 MAPK pathway independent of NF-kappaB activation and one via ERK1/2 pathway dependent on NF-kappaB activation.

Authors+Show Affiliations

Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19929981

Citation

Liu, Hong-Tao, et al. "Chitosan Oligosaccharides Inhibit the Expression of Interleukin-6 in Lipopolysaccharide-induced Human Umbilical Vein Endothelial Cells Through P38 and ERK1/2 Protein Kinases." Basic & Clinical Pharmacology & Toxicology, vol. 106, no. 5, 2010, pp. 362-71.
Liu HT, Li WM, Li XY, et al. Chitosan oligosaccharides inhibit the expression of interleukin-6 in lipopolysaccharide-induced human umbilical vein endothelial cells through p38 and ERK1/2 protein kinases. Basic Clin Pharmacol Toxicol. 2010;106(5):362-71.
Liu, H. T., Li, W. M., Li, X. Y., Xu, Q. S., Liu, Q. S., Bai, X. F., Yu, C., & Du, Y. G. (2010). Chitosan oligosaccharides inhibit the expression of interleukin-6 in lipopolysaccharide-induced human umbilical vein endothelial cells through p38 and ERK1/2 protein kinases. Basic & Clinical Pharmacology & Toxicology, 106(5), 362-71. https://doi.org/10.1111/j.1742-7843.2009.00493.x
Liu HT, et al. Chitosan Oligosaccharides Inhibit the Expression of Interleukin-6 in Lipopolysaccharide-induced Human Umbilical Vein Endothelial Cells Through P38 and ERK1/2 Protein Kinases. Basic Clin Pharmacol Toxicol. 2010;106(5):362-71. PubMed PMID: 19929981.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chitosan oligosaccharides inhibit the expression of interleukin-6 in lipopolysaccharide-induced human umbilical vein endothelial cells through p38 and ERK1/2 protein kinases. AU - Liu,Hong-Tao, AU - Li,Wen-Ming, AU - Li,Xiu-Ying, AU - Xu,Qing-Song, AU - Liu,Qi-Shun, AU - Bai,Xue-Fang, AU - Yu,Chao, AU - Du,Yu-Guang, Y1 - 2009/11/17/ PY - 2009/11/26/entrez PY - 2009/11/26/pubmed PY - 2010/12/14/medline SP - 362 EP - 71 JF - Basic & clinical pharmacology & toxicology JO - Basic Clin Pharmacol Toxicol VL - 106 IS - 5 N2 - Chitosan oligosaccharides (COS) have been reported to exert anti-fungal activities, antitumour activities and immuno-enhancing effects. However, the potential roles of COS in the treatment of vascular inflammations remain unknown. In the present study, we examined the effects of COS on interleukin-6 (IL-6) production in human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS). Induction of HUVECs with LPS (100 ng/ml) increased the mRNA expression and protein secretion of IL-6 (versus the vehicle-treated group, p < 0.01), which were significantly reverted by the pre-treatment with COS (50-200 microg/ml) for 24 hr before LPS exposure (versus the LPS-treated group, p < 0.05 or 0.01). Signal transduction studies showed that the pre-treatment of HUVECs with COS (50-200 microg/ml) for 24 hr markedly inhibited the LPS-induced over-expression of phosphorylated p38 mitogen-activated protein kinase (MAPK), phosphorylated ERK1/2 and nuclear factor kappaB (NF-kappaB). Moreover, the LPS-induced NF-kappaB activation was suppressed by the specific ERK1/2 inhibitor PD98059 (30 microM) (versus the LPS-treated group, p < 0.01), but not by the specific p38 MAPK inhibitor SB203580 (25 microM). Additionally, both MAPK inhibitors markedly suppressed LPS-induced IL-6 mRNA expression in HUVECs (versus the LPS-treated group, p < 0.01). In conclusion, our results suggest that COS inhibit LPS-induced up-regulation of IL-6 in HUVECs, and this can be regulated by at least two parallel signalling pathways: one via p38 MAPK pathway independent of NF-kappaB activation and one via ERK1/2 pathway dependent on NF-kappaB activation. SN - 1742-7843 UR - https://www.unboundmedicine.com/medline/citation/19929981/Chitosan_oligosaccharides_inhibit_the_expression_of_interleukin_6_in_lipopolysaccharide_induced_human_umbilical_vein_endothelial_cells_through_p38_and_ERK1/2_protein_kinases_ L2 - https://doi.org/10.1111/j.1742-7843.2009.00493.x DB - PRIME DP - Unbound Medicine ER -