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A novel role of kukoamine B: Inhibition of the inflammatory response in the livers of lipopolysaccharide-induced septic mice via its unique property of combining with lipopolysaccharide.

Qin WT, Wang X, Shen WC, Sun BW - Exp Ther Med (2015)

Bottom Line: In addition, KB protected against liver injury, as confirmed by improved histology and decreased aminotransferase levels in the serum.Further experiments revealed that KB attenuated liver myeloperoxidase activity and reduced the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1.These effects were accompanied by decreases in the levels of tumor necrosis factor α and interleukin-1β in the liver tissue.

View Article: PubMed Central - PubMed

Affiliation: Department of Burns and Plastic Surgery, Affiliated Hospital, Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China.

ABSTRACT

Kukoamine B (KB), derived from the traditional Chinese herb cortex Lycii, exerts anti-inflammatory effects due to its potent affinity with lipopolysaccharide (LPS) and CpG DNA; however, little is known regarding whether the in vivo administration of KB can effectively inhibit inflammation in septic mice. The present study thus aimed to investigate the inhibitory effects of KB on the inflammatory response in the livers of LPS-induced septic mice. KB treatment in the LPS-induced septic mice significantly decreased the plasma level of LPS. In addition, KB protected against liver injury, as confirmed by improved histology and decreased aminotransferase levels in the serum. Further experiments revealed that KB attenuated liver myeloperoxidase activity and reduced the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. These effects were accompanied by decreases in the levels of tumor necrosis factor α and interleukin-1β in the liver tissue. In parallel, the activity of nuclear factor-κ-gene binding (NF-κB) in the livers of LPS-induced septic mice was markedly inhibited with KB treatment. In combination, these results demonstrate that KB inhibits inflammation in septic mice by reducing the concentrations of plasma LPS, decreasing leukocyte sequestration and interfering with NF-κB activation, and, therefore, suppressing the pro-adhesive phenotype of endothelial cells.

No MeSH data available.


Related in: MedlinePlus

Effect of KB on ICAM-1 and VCAM-1 expression in the livers of LPS-induced septic mice. Mice were challenged with LPS for 4 h and then treated with KB for 4 h. The expression of the cellular adhesion molecules ICAM-1 and VCAM-1 was determined by immunohistochemical stains 4 h after KB treatment. Following LPS stimulation, the expression of ICAM-1 and VCAM-1 in the liver tissue was significantly increased compared with that in the control; however, with the in vivo administration of KB, the expression of (A-C) ICAM-1 and (D-F) VCAM-1 decreased significantly. (A and D) control group; (B and E) LPS group; (C and F) LPS + KB group. (Magnification, ×400). KB, kukoamine B; LPS, lipopolysaccharide; ICAM-1, intercellular adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1.
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f6-etm-09-03-0725: Effect of KB on ICAM-1 and VCAM-1 expression in the livers of LPS-induced septic mice. Mice were challenged with LPS for 4 h and then treated with KB for 4 h. The expression of the cellular adhesion molecules ICAM-1 and VCAM-1 was determined by immunohistochemical stains 4 h after KB treatment. Following LPS stimulation, the expression of ICAM-1 and VCAM-1 in the liver tissue was significantly increased compared with that in the control; however, with the in vivo administration of KB, the expression of (A-C) ICAM-1 and (D-F) VCAM-1 decreased significantly. (A and D) control group; (B and E) LPS group; (C and F) LPS + KB group. (Magnification, ×400). KB, kukoamine B; LPS, lipopolysaccharide; ICAM-1, intercellular adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1.

Mentions: Following LPS stimulation, the expression of ICAM-1 and VCAM-1 in the liver tissue was significantly increased compared with that in the control. With the in vivo administration of KB, the expression of ICAM-1 and VCAM-1 significantly decreased (Fig. 6).


A novel role of kukoamine B: Inhibition of the inflammatory response in the livers of lipopolysaccharide-induced septic mice via its unique property of combining with lipopolysaccharide.

Qin WT, Wang X, Shen WC, Sun BW - Exp Ther Med (2015)

Effect of KB on ICAM-1 and VCAM-1 expression in the livers of LPS-induced septic mice. Mice were challenged with LPS for 4 h and then treated with KB for 4 h. The expression of the cellular adhesion molecules ICAM-1 and VCAM-1 was determined by immunohistochemical stains 4 h after KB treatment. Following LPS stimulation, the expression of ICAM-1 and VCAM-1 in the liver tissue was significantly increased compared with that in the control; however, with the in vivo administration of KB, the expression of (A-C) ICAM-1 and (D-F) VCAM-1 decreased significantly. (A and D) control group; (B and E) LPS group; (C and F) LPS + KB group. (Magnification, ×400). KB, kukoamine B; LPS, lipopolysaccharide; ICAM-1, intercellular adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4316986&req=5

f6-etm-09-03-0725: Effect of KB on ICAM-1 and VCAM-1 expression in the livers of LPS-induced septic mice. Mice were challenged with LPS for 4 h and then treated with KB for 4 h. The expression of the cellular adhesion molecules ICAM-1 and VCAM-1 was determined by immunohistochemical stains 4 h after KB treatment. Following LPS stimulation, the expression of ICAM-1 and VCAM-1 in the liver tissue was significantly increased compared with that in the control; however, with the in vivo administration of KB, the expression of (A-C) ICAM-1 and (D-F) VCAM-1 decreased significantly. (A and D) control group; (B and E) LPS group; (C and F) LPS + KB group. (Magnification, ×400). KB, kukoamine B; LPS, lipopolysaccharide; ICAM-1, intercellular adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1.
Mentions: Following LPS stimulation, the expression of ICAM-1 and VCAM-1 in the liver tissue was significantly increased compared with that in the control. With the in vivo administration of KB, the expression of ICAM-1 and VCAM-1 significantly decreased (Fig. 6).

Bottom Line: In addition, KB protected against liver injury, as confirmed by improved histology and decreased aminotransferase levels in the serum.Further experiments revealed that KB attenuated liver myeloperoxidase activity and reduced the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1.These effects were accompanied by decreases in the levels of tumor necrosis factor α and interleukin-1β in the liver tissue.

View Article: PubMed Central - PubMed

Affiliation: Department of Burns and Plastic Surgery, Affiliated Hospital, Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China.

ABSTRACT

Kukoamine B (KB), derived from the traditional Chinese herb cortex Lycii, exerts anti-inflammatory effects due to its potent affinity with lipopolysaccharide (LPS) and CpG DNA; however, little is known regarding whether the in vivo administration of KB can effectively inhibit inflammation in septic mice. The present study thus aimed to investigate the inhibitory effects of KB on the inflammatory response in the livers of LPS-induced septic mice. KB treatment in the LPS-induced septic mice significantly decreased the plasma level of LPS. In addition, KB protected against liver injury, as confirmed by improved histology and decreased aminotransferase levels in the serum. Further experiments revealed that KB attenuated liver myeloperoxidase activity and reduced the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. These effects were accompanied by decreases in the levels of tumor necrosis factor α and interleukin-1β in the liver tissue. In parallel, the activity of nuclear factor-κ-gene binding (NF-κB) in the livers of LPS-induced septic mice was markedly inhibited with KB treatment. In combination, these results demonstrate that KB inhibits inflammation in septic mice by reducing the concentrations of plasma LPS, decreasing leukocyte sequestration and interfering with NF-κB activation, and, therefore, suppressing the pro-adhesive phenotype of endothelial cells.

No MeSH data available.


Related in: MedlinePlus