Skip to main content
Erschienen in: Inflammation 2/2014

01.04.2014

Emodin-6-O-β-d--glucoside Inhibits High-Glucose-Induced Vascular Inflammation

verfasst von: Wonhwa Lee, Sae-Kwang Ku, Doohyun Lee, Taeho Lee, Jong-Sup Bae

Erschienen in: Inflammation | Ausgabe 2/2014

Einloggen, um Zugang zu erhalten

Abstract

Emodin-6-O-β-d-glucoside (EG), a new active compound from Reynoutria japonica, has recently been shown to exert potent anti-inflammatory and barrier protective effects in human umbilical vein endothelial cells (HUVECs) and in mice. Vascular inflammatory process has been suggested to play a key role in initiation and progression of atherosclerosis, a major complication of diabetes mellitus. Thus, we attempted to determine whether EG can suppress the vascular inflammatory process induced by high glucose (HG) in HUVECs and mice. Data showed that HG induced markedly increased vascular permeability, monocyte adhesion, expressions of CAMs, formation of ROS, and activation of NF-κB. Remarkably, all of the above-mentioned vascular inflammatory effects of HG were attenuated by pretreatment with EG. Vascular inflammatory responses induced by HG are critical events underlying development of various diabetic complications; therefore, our results suggest that EG may have significant therapeutic benefits against diabetic complications and atherosclerosis.
Anhänge
Nur mit Berechtigung zugänglich
Literatur
1.
Zurück zum Zitat Kannel, W.B., and D.L. McGee. 1979. Diabetes and cardiovascular disease. The Framingham study. JAMA 241: 2035–2038.PubMedCrossRef Kannel, W.B., and D.L. McGee. 1979. Diabetes and cardiovascular disease. The Framingham study. JAMA 241: 2035–2038.PubMedCrossRef
2.
Zurück zum Zitat Kannel, W.B., and D.L. McGee. 1979. Diabetes and glucose tolerance as risk factors for cardiovascular disease: the Framingham study. Diabetes Care 2: 120–126.PubMedCrossRef Kannel, W.B., and D.L. McGee. 1979. Diabetes and glucose tolerance as risk factors for cardiovascular disease: the Framingham study. Diabetes Care 2: 120–126.PubMedCrossRef
3.
Zurück zum Zitat Chistiakov, D.A. 2011. Diabetic retinopathy: pathogenic mechanisms and current treatments. Diabetes Metabolic Syndrome 5: 165–172.PubMedCrossRef Chistiakov, D.A. 2011. Diabetic retinopathy: pathogenic mechanisms and current treatments. Diabetes Metabolic Syndrome 5: 165–172.PubMedCrossRef
4.
Zurück zum Zitat Gerrity, R.G. 1981. The role of the monocyte in atherogenesis: I. Transition of blood-borne monocytes into foam cells in fatty lesions. American Journal of Pathology 103: 181–190.PubMedCentralPubMed Gerrity, R.G. 1981. The role of the monocyte in atherogenesis: I. Transition of blood-borne monocytes into foam cells in fatty lesions. American Journal of Pathology 103: 181–190.PubMedCentralPubMed
5.
Zurück zum Zitat Wardle, E.N. 1994. Vascular permeability in diabetics and implications for therapy. Diabetes Research and Clinical Practice 23: 135–139.PubMedCrossRef Wardle, E.N. 1994. Vascular permeability in diabetics and implications for therapy. Diabetes Research and Clinical Practice 23: 135–139.PubMedCrossRef
6.
Zurück zum Zitat Esposito, C., G. Fasoli, A.R. Plati, et al. 2001. Long-term exposure to high glucose up-regulates VCAM-induced endothelial cell adhesiveness to PBMC. Kidney International 59: 1842–1849.PubMedCrossRef Esposito, C., G. Fasoli, A.R. Plati, et al. 2001. Long-term exposure to high glucose up-regulates VCAM-induced endothelial cell adhesiveness to PBMC. Kidney International 59: 1842–1849.PubMedCrossRef
7.
Zurück zum Zitat Hamuro, M., J. Polan, M. Natarajan, and S. Mohan. 2002. High glucose induced nuclear factor kappa B mediated inhibition of endothelial cell migration. Atherosclerosis 162: 277–287.PubMedCrossRef Hamuro, M., J. Polan, M. Natarajan, and S. Mohan. 2002. High glucose induced nuclear factor kappa B mediated inhibition of endothelial cell migration. Atherosclerosis 162: 277–287.PubMedCrossRef
8.
Zurück zum Zitat Morigi, M., S. Angioletti, B. Imberti, et al. 1998. Leukocyte–endothelial interaction is augmented by high glucose concentrations and hyperglycemia in a NF-κB-dependent fashion. Journal of Clinical Investigation 101: 1905–1915.PubMedCentralPubMedCrossRef Morigi, M., S. Angioletti, B. Imberti, et al. 1998. Leukocyte–endothelial interaction is augmented by high glucose concentrations and hyperglycemia in a NF-κB-dependent fashion. Journal of Clinical Investigation 101: 1905–1915.PubMedCentralPubMedCrossRef
9.
Zurück zum Zitat Tooke, J.E. 1995. Microvascular function in human diabetes. A physiological perspective. Diabetes 44: 721–726.PubMedCrossRef Tooke, J.E. 1995. Microvascular function in human diabetes. A physiological perspective. Diabetes 44: 721–726.PubMedCrossRef
10.
Zurück zum Zitat Nannipieri, M., L. Rizzo, A. Rapuano, A. Pilo, G. Penno, and R. Navalesi. 1995. Increased transcapillary escape rate of albumin in microalbuminuric type II diabetic patients. Diabetes Care 18: 1–9.PubMedCrossRef Nannipieri, M., L. Rizzo, A. Rapuano, A. Pilo, G. Penno, and R. Navalesi. 1995. Increased transcapillary escape rate of albumin in microalbuminuric type II diabetic patients. Diabetes Care 18: 1–9.PubMedCrossRef
11.
Zurück zum Zitat Lopes-Virella, M.F., and G. Virella. 1992. Immune mechanisms of atherosclerosis in diabetes mellitus. Diabetes 41(Suppl 2): 86–91.PubMedCrossRef Lopes-Virella, M.F., and G. Virella. 1992. Immune mechanisms of atherosclerosis in diabetes mellitus. Diabetes 41(Suppl 2): 86–91.PubMedCrossRef
12.
Zurück zum Zitat Bae, J.S. 2012. Role of high mobility group box 1 in inflammatory disease: focus on sepsis. Archives of Pharmacal Research 35: 1511–1523.PubMedCrossRef Bae, J.S. 2012. Role of high mobility group box 1 in inflammatory disease: focus on sepsis. Archives of Pharmacal Research 35: 1511–1523.PubMedCrossRef
13.
Zurück zum Zitat Kado, S., T. Wakatsuki, M. Yamamoto, and N. Nagata. 2001. Expression of intercellular adhesion molecule-1 induced by high glucose concentrations in human aortic endothelial cells. Life Sciences 68: 727–737.PubMedCrossRef Kado, S., T. Wakatsuki, M. Yamamoto, and N. Nagata. 2001. Expression of intercellular adhesion molecule-1 induced by high glucose concentrations in human aortic endothelial cells. Life Sciences 68: 727–737.PubMedCrossRef
14.
Zurück zum Zitat Aggarwal, B.B., H. Ichikawa, P. Garodia, et al. 2006. From traditional Ayurvedic medicine to modern medicine: identification of therapeutic targets for suppression of inflammation and cancer. Expert Opinion on Therapeutic Targets 10: 87–118.PubMedCrossRef Aggarwal, B.B., H. Ichikawa, P. Garodia, et al. 2006. From traditional Ayurvedic medicine to modern medicine: identification of therapeutic targets for suppression of inflammation and cancer. Expert Opinion on Therapeutic Targets 10: 87–118.PubMedCrossRef
15.
Zurück zum Zitat Lee, W., S.K. Ku, T.H. Kim, and J.S. Bae. 2013. Emodin-6-O-beta-d-glucoside inhibits HMGB1-induced inflammatory responses in vitro and in vivo. Food and Chemical Toxicology 52: 97–104.PubMedCrossRef Lee, W., S.K. Ku, T.H. Kim, and J.S. Bae. 2013. Emodin-6-O-beta-d-glucoside inhibits HMGB1-induced inflammatory responses in vitro and in vivo. Food and Chemical Toxicology 52: 97–104.PubMedCrossRef
16.
Zurück zum Zitat Qureshi, S.H., C. Manithody, J.S. Bae, L. Yang, and A.R. Rezaie. 2008. Autolysis loop restricts the specificity of activated protein C: analysis by FRET and functional assays. Biophysical Chemistry 134: 239–245.PubMedCentralPubMedCrossRef Qureshi, S.H., C. Manithody, J.S. Bae, L. Yang, and A.R. Rezaie. 2008. Autolysis loop restricts the specificity of activated protein C: analysis by FRET and functional assays. Biophysical Chemistry 134: 239–245.PubMedCentralPubMedCrossRef
17.
Zurück zum Zitat Kim, T.H., and J.S. Bae. 2010. Ecklonia cava extracts inhibit lipopolysaccharide induced inflammatory responses in human endothelial cells. Food and Chemical Toxicology 48: 1682–1687.PubMedCrossRef Kim, T.H., and J.S. Bae. 2010. Ecklonia cava extracts inhibit lipopolysaccharide induced inflammatory responses in human endothelial cells. Food and Chemical Toxicology 48: 1682–1687.PubMedCrossRef
18.
Zurück zum Zitat Bae, J.S., W. Lee, and A.R. Rezaie. 2012. Polyphosphate elicits proinflammatory responses that are counteracted by activated protein C in both cellular and animal models. Journal of Thrombosis and Haemostasis. Bae, J.S., W. Lee, and A.R. Rezaie. 2012. Polyphosphate elicits proinflammatory responses that are counteracted by activated protein C in both cellular and animal models. Journal of Thrombosis and Haemostasis.
19.
Zurück zum Zitat Lee, J.D., J.E. Huh, G. Jeon, et al. 2009. Flavonol-rich RVHxR from Rhus verniciflua stokes and its major compound fisetin inhibits inflammation-related cytokines and angiogenic factor in rheumatoid arthritic fibroblast-like synovial cells and in vivo models. International Immunopharmacology 9: 268–276.PubMedCrossRef Lee, J.D., J.E. Huh, G. Jeon, et al. 2009. Flavonol-rich RVHxR from Rhus verniciflua stokes and its major compound fisetin inhibits inflammation-related cytokines and angiogenic factor in rheumatoid arthritic fibroblast-like synovial cells and in vivo models. International Immunopharmacology 9: 268–276.PubMedCrossRef
20.
Zurück zum Zitat Akeson, A.L., and C.W. Woods. 1993. A fluorometric assay for the quantitation of cell adherence to endothelial cells. Journal of Immunological Methods 163: 181–185.PubMedCrossRef Akeson, A.L., and C.W. Woods. 1993. A fluorometric assay for the quantitation of cell adherence to endothelial cells. Journal of Immunological Methods 163: 181–185.PubMedCrossRef
21.
Zurück zum Zitat Kim, I., S.O. Moon, S.H. Kim, H.J. Kim, Y.S. Koh, and G.Y. Koh. 2001. Vascular endothelial growth factor expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin through nuclear factor-kappa B activation in endothelial cells. Journal of Biological Chemistry 276: 7614–7620.PubMedCrossRef Kim, I., S.O. Moon, S.H. Kim, H.J. Kim, Y.S. Koh, and G.Y. Koh. 2001. Vascular endothelial growth factor expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin through nuclear factor-kappa B activation in endothelial cells. Journal of Biological Chemistry 276: 7614–7620.PubMedCrossRef
22.
Zurück zum Zitat Mackman, N., K. Brand, and T.S. Edgington. 1991. Lipopolysaccharide-mediated transcriptional activation of the human tissue factor gene in THP-1 monocytic cells requires both activator protein 1 and nuclear factor kappa B binding sites. Journal of Experimental Medicine 174: 1517–1526.PubMedCrossRef Mackman, N., K. Brand, and T.S. Edgington. 1991. Lipopolysaccharide-mediated transcriptional activation of the human tissue factor gene in THP-1 monocytic cells requires both activator protein 1 and nuclear factor kappa B binding sites. Journal of Experimental Medicine 174: 1517–1526.PubMedCrossRef
23.
Zurück zum Zitat Laakso, M. 1999. Hyperglycemia and cardiovascular disease in type 2 diabetes. Diabetes 48: 937–942.PubMedCrossRef Laakso, M. 1999. Hyperglycemia and cardiovascular disease in type 2 diabetes. Diabetes 48: 937–942.PubMedCrossRef
24.
Zurück zum Zitat Sander, B., M. Larsen, C. Engler, H. Lund-Andersen, and H.H. Parving. 1994. Early changes in diabetic retinopathy: capillary loss and blood–retina barrier permeability in relation to metabolic control. Acta Ophthalmologica 72: 553–559.PubMedCrossRef Sander, B., M. Larsen, C. Engler, H. Lund-Andersen, and H.H. Parving. 1994. Early changes in diabetic retinopathy: capillary loss and blood–retina barrier permeability in relation to metabolic control. Acta Ophthalmologica 72: 553–559.PubMedCrossRef
25.
Zurück zum Zitat Hansson, G.K., and P. Libby. 2006. The immune response in atherosclerosis: a double-edged sword. Nature Reviews Immunology 6: 508–519.PubMedCrossRef Hansson, G.K., and P. Libby. 2006. The immune response in atherosclerosis: a double-edged sword. Nature Reviews Immunology 6: 508–519.PubMedCrossRef
26.
Zurück zum Zitat Boisvert, W.A. 2004. Modulation of atherogenesis by chemokines. Trends in Cardiovascular Medicine 14: 161–165.PubMedCrossRef Boisvert, W.A. 2004. Modulation of atherogenesis by chemokines. Trends in Cardiovascular Medicine 14: 161–165.PubMedCrossRef
27.
Zurück zum Zitat Inoguchi, T., P. Li, F. Umeda, et al. 2000. High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C-dependent activation of NAD(P)H oxidase in cultured vascular cells. Diabetes 49: 1939–1945.PubMedCrossRef Inoguchi, T., P. Li, F. Umeda, et al. 2000. High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C-dependent activation of NAD(P)H oxidase in cultured vascular cells. Diabetes 49: 1939–1945.PubMedCrossRef
28.
Zurück zum Zitat Dunlop, M. 2000. Aldose reductase and the role of the polyol pathway in diabetic nephropathy. Kidney International. Supplement 77: S3–S12.PubMedCrossRef Dunlop, M. 2000. Aldose reductase and the role of the polyol pathway in diabetic nephropathy. Kidney International. Supplement 77: S3–S12.PubMedCrossRef
29.
Zurück zum Zitat Han, H.J., Y.J. Lee, S.H. Park, J.H. Lee, and M. Taub. 2005. High glucose-induced oxidative stress inhibits Na+/glucose cotransporter activity in renal proximal tubule cells. American Journal of Physiology. Renal Physiology 288: F988–F996.PubMedCrossRef Han, H.J., Y.J. Lee, S.H. Park, J.H. Lee, and M. Taub. 2005. High glucose-induced oxidative stress inhibits Na+/glucose cotransporter activity in renal proximal tubule cells. American Journal of Physiology. Renal Physiology 288: F988–F996.PubMedCrossRef
30.
Zurück zum Zitat Rimbach, G., G. Valacchi, R. Canali, and F. Virgili. 2000. Macrophages stimulated with IFN-gamma activate NF-kappa B and induce MCP-1 gene expression in primary human endothelial cells. Molecular Cell Biology Research Communications 3: 238–242.PubMedCrossRef Rimbach, G., G. Valacchi, R. Canali, and F. Virgili. 2000. Macrophages stimulated with IFN-gamma activate NF-kappa B and induce MCP-1 gene expression in primary human endothelial cells. Molecular Cell Biology Research Communications 3: 238–242.PubMedCrossRef
31.
Zurück zum Zitat Uemura, S., H. Matsushita, W. Li, et al. 2001. Diabetes mellitus enhances vascular matrix metalloproteinase activity: role of oxidative stress. Circulation Research 88: 1291–1298.PubMedCrossRef Uemura, S., H. Matsushita, W. Li, et al. 2001. Diabetes mellitus enhances vascular matrix metalloproteinase activity: role of oxidative stress. Circulation Research 88: 1291–1298.PubMedCrossRef
Metadaten
Titel
Emodin-6-O-β-d--glucoside Inhibits High-Glucose-Induced Vascular Inflammation
verfasst von
Wonhwa Lee
Sae-Kwang Ku
Doohyun Lee
Taeho Lee
Jong-Sup Bae
Publikationsdatum
01.04.2014
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 2/2014
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-013-9741-9

Weitere Artikel der Ausgabe 2/2014

Inflammation 2/2014 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.