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Rosuvastatin suppresses the inflammatory responses through inhibition of c-Jun N-terminal kinase and Nuclear Factor-kappaB in endothelial cells.
J Cardiovasc Pharmacol. 2007 Jun; 49(6):376-83.JC

Abstract

BACKGROUND

Rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, has pleiotropic effects that are anti-inflammatory and antiatherothrombotic. It is important to understand the cardioprotective effects of rosuvastatin in order to optimize its additional advantages in the treatment and prevention of cardiovascular diseases.

METHODS

Human umbilical vein endothelial cells (HUVEC) were treated with tumor necrosis factor (TNF)-alpha (10 ng/mL) alone or with rosuvastatin (100 microM). The extent of inflammation was determined by U937 adhesion assay as well as analysis of the expression of intercellular adhesion molecule (ICAM)-1, monocyte chemoattractant protein (MCP)-1, interleukin (IL)-8, IL-6, cyclooxygenase (COX)-2, c-Jun N-terminal kinase (JNK), extracellular signal-regulated protein kinase (ERK), p38, and signal transducer and activator of transcription (STAT)-3. The activation of nuclear factor kappa B (NF-kappaB) was determined by Western blot.

RESULTS

Rosuvastatin decreased the extent of U937 adhesion to TNF-alpha-stimulated HUVEC. Rosuvastatin inhibited the expressions of ICAM-1, MCP-1, IL-8, IL-6, and COX-2 mRNA and protein levels. The activation of JNK and NF-kappaB was also blocked by rosuvastatin. The inhibitors of JNK, NF-kappaB, and STAT-3 produced a statistically significant decrease of the TNF-alpha induced U937 adhesion and IL-6 protein release.

CONCLUSIONS

This study suggests that the anti-inflammatory activity of rosuvastatin is accompanied by the inhibition of JNK and NF-kappaB.

Authors+Show Affiliations

The Heart Center of Chonnam National University Hospital, Gwangju, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

17577102

Citation

Kim, Yong Sook, et al. "Rosuvastatin Suppresses the Inflammatory Responses Through Inhibition of c-Jun N-terminal Kinase and Nuclear Factor-kappaB in Endothelial Cells." Journal of Cardiovascular Pharmacology, vol. 49, no. 6, 2007, pp. 376-83.
Kim YS, Ahn Y, Hong MH, et al. Rosuvastatin suppresses the inflammatory responses through inhibition of c-Jun N-terminal kinase and Nuclear Factor-kappaB in endothelial cells. J Cardiovasc Pharmacol. 2007;49(6):376-83.
Kim, Y. S., Ahn, Y., Hong, M. H., Kim, K. H., Park, H. W., Hong, Y. J., Kim, J. H., Kim, W., Jeong, M. H., Cho, J. G., Park, J. C., & Kang, J. C. (2007). Rosuvastatin suppresses the inflammatory responses through inhibition of c-Jun N-terminal kinase and Nuclear Factor-kappaB in endothelial cells. Journal of Cardiovascular Pharmacology, 49(6), 376-83.
Kim YS, et al. Rosuvastatin Suppresses the Inflammatory Responses Through Inhibition of c-Jun N-terminal Kinase and Nuclear Factor-kappaB in Endothelial Cells. J Cardiovasc Pharmacol. 2007;49(6):376-83. PubMed PMID: 17577102.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rosuvastatin suppresses the inflammatory responses through inhibition of c-Jun N-terminal kinase and Nuclear Factor-kappaB in endothelial cells. AU - Kim,Yong Sook, AU - Ahn,Youngkeun, AU - Hong,Moon Hwa, AU - Kim,Kye Hun, AU - Park,Hyung Wook, AU - Hong,Young Joon, AU - Kim,Ju Han, AU - Kim,Weon, AU - Jeong,Myung Ho, AU - Cho,Jeong Gwan, AU - Park,Jong Chun, AU - Kang,Jung Chaee, PY - 2007/6/20/pubmed PY - 2007/7/21/medline PY - 2007/6/20/entrez SP - 376 EP - 83 JF - Journal of cardiovascular pharmacology JO - J Cardiovasc Pharmacol VL - 49 IS - 6 N2 - BACKGROUND: Rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, has pleiotropic effects that are anti-inflammatory and antiatherothrombotic. It is important to understand the cardioprotective effects of rosuvastatin in order to optimize its additional advantages in the treatment and prevention of cardiovascular diseases. METHODS: Human umbilical vein endothelial cells (HUVEC) were treated with tumor necrosis factor (TNF)-alpha (10 ng/mL) alone or with rosuvastatin (100 microM). The extent of inflammation was determined by U937 adhesion assay as well as analysis of the expression of intercellular adhesion molecule (ICAM)-1, monocyte chemoattractant protein (MCP)-1, interleukin (IL)-8, IL-6, cyclooxygenase (COX)-2, c-Jun N-terminal kinase (JNK), extracellular signal-regulated protein kinase (ERK), p38, and signal transducer and activator of transcription (STAT)-3. The activation of nuclear factor kappa B (NF-kappaB) was determined by Western blot. RESULTS: Rosuvastatin decreased the extent of U937 adhesion to TNF-alpha-stimulated HUVEC. Rosuvastatin inhibited the expressions of ICAM-1, MCP-1, IL-8, IL-6, and COX-2 mRNA and protein levels. The activation of JNK and NF-kappaB was also blocked by rosuvastatin. The inhibitors of JNK, NF-kappaB, and STAT-3 produced a statistically significant decrease of the TNF-alpha induced U937 adhesion and IL-6 protein release. CONCLUSIONS: This study suggests that the anti-inflammatory activity of rosuvastatin is accompanied by the inhibition of JNK and NF-kappaB. SN - 0160-2446 UR - https://www.unboundmedicine.com/medline/citation/17577102/Rosuvastatin_suppresses_the_inflammatory_responses_through_inhibition_of_c_Jun_N_terminal_kinase_and_Nuclear_Factor_kappaB_in_endothelial_cells_ L2 - https://doi.org/10.1097/FJC.0b013e31804a5e34 DB - PRIME DP - Unbound Medicine ER -