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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2016.1
- 수록면
- 321 - 327 (7page)
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Purpose: Increased lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and Rho kinase activity may be associated with atherosclerosis. The principal aim of this study was to examine whether darapladib (a selective Lp-PLA2 inhibitor) could reduce the elevated Lp-PLA2 and Rho kinase activity in atherosclerosis.
Materials and Methods: Studies were performed in male Sprague-Dawley rats. The atherosclerosis rats were prepared by feeding them with a high-cholesterol diet for 10 weeks. Low-dose darapladib (25 mg·kg-1·d-1) and high-dose darapladib (50 mg·kg-1·d-1) interventions were then administered over the course of 2 weeks.
Results: The serum levels of triglycerides, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoproteincholesterol (HDL-C), high-sensitivity C-reactive protein (hs-CRP), and Lp-PLA2, significantly increased in atherosclerosis model groups, as did Rho kinase activity and cardiomyocyte apoptosis (p<0.05 vs. sham group), whereas nitric oxide (NO) productionwas reduced. Levels of TC, LDL-C, CRP, Lp-PLA2, and Rho kinase activity were respectively reduced in darapladib groups, whereas NO production was enhanced. When compared to the low-dose darapladib group, the reduction of the levels of TC, LDL-C, CRP, and Lp-PLA2 was more prominent in the high-dose darapladib group (p<0.05), and the increase of NO productionwas more prominent (p<0.05). Cardiomyocyte apoptosis of the high-dose darapladib group was also significantly reduced compared to the low-dose darapladib group (p<0.05). However, there was no significant difference in Rho kinase activity between the low-dose darapladib group and the high-dose darapladib group (p>0.05).
Conclusion: Darapladib, a Lp-PLA2 inhibitor, leads to cardiovascular protection that might be mediated by its inhibition of both Rho kinase and Lp-PLA2 in atherosclerosis.
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참고문헌 (32)
참고문헌 신청
Murray CJ / 1997 / Alternative projections of mortality and disability by cause 1990-2020: Global Burden of Disease Study / Lancet 349:1498~1504
Ocaranza MP / 2011 / Rho kinase inhibition activates the homologous angiotensinconverting enzyme-angiotensin-(1-9) axis in experimental hypertension / J Hypertens 29:706~715
Soga J / 2011 / Rho-associated kinase activity, endothelial function, and cardiovascular risk factors / Arterioscler Thromb Vasc Biol 31:2353~2359
Ocaranza MP / 2011 / Markedly increased Rho-kinase activity in circulating leukocytes in patients with chronic heart failure / Am Heart J 161:931~937
Zhang J / 2010 / ERK-MAPK signaling opposes rho-kinase to reduce cardiomyocyte apoptosis in heart ischemic preconditioning / Mol Med 16:307~315
Ocaranza MP / 2011 / Rho kinase inhibition activates the homologous angiotensinconverting enzyme-angiotensin-(1-9) axis in experimental hypertension / J Hypertens 29:706~715
Soga J / 2011 / Rho-associated kinase activity, endothelial function, and cardiovascular risk factors / Arterioscler Thromb Vasc Biol 31:2353~2359
Ocaranza MP / 2011 / Markedly increased Rho-kinase activity in circulating leukocytes in patients with chronic heart failure / Am Heart J 161:931~937
Zhang J / 2010 / ERK-MAPK signaling opposes rho-kinase to reduce cardiomyocyte apoptosis in heart ischemic preconditioning / Mol Med 16:307~315
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