JOURNAL BROWSE
Search
Advanced SearchSearch Tips
Dose-dependent Effects of Dietary Folate on Aortic Relaxation and Hepatic C-reactive protein Levels in C57BL/6 Mice
facebook(new window)  Pirnt(new window) E-mail(new window) Excel Download
  • Journal title : Journal of Life Science
  • Volume 25, Issue 8,  2015, pp.889-895
  • Publisher : Korean Society of Life Science
  • DOI : 10.5352/JLS.2015.25.8.889
 Title & Authors
Dose-dependent Effects of Dietary Folate on Aortic Relaxation and Hepatic C-reactive protein Levels in C57BL/6 Mice
Kong, Eunhee; Hasan, Syeda T.; Jang, Hyeran; Zimmerly, Ella M.; Choi, Sang-Woon; Meydani, Mohsen;
  PDF(new window)
 Abstract
Endothelial dysfunction is an initial step in atherosclerosis. B vitamins (B6, B12, and folate) are important contributing factors to vascular homeostasis. Deficiencies in these B vitamins induce cardiovascular diseases by altering vascular homeostasis. Folate plays important roles in nitric oxide homeostasis in the endothelium. To determine the dose-dependent effect of dietary folate on atherosclerosis, we studied aortic relaxation and hepatic C-reactive protein (CRP) levels in C57BL/6 mice. In this study, a total of 54 male C57BL/6, 8-wk old mice were split into 2 dietary groups (control and Western style diet). Each diet group was divided into 3 subgroups according to dietary folate dosage (0.2, 2, and 8 mg/kg). After 18 months, the relaxation response seen in aortic rings from mice fed 0.2 or 2 mg folate/kg in both diet groups. However, the aortic relaxation response was not seen and no differences were observed in mice fed 8mg folate/kg in either diet group (p<0.05). Hepatic CRP levels at all folate dosages (0.2, 2, 8 mg folate/kg) were higher in the groups fed a Western style diet than in mice fed a control diet (p=0.035). CRP levels were lower in mice fed 0.2 mg folate/kg than in mice fed 2 or 8 mg folate/kg in both diet groups (p<0.05). These results indicate that in C57BL/6 mice 0.2 mg folate/kg may be enough to prevent atherosclerosis by inducing the relaxation responses of the aorta and by reducing levels of hepatic CRP, regardless of dietary style.
 Keywords
C-reactive protein;folate;relaxation;
 Language
English
 Cited by
 References
1.
Brandes, R. P., Schmitz-Winnenthal, F. H., Feletou, M., Godecke, A., Huang, P. L., Vanhoutte, P. M., Fleming, I. and Busse, R. 2000. An endothelium-derived hyperpolarizing factor distinct from NO and prostacyclin is a major endothelium-dependent vasodilator in resistance vessels of wild-type and endothelial NO synthase knockout mice. Proc. Natl. Acad. Sci. USA 97, 9747-9752. crossref(new window)

2.
Breve, J. J., Drukarch, B., van Strien, M. and van Dam, A. M. 2008. Validated sandwich ELISA for the quantification of tissue transglutaminase in tissue homogenates and cell lysates of multiple species. J. Immunol. Methods 332, 142-150. crossref(new window)

3.
Calabro, P., Willerson, J. T. and Yeh, E. T. 2003. Inflammatory cytokines stimulated C-reactive protein production by human coronary artery smooth muscle cells. Circulation 108, 1930-1932. crossref(new window)

4.
Choi, M. S., Jang, Y. Y., Lee, W. S., Song, J. H. and Shin, Y. K. 2003. Dietary ascorbate supplementation reduces oxidative tissue damage and expression of iNOS in the kidney of streptozotocin induced diabetic rats. Kor. J. Physiol. Pharmacol. 7, 39-45.

5.
Edith-Rodriguez, J., Resendiz-Albor, A. A., ArciniegaMartinez, I. M., Campos-Rodriguez, R., Hong, E., Huang, F. and Villafana, S. 2013. Effect of early diabetes on the expression of alpha-1 adrenergic receptors in aorta and carotidarteries of Wistar Kyoto and spontaneously hypertensive rats. Clin. Exp. Hypertens. 35, 389-395. crossref(new window)

6.
Feletou, M., Kohler, R. and Vanhoutte, P. M. 2012. Nitric oxide: orchestrator of endothelium-dependent responses. Ann. Med. 44, 694-716. crossref(new window)

7.
Fletcher, R. H. and Fairfield, K. M. 2002. Vitamins for chronic disease prevention in adults: clinical applications. JAMA 287, 3127-3129. crossref(new window)

8.
Gentile, M., Panico, S., Rubba, F., Mattiello, A., Chiodini, P., Jossa, F., Marotta, G., Pauciullo, P. and Rubba, P. 2010. Obesity, overweight, and weight gain over adult life are main determinants of elevated hs-CRP in a cohort of Mediterranean women. Eur. J. Clin. Nutr. 64, 873-878. crossref(new window)

9.
Hsu, T. C., Huang, C. Y., Chiang, S. Y., Lai, W. X., Tsai, C. H. and Tzang, B. S. 2008. Transglutaminase inhibitor cystamine alleviates the abnormality in liver from NZB/W F1 mice. Eur. J. Pharmacol. 579, 382-389. crossref(new window)

10.
Jialal, I., Verma, S. and Devaraj, S. 2009. Inhibition of endothelial nitric oxide synthase by C-reactive protein: clinical relevance. Clin Chem. 55, 206-208.

11.
Lentz, S. R., Piegors, D. J., Malinow, M. R. and Heistad, D. D. 2001. Supplementation of atherogenic diet with B vitamins does not prevent atherosclerosis or vascular dysfunction in monkeys. Circulation 103, 1006-1011. crossref(new window)

12.
Libby, P., Ridker, P. M. and Maseri, A. 2002. Inflammation and atherosclerosis. Circulation 105, 1135-1143. crossref(new window)

13.
Moens, A. L., Vrints, C. J., Claeys, M. J., Timmermans, J. P., Champion, H. C. and Kass, D. A. 2008. Mechanisms and potential therapeutic targets for folic acid in cardiovascular disease. Am. J. Physiol. Heart Circ. Physiol. 294, H1971-1977. crossref(new window)

14.
Rasouli, M. L., Nasir, K., Blumenthal, R. S., Park, R., Aziz, D. C. and Budoff, M. J. 2005. Plasma homocysteine predicts progression of atherosclerosis. Atherosclerosis 181, 159-165. crossref(new window)

15.
Singh, U., Devaraj, S., Vasquez-Vivar, J. and Jialal, I. 2007. C-reactive protein decreases endothelial nitric oxide synthase activity via uncoupling. J. Mol. Cell. Cardiol. 43, 780-791. crossref(new window)

16.
Stroes, E. S., van Faassen, E. E., Yo, M., Martasek, P., Boer, P., Govers, R. and Rabelink, T. J. 2000. Folic acid reverts dysfunction of endothelial nitric oxide synthase. Circ. Res. 86, 1129-1134. crossref(new window)

17.
Symons, J. D., Rutledge, J. C., Simonsen, U. and Pattathu, R. A. 2006. Vascular dysfunction produced by hyperhomocysteinemia is more severe in the presence of low folate. Am. J. Physiol. Heart Circ. Physiol. 290, H181-191.

18.
Symons, J. D., Zaid, U. B., Athanassious, C. N., Mullick, A. E., Lentz, S. R. and Rutledge, J. C. 2006. Influence of folate on arterial permeability and stiffness in the absence or presence of hyperhomocysteinemia. Arterioscler. Thromb. Vasc. Biol. 26, 814-818. crossref(new window)

19.
van Dijk, R. A., Rauwerda, J. A., Steyn, M., Twisk, J. W. and Stehouwer, C. D. 2001. Long-term homocysteine-lowering treatment with folic acid plus pyridoxine is associated with decreased blood pressure but not with improved brachial artery endothelium-dependent vasodilation or carotid artery stiffness: a 2-year, randomized, placebo-controlled trial. Arterioscler. Thromb. Vasc Biol. 21, 2072-2079. crossref(new window)

20.
Venugopal, S. K., Devaraj, S., Yuhanna, I., Shaul, P. and Jialal, I. 2002. Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells. Circulation 106, 1439-1441. crossref(new window)

21.
Wilmink, H. W., Stroes, E. S., Erkelens, W. D., Gerritsen, W. B., Wever, R., Banga, J. D. and Rabelink, T. J. 2000. Influence of folic acid on postprandial endothelial dysfunction. Arterioscler. Thromb. Vasc. Biol. 20, 185-188. crossref(new window)

22.
Zhu, Y., Bian, Z., Lu, P., Karas, R. H., Bao, L., Cox, D., Hodgin, J., Shaul, P. W., Thoren, P., Smithies, O., Gustafsson, J. A. and Mendelsohn, M. E. 2002. Abnormal vascular function and hypertension in mice deficient in estrogen receptor beta. Science 295, 505-508. crossref(new window)