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      Investigating the effect of Fenofibrate on biomarkers of vascular inflammation in L-NAME induced hypertensive rats

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      Journal: Pharmacia
      Publisher: Pensoft Publishers

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          Abstract

          This study aims to evaluate the impact of fenofibrate on the levels of (IL-6, hsCRP, Lp-PLA2, sCD40L, and cystatin C) in hypertensive rats. Twenty-four rats were divided into two groups each of twelve. The first group served as the normotensive group, while the second group was regarded as the hypertensive group. Each group was further divided into two subgroups (control and treated). The control subgroups only received a placebo and the treated subgroups were given fenofibrate 30 mg/kg daily orally by gastric gavage for 4 weeks. The level of hsCRP, IL6, and Lp-PLA2 significantly increased, but sCD40L and cystatin C levels were not changed in hypertensive rats. Fenofibrate has significantly reduced the levels of hsCRP and Lp-LPA2 in hypertensive rats while IL6 and sCD40s have not been changed in both groups. In conclusion, Fenofibrate has revealed a pleiotropic anti-inflammatory effect by reducing the level of hsCRP and Lp-LPA2 in hypertensive rats.

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          2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.

          Neil J Stone, Jennifer G Robinson, Alice H. Lichtenstein … (2014)
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            Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies.

            Nadeem Sarwar, John Danesh, Gudny Eiriksdottir … (2007)
            Many epidemiological studies have reported on associations between serum triglyceride concentrations and the risk of coronary heart disease, but this association has not been reliably quantified. In the present study, we report 2 separate nested case-control comparisons in 2 different prospective, population-based cohorts, plus an updated meta-analysis of 27 additional prospective studies in general Western populations. Measurements were made in a total of 3582 incident cases of fatal and nonfatal coronary heart disease and 6175 controls selected from among the 44,237 men and women screened in the Reykjavik and the European Prospective Investigation of Cancer (EPIC)-Norfolk studies. Repeat measurements were obtained an average of 4 years apart in 1933 participants in the EPIC-Norfolk Study and an average of 12 years apart in 379 participants in the Reykjavik study. The long-term stability of log-triglyceride values (within-person correlation coefficients of 0.64 [95% CI, 0.60 to 0.68] over 4 years and 0.63 [95% CI, 0.57 to 0.70] over 12 years) was similar to those of blood pressure and total serum cholesterol. After adjustment for baseline values of several established risk factors, the strength of the association was substantially attenuated, and the adjusted odds ratio for coronary heart disease was 1.76 (95% CI, 1.39 to 2.21) in the Reykjavik study and 1.57 (95% CI, 1.10 to 2.24) in the EPIC-Norfolk study in a comparison of individuals in the top third with those in the bottom third of usual log-triglyceride values. Similar overall findings (adjusted odds ratio, 1.72; 95% CI, 1.56 to 1.90) were observed in an updated meta-analysis involving a total of 10,158 incident coronary heart disease cases from 262,525 participants in 29 studies. Available prospective studies in Western populations consistently indicate moderate and highly significant associations between triglyceride values and coronary heart disease risk. Because these associations depend considerably on levels of established risk factors, however, further studies are needed to help assess the nature of any independent associations.
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              Roles of Inflammation, Oxidative Stress, and Vascular Dysfunction in Hypertension

              Quynh Dinh, Grant Drummond, Christopher Sobey … (2014)
              Hypertension is a complex condition and is the most common cardiovascular risk factor, contributing to widespread morbidity and mortality. Approximately 90% of hypertension cases are classified as essential hypertension, where the precise cause is unknown. Hypertension is associated with inflammation; however, whether inflammation is a cause or effect of hypertension is not well understood. The purpose of this review is to describe evidence from human and animal studies that inflammation leads to the development of hypertension, as well as the evidence for involvement of oxidative stress and endothelial dysfunction—both thought to be key steps in the development of hypertension. Other potential proinflammatory conditions that contribute to hypertension—such as activation of the sympathetic nervous system, aging, and elevated aldosterone—are also discussed. Finally, we consider the potential benefit of anti-inflammatory drugs and statins for antihypertensive therapy. The evidence reviewed suggests that inflammation can lead to the development of hypertension and that oxidative stress and endothelial dysfunction are involved in the inflammatory cascade. Aging and aldosterone may also both be involved in inflammation and hypertension. Hence, in the absence of serious side effects, anti-inflammatory drugs could potentially be used to treat hypertension in the future.
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                Author and article information

                Contributors
                Journal
                Title: Pharmacia
                Abbreviated Title: PHAR
                Publisher: Pensoft Publishers
                ISSN (Electronic): 2603-557X
                ISSN (Print): 0428-0296
                Publication date Created: May 19 2022
                Publication date (Electronic): May 19 2022
                Volume: 69
                Issue: 2
                Pages: 459-465
                Article
                DOI: 10.3897/pharmacia.69.e81078
                SO-VID: f7a16d57-2ab4-40f2-8ee6-57388591fe64
                Copyright © © 2022
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                http://creativecommons.org/licenses/by/4.0/

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