Effect of Limonene and Sobrerol on Monocrotaline-lnduced Lung Alterations and Pulmonary Hypertension

Touvay, Caroline; Vilain, B.; Carré, C.; Mencia‐Huerta, Jean‐Michel; Braquet, P.

doi:10.1159/000237000

Cited by 20 publications

(10 citation statements)

References 4 publications

(4 reference statements)

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“…After daily oral administrations at a dose of 400 mg/rat, both limonene and sobrerol were able to significantly decrease the changes induced by MCT. Moreover, both monoterpenes also reduced the increase in medial thickness of the pulmonary artery (Touvay et al, 1995).…”

Section: Limonene and Sobrerolmentioning

confidence: 83%

“…It is the major constituent in several citrus oils (orange, lemon, mandarin, lime, and grapefruit) (Sun, 2007). Touvay et al (1995) studied the effects of limonene (13) and sobrerol (28) on pulmonary hypertension and right ventricular hypertrophy induced by monocrotaline (MCT) in rats. After daily oral administrations at a dose of 400 mg/rat, both limonene and sobrerol were able to significantly decrease the changes induced by MCT.…”

Section: Limonene and Sobrerolmentioning

confidence: 99%

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Cardiovascular effects of monoterpenes: a review

Santos¹,

Moreira²,

Fraga³

et al. 2011

Rev. bras. farmacogn.

158

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Abstract:The monoterpenes are secondary metabolites of plants. They have various pharmacological properties including antifungal, antibacterial, antioxidant, anticancer, anti-spasmodic, hypotensive, and vasorelaxant. The purpose of this research was to review the cardiovascular effects of monoterpenes. The data in this resarch were collected using the Internet portals Pubmed, Scopus, and ISI Web of Knowledge between the years 1987 and 2010. In the study 33 monoterpenes were included, which were related to each of the thirteen individual words: artery, cardiovascular, heart, myocyte, vasorelaxant, vessel, hypotension, hypotensive, cardiomyocyte, ventricular, vasodilatory, aorta, and aortic. The research utilized 22 articles published mainly in the journals Phytomedicine, Fundamental Clinical Pharmacology, Planta Medica, Life Science, European Journal of Pharmacology, and Brazilian Journal of Medical and Biological Research. Of the 33 monoterpenes studied surveyed, sixteen of them had already been studied for their effects on the cardiovascular system: carvacrol, citronellol, p-cymene, eucalyptol (1,8-cineole), linalool, menthol, myrtenal, myrtenol, α-pinene, rotundifolone (piperitenone oxide), sobrerol, thymol, α-limonene, α-terpinen-4-ol, α-terpineol, and perillyl alcohol. The main effects observed were vasorelaxation, decreased heart rate and blood pressure. This review showed that the monoterpenes may be considered promising agents for prevention or treatment of diseases of the cardiovascular system.

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Section: Limonene and Sobrerolmentioning

confidence: 83%

Section: Limonene and Sobrerolmentioning

confidence: 99%

Cardiovascular effects of monoterpenes: a review

Santos¹,

Moreira²,

Fraga³

et al. 2011

Rev. bras. farmacogn.

158

View full text Add to dashboard Cite

show abstract

“…A recent report demonstrating the dramatic effect of simvastatin on the development of pulmonary hypertension and neointimal proliferation in a monocrotaline plus pneumonectomy rat model (37) is consistent with our data. Additional evidence supporting the potential usefulness of these agents is the abrogation of monocrotaline-induced pulmonary hypertension and vascular remodeling by limonene and sobrerol (45). These compounds are structurally related to isoprenoids and, like statins, inhibit the posttranslational lipid modification of small G proteins.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of chronic hypoxic pulmonary hypertension by simvastatin

Girgis¹,

Li²,

Zhan³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

145

127

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. Attenuation of chronic hypoxic pulmonary hypertension by simvastatin. Am J Physiol Heart Circ Physiol 285: H938-H945, 2003. First published May 15, 2003 10.1152/ ajpheart.01097.2002The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been shown to improve multiple normal endothelial cell functions and inhibit vascular wall cell proliferation. We hypothesized that one such agent, simvastatin, would attenuate chronic hypoxic pulmonary hypertension. Male adult Sprague-Dawley rats were exposed (14 days) to normoxia (N), normoxia plus once-a-day administered simvastatin (20 mg/kg ip) (NS), hypoxia (10% inspired O 2 fraction) (H), or hypoxia plus simvastatin (HS). Mean pulmonary artery pressure, measured in anesthetized, ventilated rats with an open-chest method, was reduced from 25 Ϯ 2 mmHg in H to 18 Ϯ 1 in HS (P Ͻ 0.001) but did not reach normoxic values (12 Ϯ 1 mmHg). Similarly, right ventricular/left ventricular plus interventricular septal weight was reduced from 0.53 Ϯ 0.02 in the H group to 0.36 Ϯ 0.02 in the HS group (P Ͻ 0.001). The increased hematocrit in H (0.65 Ϯ 0.02) was prevented by simvastatin treatment (0.51 Ϯ 0.01, P Ͻ 0.001). Hematocrit was similar in N versus NS. Alveolar vessel muscularization and medial thickening of vessels 50-200 M in diameter induced by hypoxia were also significantly attenuated in the HS animals. Lung endothelial nitric oxide synthase (eNOS) protein expression in the HS group was less than H (P Ͻ 0.01) but was similar in N versus NS. We conclude that simvastatin treatment potently attenuates chronic hypoxic pulmonary hypertension and polycythemia in rats and inhibits vascular remodeling. Enhancement of lung eNOS expression does not appear to be involved in mediating this effect. pulmonary vascular remodeling; 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibition; nitric oxide; polycythemia; small G proteins CHRONIC PULMONARY HYPERTENSION is characterized by a component of abnormal pulmonary vasoconstriction and by structural remodeling of the small pulmonary arteries. Both processes lead to a progressive increase in pulmonary vascular resistance, which, when extreme, culminates in right ventricular (RV) failure and death. The syndrome occurs in diverse clinical settings, including lung disease associated with alveolar hypoxia. Endothelial cell injury-dysfunction is considered to be a key factor in the pathogenesis of pulmonary hypertension (3), leading to increased vascular smooth muscle tone, cell proliferation in the vascular wall, and activation of thrombotic mechanisms, all of which participate in the process of remodeling. Currently available therapies have a beneficial clinical effect yet cannot reverse the disease process. Therefore, the response is variable with considerable morbidity and mortality despite therapy (33). Clearly, there is an urgent need for new therapies.The 3-hydroxy-3-methylglutaryl-coenzyme A (HMGCoA) reductase inhibitors (statins) have been shown to exert numerous effects on vascular wall function, independent of t...

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“…Then it primarily reaches the lung and may directly affect lung tissues and alveo lar macrophages (MO). On the other hand, there are some reports that terpenoids including D-limonene may irritate the mucous membrane and the skin (14), and further prolonged exposure of D-limonene may result in an impairment of lung function (15)(16)(17)(18) and kidney (19)(20)(21)(22)(23).…”

Section: Discussionmentioning

confidence: 99%