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Métodos Terapéuticos y Terapias MTCI
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1.
Nat Prod Res ; 35(10): 1657-1661, 2021 May.
Artículo en Inglés | MEDLINE | ID: mdl-31140298

RESUMEN

Aerial parts (leaves, flowers, stem) of Peperomia galioides extract administered to mice, was used to confirm its anti-inflammatory and sedative folk uses. The anti-inflammatory activity was assessed by croton oil-induced ear oedema and myeloperoxidase (acute inflammation); cotton pellet-induced granuloma (sub-acute inflammation) and Escherichia coli Lipopolysaccharide (LPS) induced inflammation (cellular mediators). The sedative activity was studied by the pentobarbital-induced sleeping time test. Single doses (300 and 600 mg/kg; i.p.) of the extract reduced croton oil-induced ear oedema and myeloperoxidase activity. Six days administration of the extract (300 mg/kg, i.p.) to mice implanted with cotton pellets diminished granuloma formation. LPS (20 mg/kg, i.p.) enhanced plasma nitrites and TNF-α levels that were inhibited by the extract. The duration but not the onset of sleeping time was enhanced by 300 and 600 mg/kg of the extract. Our results show that P. galioides has anti-inflammatory and sedative activities in mice, which validates its traditional use.


Asunto(s)
Antiinflamatorios no Esteroideos/farmacología , Hipnóticos y Sedantes/farmacología , Peperomia/química , Extractos Vegetales/farmacología , Animales , Antiinflamatorios no Esteroideos/química , Aceite de Crotón/toxicidad , Edema/inducido químicamente , Edema/tratamiento farmacológico , Hipnóticos y Sedantes/química , Inflamación/inducido químicamente , Inflamación/tratamiento farmacológico , Masculino , Ratones , Peroxidasa/metabolismo , Extractos Vegetales/química , Hojas de la Planta/química , Plantas Medicinales/química , Sueño/efectos de los fármacos , Factor de Necrosis Tumoral alfa/sangre
2.
Front Cardiovasc Med ; 7: 588692, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-33195477

RESUMEN

Cardiovascular disease causes almost one third of deaths worldwide, and more than half are related to primary arterial hypertension (PAH). The occurrence of several deleterious events, such as hyperactivation of the renin-angiotensin system (RAS), and oxidative and inflammatory stress, contributes to the development of small vessel disease in PAH. Small resistance arteries are found at various points through the arterial tree, act as the major site of vascular resistance, and actively regulate local tissue perfusion. Experimental and clinical studies demonstrate that alterations in small resistance artery properties are important features of PAH pathophysiology. Diseased small vessels in PAH show decreased lumens, thicker walls, endothelial dysfunction, and oxidative stress and inflammation. These events may lead to altered blood flow supply to tissues and organs, and can increase the risk of thrombosis. Notably, PAH is prevalent among patients diagnosed with COVID-19, in whom evidence of small vessel disease leading to cardiovascular pathology is reported. The SARS-Cov2 virus, responsible for COVID-19, achieves cell entry through an S (spike) high-affinity protein binding to the catalytic domain of the angiotensin-converting enzyme 2 (ACE2), a negative regulator of the RAS pathway. Therefore, it is crucial to examine the relationship between small resistance artery disease, ACE2, and PAH, to understand COVID-19 morbidity and mortality. The scope of the present review is to briefly summarize available knowledge on the role of small resistance artery disease and ACE2 in PAH, and critically discuss their clinical relevance in the context of cardiovascular pathology associated to COVID-19.

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