ArticleBMC complementary and alternative medicine2019
Rosmarinic acid improves hypertension and skeletal muscle glucose transport in angiotensin II-treated rats.
Article in BMC complementary and alternative medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- In-vitro ACE-1 Inhibitory Activity ofActa medica Philippina · 2026Article
- Rosmarinic Acid Induces Vasorelaxation via Endothelium-Dependent, Potassium Channel-Related, and Calcium-Modulated Pathways: Evidence from Rat Aortic Rings.Biomedicines · 2025Article
- In vitro biological activities of Calamintha nepeta L. aqueous extracts.Journal of applied biomedicine · 2024Article
- Review
- Effect of the Combination ofFoods (Basel, Switzerland) · 2023Review
- Deciphering the therapeutical potentials of rosmarinic acid.Scientific reports · 2022Article
- Biomedical features and therapeutic potential of rosmarinic acid.Archives of pharmacal research · 2022Review
- Review
- Rosmarinic Acid as a Candidate in a Phenotypic Profiling Cardio-/Cytotoxicity Cell Model Induced by Doxorubicin.Molecules (Basel, Switzerland) · 2020Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundRosmarinic acid (RA) is a natural pure compound from herbs belonging to the Lamiaceae family, such as rosemary, sage, basil, and mint. The antioxidant, angiotensin-converting enzyme inhibitory, and vasodilatory effects of RA have been revealed. Angiotensin II (ANG II) is a potent agent that generates hypertension and oxidative stress. Hypertension and skeletal muscle insulin resistance are strongly related. The aim of this study was to evaluate the effects of acute and chronic RA treatment on blood pressure and skeletal muscle glucose transport in ANG II-induced hypertensive rats.
methodsEight-week-old male Sprague Dawley rats were separated into SHAM and ANG II-infused (250 ng/kg/min) groups. ANG II rats were treated with or without acute or chronic RA at 10, 20, or 40 mg/kg. At the end of the experiment, body weight, liver and heart weights, oral glucose tolerance, skeletal muscle glucose transport activity, and signaling proteins were evaluated.
resultsBoth acute and chronic RA treatment decreased systolic, diastolic, and mean arterial blood pressure. Only acute RA at 40 mg/kg resulted in a reduction of fasting plasma glucose levels and an induction of skeletal muscle glucose transport activity. These effects might involve increased ERK activity in skeletal muscle. Meanwhile, chronic RA treatment with 10, 20, and 40 mg/kg prevented ANG II-induced hyperglycemia.
conclusionsBoth acute and chronic RA treatment attenuated ANG II-induced cardiometabolic abnormalities in rats. Therefore, RA would be an alternative strategy for improving skeletal muscle glucose transport and protecting against ANG II-induced hypertension and hyperglycemia.
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