Publication: Rosmarinic acid improves hypertension and skeletal muscle glucose transport in angiotensin II-treated rats
Issued Date
2019-07-08
Resource Type
ISSN
14726882
Other identifier(s)
2-s2.0-85068844277
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
BMC Complementary and Alternative Medicine. Vol.19, No.1 (2019)
Suggested Citation
Mujalin Prasannarong, Vitoon Saengsirisuwan, Juthamard Surapongchai, Jariya Buniam, Natsasi Chukijrungroat, Yupaporn Rattanavichit Rosmarinic acid improves hypertension and skeletal muscle glucose transport in angiotensin II-treated rats. BMC Complementary and Alternative Medicine. Vol.19, No.1 (2019). doi:10.1186/s12906-019-2579-4 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/51533
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Rosmarinic acid improves hypertension and skeletal muscle glucose transport in angiotensin II-treated rats
Abstract
© 2019 The Author(s). Background: Rosmarinic 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. Methods: Eight-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. Results: Both 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. Conclusions: Both 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.