Publication:
Rosmarinic acid improves hypertension and skeletal muscle glucose transport in angiotensin II-treated rats

2
0

Issued Date

2019

Resource Type

Article

File Type

application/pdf

ISSN

14726882

DOI

10.1186/s12906-019-2579-4

Other identifier(s)

2-s2.0-85068844277

Rights Holder(s)

Scopus

Bibliographic Citation

BMC Complementary and Alternative Medicine. Vol 19, No.1 (2019)

Suggested Citation

Prasannarong M., Saengsirisuwan V., Surapongchai J., Buniam J., Chukijrungroat N., Rattanavichit Y. 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://hdl.handle.net/20.500.14740/5208

Title

Rosmarinic acid improves hypertension and skeletal muscle glucose transport in angiotensin II-treated rats

Author(s)

Prasannarong M.
 Saengsirisuwan V.
 Surapongchai J.
 Buniam J.
 Chukijrungroat N.
 Rattanavichit Y.

Abstract

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. © 2019 The Author(s).

Subject(s)

Angiotensin II
 Glucose
 Glyceraldehyde 3 phosphate dehydrogenase
 Glycogen synthase kinase 3alpha
 Glycogen synthase kinase 3beta
 Janus kinase
 Mitogen activated protein kinase
 Mitogen activated protein kinase 1
 Mitogen activated protein kinase 3
 Mitogen activated protein kinase p38
 Protein kinase B
 Rosmarinic acid
 Angiotensin II
 Cinnamic acid derivative
 Depside
 Glucose
 Insulin
 Rosmarinic acid
 Animal tissue
 Article
 Body weight
 Controlled study
 Diastolic blood pressure
 Drug effect
 Enzyme activity
 Glucose blood level
 Glucose transport
 Heart weight
 Hypertension
 Liver weight
 Long term care
 Male
 Mean arterial pressure
 Nonhuman
 Oral glucose tolerance test
 Rat
 Sham procedure
 Single drug dose
 Skeletal muscle
 Sprague Dawley rat
 Systolic blood pressure
 Treatment duration
 Animal
 Blood pressure
 Hypertension
 Metabolism
 Organ size
 Signal transduction
 Skeletal muscle
 Angiotensin II
 Animals
 Blood Pressure
 Body Weight
 Cinnamates
 Depsides
 Glucose
 Hypertension
 Insulin
 Male
 Muscle, Skeletal
 Organ Size
 Rats
 Rats, Sprague-Dawley
 Signal Transduction

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URI

https://hdl.handle.net/20.500.14740/5208

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Scopus: Year 1983-2021

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