Affiliations 

  • 1 Faculty of Dentistry, Lincoln University College, Petaling Jaya, Selangor 47301, Malaysia
  • 2 Institute of Systems Biology (INBIOSIS), Universiti Kebangsaan Malaysia, UKM, Bangi, Selangor 43600, Malaysia
  • 3 Faculty of Applied Sciences, Universiti Teknologi MARA, Shah Alam, Selangor 40450, Malaysia
  • 4 Faculty of Applied Sciences, Universiti Teknologi MARA, Shah Alam, Selangor 40450, Malaysia; Atta-ur-Rahman Institute of Natural Product Discovery (AuRIns), Universiti Teknologi MARA, Cawangan Selangor, Puncak Alam Campus, Selangor, Malaysia
  • 5 Faculty of Medicine, Universiti Teknologi MARA, Cawangan Selangor, Sungai Buloh Campus, Selangor, Malaysia
  • 6 Faculty of Medicine, Universiti Teknologi MARA, Cawangan Selangor, Sungai Buloh Campus, Selangor, Malaysia; Institute for Pathology, Laboratory and Forensic Medicine (I-PPerFORM), Universiti Teknologi MARA, Cawangan Selangor, Sungai Buloh Campus, Selangor, Malaysia. Electronic address: hjsingh@uitm.edu.my
J Pharm Biomed Anal, 2022 Feb 20;210:114579.
PMID: 35016031 DOI: 10.1016/j.jpba.2021.114579

Abstract

Ficus deltoidea var angustifolia (FD-A) reduces blood pressure in spontaneously hypertensive rats (SHR) but the mechanism remains unknown. Changes in urine metabolites following FD-A treatment in SHR were, therefore, examined to identify the mechanism of its antihypertensive action. Male SHR were given either FD-A (1000 mg kg-1 day-1) or losartan (10 mg kg-1 day-1) or 0.5 mL of ethanolic-water (control) daily for 4 weeks. Systolic blood pressure (SBP) was measured every week and urine spectra data acquisition, on urine collected after four weeks of treatment, were compared using multivariate data analysis. SBP in FD-A and losartan treated rats was significantly lower than that in the controls after four weeks of treatment. Urine spectra analysis revealed 24 potential biomarkers with variable importance projections (VIP) above 0.5. These included creatine, hippurate, benzoate, trimethylamine N-oxide, taurine, dimethylamine, homocysteine, allantoin, methylamine, n-phenylacetylglycine, guanidinoacetate, creatinine, lactate, glucarate, kynurenine, ethanolamine, betaine, 3-hydroxybutyrate, glycine, lysine, glutamine, 2-hydroxyphenylacetate, 3-indoxylsulfate and sarcosine. From the profile of these metabolites, it seems that FD-A affects urinary levels of metabolites like taurine, hypotaurine, glycine, serine, threonine, alanine, aspartate and glutamine. Alterations in these and the pathways involved in their metabolism might underlie the molecular mechanism of its antihypertensive action.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.