Spasmolytic Effect of Grewia asiatica Fruit Extract on Isolated Smooth Muscles is Mediated via Multiple Pathways

Muhammad Nabeel Ghayur; Saeed Ahmad; Anwarul Hassan Gilani

doi:10.1155/2021/5583372

Spasmolytic Effect of Grewia asiatica Fruit Extract on Isolated Smooth Muscles is Mediated via Multiple Pathways

Evid Based Complement Alternat Med. 2021 Sep 13:2021:5583372. doi: 10.1155/2021/5583372. eCollection 2021.

Authors

Muhammad Nabeel Ghayur^{1

2}, Saeed Ahmad¹, Anwarul Hassan Gilani^{1

3}

Affiliations

¹ Department of Biological and Biomedical Sciences, Aga Khan University, Karachi 74800, Sind, Pakistan.
² Kentucky College of Osteopathic Medicine, University of Pikeville, Pikeville 41501, KY, USA.
³ Department of Public Health and Nutrition, The University of Haripur, Haripur 22620, Khyber Pakhtunkhwa, Pakistan.

Abstract

Background: Grewia asiatica Linn, or phalsa, is a commonly consumed fruit in Pakistan. The fruit is employed in the traditional medicine practice of Pakistan as a smooth muscle relaxant in different gastrointestinal (GI) and cardiovascular diseases. In this investigation, we show the antispasmodic and vasorelaxant actions of Grewia asiatica fruit extract.

Methods: A 70% methanolic crude extract of the plant material was prepared (Ga.Cr). Different isolated GI tissue preparations and endothelium-intact aortas from rats were utilized to observe the pharmacological actions of the extract.

Results: Ga.Cr, in increasing concentrations, inhibited the spontaneously contracting rabbit jejunum. In an effort to determine the mechanism of this relaxant action, contractions were induced in jejunum and ileum tissues with K⁺ (80 mM). Ga.Cr was able to only partially inhibit these induced contractions indicating that the mechanism might not be completely through a blockade of Ca²⁺ channels (CCB). When tested on low K⁺-(25 mM) sustained contractions, Ga.Cr cumulatively suppressed these contractions (0.1-10 mg/ml), indicating an opening of K⁺ channels (KCO) as the mechanism. Cromakalim, a standard KCO, was also more specific in blocking low K⁺-induced contractions. For the effect in aorta tissues, Ga.Cr suppressed the agonist-induced contractions from 0.3 mg/ml to 10 mg/ml. Upon challenge with L-NAME, a nitric oxide (NO) blocker, the extract response curve shifted right, indicating vasodilation was mediated via endothelial NO.

Conclusion: This study shows that GI antispasmodic and vasodilator activities of Ga.Cr may be mediated via a KCO mechanism in the GI tract and through the release of NO from vascular endothelium.