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Original Research Article | OPEN ACCESS

Supercritical fluid carbon dioxide extract of Alpinia oxyphylla ameliorates dextran sulfate sodium-induced intestinal barrier damage in mice

Fan Yang1, Yongqing Tao1 , Chen Chen1, Wei Zhao1, Juan Wang1, Beibei Peng1, Ke Lv1, Patrick O Erah2 , Hui Zhao1

1Tianjin Key Laboratory of Food and Biotechnology, Tianjin International Joint Center of Food Science and Engineering, State Experimental and Training Centre of Food and Drug, School of Biotechnology and Food Science, Tianjin University of Commerce, No. 409 Guangrong Road, Tianjin, 300134 China; 2Department of Clinical Pharmacy and Pharmacy Practice, Faculty of Pharmacy, University of Benin, Benin City, Nigeria.

For correspondence:-  Yongqing Tao   Email: tyqing@tjcu.edu.cn

Accepted: 1 May 2024        Published: 29 May 2024

Citation: Yang F, Tao Y, Chen C, Zhao W, Wang J, Peng B, et al. Supercritical fluid carbon dioxide extract of Alpinia oxyphylla ameliorates dextran sulfate sodium-induced intestinal barrier damage in mice. Trop J Pharm Res 2024; 23(5):833-845 doi: 10.4314/tjpr.v23i5.5

© 2024 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: Inflammation and oxidative stress are the leading causes of intestinal barrier dysfunction and a wide range of diseases. The purpose of this study was to explore the protective effect and elucidate potential mechanisms of supercritical carbon dioxide extract from Alpinia oxyphylla Miq. (AOE) on intestinal inflammation.
Methods: The AOE was extracted by supercritical carbon dioxide extraction and its components were determined. Cytotoxicity of the extract (0.05 to 20μg/mL) was determined on Caco-2 cells. In vitro assessment of whether AOE protected against LPS-induced intestinal barrier dysfunction was done on Caco-2 cells pretreated with non-cytotoxic concentrations (0.5μg/mL and 1 μg/mL) of the extract. Experimental colitis of mouse model was induced by drinking water containing 3% dextran sulfate sodium (DSS). The intestinal permeability was assessed by TEER and fluorescein isothiocyanate conjugated dextran (FITC). Pathological evidence and possible mechanism were verified by tissue staining and molecular methods including quantitative real-time polymerase chain reaction (qRT-PCR) and western blot.
Results: TEER and FITC testing indicated that AOE pretreatment significantly improved intestinal barrier hemostasis (p<0.05). Furthermore, AOE pretreatment counteracted DSS-induced upregulation of pro-inflammatory cytokines and oxidative stress (p<0.05). Lastly, two crucial signal pathways regarding hemostasis of intestinal barrier, NF-κB and NOX1-LCN2, were significantly attenuated upon AOE pretreatment (p<0.05).
Conclusion: This study sheds lights on the protective effect of AOE for intestinal hemostasis and supports the development of AOE-based intestinal protective agents.

Keywords: Alpinia oxyphylla extract; Intestinal inflammation; Dextran Sulfate Sodium Salt; NF-?B; Oxidative stress

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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