Publication:
α-mangostin preserves hepatic microvascular architecture in fibrotic rats as shown by scanning electron microscopy of vascular corrosion casts

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Issued Date

2021

Resource Type

Article

Language

eng

File Type

application/pdf

ISSN

20499434

DOI

10.3892/br.2021.1424

Other identifier(s)

2-s2.0-85107782713

Rights Holder(s)

Scopus

Bibliographic Citation

Biomedical Reports. Vol 14, No.6 (2021)

Suggested Citation

Tangphokhanon W., Pradidarcheep W., Lametschwandtner A. α-mangostin preserves hepatic microvascular architecture in fibrotic rats as shown by scanning electron microscopy of vascular corrosion casts. Biomedical Reports. Vol 14, No.6 (2021). doi:10.3892/br.2021.1424 Retrieved from: https://hdl.handle.net/20.500.14740/8033

Title

α-mangostin preserves hepatic microvascular architecture in fibrotic rats as shown by scanning electron microscopy of vascular corrosion casts

Author(s)

Tangphokhanon W.
 Pradidarcheep W.
 Lametschwandtner A.

Abstract

Liver fibrosis is a dynamic condition caused by wound-healing in which scar tissue replaces the liver parenchyma following repetitive injuries. It is hypothesized that α-mangostin (AM), the major constituent of the xanthone fraction in extracts of Garcinia mangostana L., may protect the hepatic microvascular bed from thioacetamide (TAA)-induced fibrosis. In the present study, rats were divided into 4 groups: Control rats received no treatment; TAA-treated rats received 150 mg/kg TAA 3 times per week intraperitoneally; AM-treated rats received 75 mg/kg AM twice per week intraperitoneally; and TAA+AM-treated rats received both TAA and AM as described above. Rat livers were processed either for light microscopy or for vascular corrosion casting after 30 and 60 days of treatment. Vascular parameters were measured by 3D morphometry analysis of scanning electron micrographs. AM attenuated hepatocellular injuries and delayed both periportal and pericentral fibrosis in the TAA-treated rats. The comparison of findings at day 30 and 60 showed that TAA-induced fibrotic changes were progressive in time, and that the beneficial effects of AM only became apparent after prolonged treatment. The livers of rats treated with both TAA and AM had less space surrounding the portal vessels, improved preservation of the hepatic microvascular pattern, and minimally altered sinusoidal patterns with few signs of terminal portal venule remodeling. AM therefore partially protected the liver against hepatotoxin-induced fibrosis and the associated microvascular changes. The mechanism of the protective effect of AM on the liver remains to be investigated. © 2021, Spandidos Publications. All rights reserved.

Subject(s)

Alanine aminotransferase
 Alkaline phosphatase
 Alpha mangostin
 Aspartate aminotransferase
 Natural product
 Pentobarbital
 Thioacetamide
 Unclassified drug
 3 dimentional morphometry
 Animal model
 Animal tissue
 Article
 Cadaver
 Controlled study
 Corrosion casting
 Drug mechanism
 Endothelium cell
 Experimental liver fibrosis
 Garcinia mangostana
 Hepatic portal vein
 Histopathology
 Liver blood vessel
 Liver cell
 Liver fibrosis
 Male
 Microvasculature
 Morphometry
 Nonhuman
 Quantitative analysis
 Rat
 Scanning electron microscopy
 Staining

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URI

https://hdl.handle.net/20.500.14740/8033

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Scopus: Year 1983-2021

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