α-mangostin preserves hepatic microvascular architecture in fibrotic rats as shown by scanning electron microscopy of vascular corrosion casts
- Wasan Tangphokhanon
- Wisuit Pradidarcheep
- Alois Lametschwandtner
Affiliations: Center of Excellence in Veterinary Biosciences, Department of Veterinary Biosciences and Public Health, Faculty of Veterinary Medicine, Chiang Mai University, Chiang Mai 50100, Thailand, Department of Anatomy, Faculty of Medicine, Srinakharinwirot University, Bangkok 10110, Thailand, Department of Biosciences, Vascular and Exercise Biology Unit, University of Salzburg, Salzburg 5020, Austria
- Published online on: March 23, 2021 https://doi.org/10.3892/br.2021.1424
Copyright: © Tangphokhanon
et al. This is an open access article distributed under the
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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.