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Antidotal and protective effects of mangosteen (Garcinia mangostana) against natural and chemical toxicities: A review

Journal

IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES
Volume 26, Issue 5, Pages 492-503

Publisher

MASHHAD UNIV MED SCIENCES
DOI: 10.22038/IJBMS.2023.66900.14674

Keywords

Analgesics; Anti-inflammatory agents; Anti-oxidants; Apoptosis; Hypoglycemic Agents; Neuroprotective Agents; Phytotherapy; Xanthones

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This review evaluates the protective activities of mangosteen and its major components against natural and chemical toxicities. The protective effects are mediated through various mechanisms, including oxidative stress inhibition, modulation of inflammation, apoptosis and MAPK signaling pathways, and improvement of histological conditions.
Chemical and natural toxic compounds can harm human health through a variety of mechanisms. Nowadays, herbal therapy is widely accepted as a safe method of treating toxicity. Garcinia mangostana (mangosteen) is a tree in the Clusiaceae family, and isoprenylated xanthones, its main constituents, are a class of secondary metabolites having a variety of biological properties, such as anti-inflammatory, anti-oxidant, pro-apoptotic, anti-proliferative, antinociceptive, neuroprotective, hypoglycemic, and anti-obesity. In this review, the protective activities of mangosteen and its major components against natural and chemical toxicities in both in vivo and in vitro experiments were evaluated. The protective effects of mangosteen and its components are mediated primarily through oxidative stress inhibition, a decrease in the number of inflammatory cells such as lymphocytes, neutrophils, and eosinophils, reduction of inflammatory mediators such as tumor necrosis factor -alpha (TNF-alpha), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), cyclooxygenase-2 (COX -2), prostaglandin (PG) E2, inducible nitric oxide synthase, and nuclear factor-KB (NF-KB), modulation of apoptosis and mitogen-activated protein kinase (MAPK) signaling pathways, reducing p65 entrance into the nucleus, alpha-smooth muscle actin (alpha-SMA), transforming growth factor [31 (TGF[31), improving histological conditions, and inhibition in acetylcholinesterase activity.

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