Abstract

Cratoxylum arborescens (Vahl) Blume is an Asian herbal medicine with versatile ethnobiological properties including treatment of gastric ulcer. This study evaluated the antiulcerogenic mechanism(s) of α-mangostin (AM) in a rat model of ulcer. AM is a prenylated xanthone derived through biologically guided fractionation of C. arborescens. Rats were orally pretreated with AM and subsequently exposed to acute gastric lesions induced by ethanol. Following treatment, ulcer index, gastric juice acidity, mucus content, histological and immunohistochemical analyses, glutathione (GSH), malondialdehyde (MDA), nitric oxide (NO), and nonprotein sulfhydryl groups (NP-SH) were evaluated. The anti-Helicobacter pylori, cyclooxygenase-2 (COX-2) inhibitory effect, and antioxidant activity of AM were also investigated in vitro. AM (10 and 30 mg/kg) inhibited significantly (P < 0.05) ethanol-induced gastric lesions by 66.04% and 74.39 %, respectively. The compound induces the expression of Hsp70, restores GSH levels, decreases lipid peroxidation, and inhibits COX-2 activity. The minimum inhibitory concentration (MIC) of AM showed an effective in vitro anti-H. pylori activity. The efficacy of the AM was accomplished safely without presenting any toxicological parameters. The results of the present study indicate that the antioxidant properties and the potent anti-H. pylori, in addition to activation of Hsp70 protein, may contribute to the gastroprotective activity of α-mangostin.

Highlights

  • Peptic ulcer disease (PUD) is the most common gastrointestinal tract aliment of multiple causes which hinders a lot of people worldwide

  • Histological examination to the liver and kidney and serum biochemical analysis did not show any difference in comparison to the control group

  • Results showed that animals pretreated with antiulcerogenic mechanism(s) of α-mangostin (AM) and omeprazole considerably reduced ulcer area formation compared to animal group pretreated with only 5% Tween80 (Table 1). αMangostin (AM) at doses of 10 and 30 mg/kg b.w. significantly (P < 0.05) inhibited ulcer formation by 66.04% and 74.39%, respectively, as shown in Table 1 and Figure 2

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Summary

Introduction

Peptic ulcer disease (PUD) is the most common gastrointestinal tract aliment of multiple causes which hinders a lot of people worldwide. There are many noxious agents that attack the stomach resulting in mucosal ulceration such as Helicobacter pylori infection, excessive ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs), or alcohol as well as psychological stress and cigarette smoking. The stomach protects itself by many defensive mechanisms, mainly the entire mucosal layer which acts as a barrier against inflammatory and cytotoxic agents [3]. It is reported that accumulation of reactive oxygen species is in charge of peptic ulcer aetiology in various gastric ulcer models suggesting the participation of antioxidant enzymes, and there is a trend to explore antioxidant drugs from natural resources [2]. The reciprocal antiulcer medication to treat the peptic ulcer is either by inhibiting gastric acid secretion or by enhancing mucus layer protection.

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