Abstract

Black rice is a type of rice in the Oryza sativa L. species. There are numerous reports regarding the pharmacological actions of black rice bran, but scientific evidence on its gastroprotection is limited. This study aimed to evaluate the gastroprotective activities of black rice bran ethanol extract (BRB) from the Thai black rice variety Hom Nil (O. sativa L. indica) as well as its mechanisms of action, acute oral toxicity in rats, and phytochemical screening. Rat models of gastric ulcers induced by acidified ethanol, indomethacin, and restraint water immersion stress were used. After pretreatment with 200, 400, and 800 mg/kg of BRB in test groups, BRB at 800 mg/kg significantly inhibited the formation of gastric ulcers in all gastric ulcer models, and this inhibition seemed to be dose dependent in an indomethacin-induced gastric ulcer model. BRB could not normalize the amount of gastric wall mucus, reduce gastric volume and total acidity, or increase gastric pH. Although BRB could not increase NO levels in gastric tissue, the tissue MDA levels could be normalized with DPPH radical scavenging activity. These results confirm the gastroprotective activities of BRB with a possible mechanism of action via antioxidant activity. The major phytochemical components of BRB comprise carotenoid derivatives with the presence of phenolic compounds. These components may be responsible for the gastroprotective activities of BRB. The 2000 mg/kg dose of oral BRB showed no acute toxicity in rats and confirmed, in part, the safe uses of BRB.

Highlights

  • Peptic ulcer disease (PUD) is one of the most common gastrointestinal diseases worldwide

  • L. indica) at the dose of 800 mg/kg displayed effective gastroprotection against gastric ulcers in all gastric ulcer models, and this inhibition appeared to be dose dependent in the indomethacin-induced gastric ulcer model

  • black rice bran ethanol extract (BRB) could not normalize the amount of gastric wall mucus, reduce gastric volume and total acidity, or increase gastric pH

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Summary

Introduction

Peptic ulcer disease (PUD) is one of the most common gastrointestinal diseases worldwide. The etiology of PUD is an imbalance between the defensive factors of gastroduodenal mucosa Bicarbonate barrier, prostaglandin (PG), and mucosal blood flow) and the aggressive factors (such as hydrochloric acid and pepsin secretion, alcohol, psychological stress, and Helicobacter pylori). The increased aggressive factors cause erosive damage on gastroduodenal mucosa, while the compromised defensive factors expose the inner epithelial layer to acidity, leading to gastric ulcer formation. Proton pump inhibitors (PPIs) are the first-line antisecretory drug for PUD. Their mechanism of action is to irreversibly inhibit H+ /K+ -ATPase. PPIs are not recommended for long-term use because of their possible adverse effects. Other treatment options of PUD include acid neutralizing/inhibitory agents (such as antacids and histamine H2 -receptor antagonists) and mucosal protective agents (such as PG analogs, sucralfate, colloidal bismuth compounds, and carbenoxolone) [2]

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