In vivo antioxidant and antiulcer activity of Parkia speciosa ethanolic leaf extract against ethanol-induced gastric ulcer in rats.

Rami Al Batran,Fouad Al-Bayaty,Abdualrahman Mohammed Abdualkader,Hapipah Mohd Ali,Hamid A Hadi,Mahmood Ameen Abdulla,Mazen M Jamil Al-Obaidi,Herbert B Tanowitz

doi:10.1371/journal.pone.0064751

Abstract

BackgroundThe current study was carried out to examine the gastroprotective effects of Parkia speciosa against ethanol-induced gastric mucosa injury in rats.Methodology/Principal FindingsSprague Dawley rats were separated into 7 groups. Groups 1–2 were orally challenged with carboxymethylcellulose (CMC); group 3 received 20 mg/kg omeprazole and groups 4–7 received 50, 100, 200 and 400 mg/kg of ethanolic leaf extract, respectively. After 1 h, CMC or absolute ethanol was given orally to groups 2–7. The rats were sacrificed after 1 h. Then, the injuries to the gastric mucosa were estimated through assessment of the gastric wall mucus, the gross appearance of ulcer areas, histology, immunohistochemistry and enzymatic assays. Group 2 exhibited significant mucosal injuries, with reduced gastric wall mucus and severe damage to the gastric mucosa, whereas reductions in mucosal injury were observed for groups 4–7. Groups 3–7 demonstrated a reversal in the decrease in Periodic acid-Schiff (PAS) staining induced by ethanol. No symptoms of toxicity or death were observed during the acute toxicity tests.ConclusionTreatment with the extract led to the upregulation of heat-shock protein 70 (HSP70) and the downregulation of the pro-apoptotic protein BAX. Significant increases in the levels of the antioxidant defense enzymes glutathione (GSH) and superoxide dismutase (SOD) in the gastric mucosal homogenate were observed, whereas that of a lipid peroxidation marker (MDA) was significantly decreased. Significance was defined as p<0.05 compared to the ulcer control group (Group 2).

Highlights

Peptic ulcers, which are characterized by the presence of mucosal damage, are predominantly caused by infection with Helicobacter pylori, antiplatelet agents such as acetylsalicylic acid [1], non-steroidal anti-inflammatory drugs (NSAIDs) such as oral bisphosphonates, potassium chloride, immunosuppressive medications [2], serotonin reuptake inhibitors [3], alcohol consumption and cigarette smoking [4]
Acute Toxicity Study No death or significant toxicity was observed in the control or treatment groups, as evaluated based on clinical and histopathological observations
The results demonstrated that rats pretreated with omeprazole or Parkia speciosa extracts prior to treatment with absolute ethanol exhibited significantly smaller areas of gastric ulceration than did group 2 (Figure 1)

Summary

Introduction

Peptic ulcers, which are characterized by the presence of mucosal damage, are predominantly caused by infection with Helicobacter pylori, antiplatelet agents such as acetylsalicylic acid [1], non-steroidal anti-inflammatory drugs (NSAIDs) such as oral bisphosphonates, potassium chloride, immunosuppressive medications [2], serotonin reuptake inhibitors [3], alcohol consumption and cigarette smoking [4]. These factors can cause submucosal erosion and inhibit cyclooxygenase, disturbing the protection of the gastric mucosal layer [5]. Parkia speciosa is known as stink bean or ‘‘petai.’’ It bears long, flat bean pods with green seeds. The current study was carried out to examine the gastroprotective effects of Parkia speciosa against ethanolinduced gastric mucosa injury in rats

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Conclusion