Abstract

Current anti-gastric ulcer agents have side effects, despite the progression and expansion of advances in treatment. This study aimed to investigate the gastroprotective mechanisms of Pithecellobium jiringa ethanol extract against ethanol-induced gastric mucosal ulcers in rats. For this purpose, Sprague Dawley rats were randomly divided into five groups: Group 1 (normal control) rats were orally administered with vehicle (carboxymethyl cellulose), Group 2 (ulcer control) rats were also orally administered with vehicle. Group 3 (positive control) rats were orally administered with 20 mg/kg omeprazole, Groups 4 and 5 (experimental groups) received ethanol extract of Pithecellobium jiringa ethanol extract at a concentration of 250 and 500 mg/kg, respectively. Sixty minutes later, vehicle was given orally to the normal control group, and absolute ethanol was given orally to the ulcer control, positive control and experimental groups to generate gastric mucosal injury. The rats were sacrificed an hour later. The effect of oral administration of plant extract on ethanol-induced gastric mucosal injury was studied grossly and histology. The level of lipid peroxidation, (malondialdehyde—MDA), superoxide dismutase (SOD) and gastric wall mucus were measured from gastric mucosal homogenate. The ulcer control group exhibited severe gastric mucosal injury, and this finding was also confirmed by histology of gastric mucosa which showed severe damage to the gastric mucosa with edema and leucocyte infiltration of the submucosal layer. Pre-treatment with plant extract significantly reduced the formation of ethanol-induced gastric lesions, and gastric wall mucus was significantly preserved. The study also indicated a significant increase in SOD activity in gastric mucosal homogenate, whereas a significant decrease in MDA was observed. Acute toxicity tests did not show any signs of toxicity and mortality up to 5 g/kg. The ulcer protective effect of this plant may possibly be due to its preservation of gastric wall mucus along with increased SOD activity and reduction of oxidative stress (MDA). The extract is non-toxic, even at relatively high concentrations.

Highlights

  • IntroductionPithecellobium jiringa (djengkol bean) is one of the members of the Leguminosae family

  • Pithecellobium jiringa is one of the members of the Leguminosae family

  • Rats pretreated with omeprazole (GIII), or with both doses of ethanol extract (GIV and GV) before being given absolute alcohol showed significantly reduced areas of gastric ulcer formation compared to gastric lesions in ulcers control rats (GII) (Figure 2, Table 3)

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Summary

Introduction

Pithecellobium jiringa (djengkol bean) is one of the members of the Leguminosae family. Its other scientific name is Archidendron jiringa This plant originated from Southeast Asia, where it is known as jering in Malaysia, djengkol in Indonesian, krakos in Cambodia, and niang-yai in Thailand. In those countries, P. jiringa beans are typically consumed as a side dish with rice. Today P. jiringa is used in the production of organic pesticides It contains djenkolic acid and sulphur which are able to inhibit and kill pests [2]. The methanolic extract of P. jiringa was found to inhibit the activation of Epstein-Barr virus (EBV) by 30% or more. The present study was undertaken to investigate the gastroprotective mechanisms of P. jiringa ethanol extract against ethanol-induced gastric mucosal injury in experimental rats

Acute Toxicity Study
Gross Appearance of Gastric Lesions
Histological Changes of Gastric Mucosa
Drugs and Chemicals
Preparation of the Ethanol Extraction
Acute Toxicity Test and Experimental Animals
Experimental Animals for Gastric Ulcer
Treatment
Gross Gastric Lesions Evaluation
Determination of Gastric Wall Mucus
Microscopic Studies
3.10. Estimation of SOD Antioxidant Enzyme and Proteins Concentration
3.11. Measurement of the Membrane Lipids Peroxidation
Conclusions
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