Activity of Brucea javanica oil emulsion against gastric ulcers in rodents

Abstract

The present study aims to investigate the gastroprotective effect of Brucea javanica oil emulsion (BJOE) in animals. Gastroprotective potential of BJOE was studied on absolute ethanol, aspirin, reserpine and restraint plus water immersion-induced gastric ulcers in mice as well as glacial acetic acid (GAA) and pyloric ligation (PL)-induced gastric ulcers in rats. Except for ulcer scores, total acidity as well as pepsin activity as for the PL-induced gastric ulcer model and ulcer incidence as for the GAA-induced gastric ulcer model were also determined. Histopathological evaluation as for aspirin, reserpine, PL-induced models was conducted. Results showed that BJOE significantly (P < 0.05) reduced ulcer index in the mouse and rat models in a dose-dependent manner. It had significant (P < 0.05) suppressive effect on total activity of gastric juice as well in PL-induced model. Histopathological examination for the stomach samples confirmed the findings in the aspirin, reserpine or PL-induced gastric lesion models, which showed relatively complete mucosa structure and less inflammation. It is concluded that BJOE could be effective on gastric ulcer in rodents and its gastroprotective activity might be related to antioxidant, anti-inflammatory ability and promote gastric mucus secreted. The results may provide beneficial basis for increasing BJOE's clinical indication in future.

Keywords: Brucea javanica oil emulsion; Gastric mucosa; Gastric ulcer; Glacial acetic acid; Pepsin activity; Ulcer scores.

Graphical abstract

Fig. 1

BJOE administration reduces dose-dependently ulcer index in mice with gastric ulcers induced by oral ethanol. Data were expressed as mean ± SD (n = 10) and analyzed with one-way ANOVA followed by LSD with SPSS (Version 20.0). The asterisk * stands for P < 0.05 compared with model control (gastric ulcer mice treated with normal saline). Superscripts were the protection percentage of gastric ulcer in each dosage group.

Fig. 2

BJOE administration reduces dose-dependently ulcer index in mice with gastric ulcers induced by aspirin. Data were expressed as mean ± SD (n = 10) and analyzed with one-way ANOVA followed by LSD with SPSS (Version 20.0). The asterisk * stands for P < 0.05 compared with model control (gastric ulcer mice treated with normal saline). Superscripts were the protection percentage of gastric ulcer in each dosage group.

Fig. 3

Slices of the mouse stomach mucus which is subjected to the gastric ulcer induced by aspirin. Samples are from the mice with the gastric ulcer treated with saline (A), BJOE 0.2, 0.4 and 0.8 ml/kg (B, C, D) and cimetidine 200 mg/kg (E), respectively. The slices are stained with hematoxylin and eosine and then examined under optical microscope (40×). Mucosa desquamation (white arrows); Edematous mucosa (black arrows); Local disruption of gastric mucosa (yellow arrows); Undamaged gastric mucosal architecture (arrowheads).

Fig. 4

BJOE administration reduces dose-dependently ulcer index in mice with gastric ulcers induced by reserpine. Data were expressed as mean ± SD (n = 10) and analyzed with one-way ANOVA followed by LSD with SPSS (Version 20.0). The single asterisk * stands for P < 0.05 and the double asterisks **P < 0.01 compared with model control (gastric ulcer mice treated with normal saline). Superscripts were the protection percentage of gastric ulcer in each dosage group.

Fig. 5

Slices of the mouse stomach mucus which is subjected to the gastric ulcer induced by reserpine. Samples are from the mice with the gastric ulcer treated with saline (A), BJOE 0.4 and 0.8 ml/kg (B and C) and cimetidine 200 mg/kg (D), respectively. The slices are stained with hematoxylin and eosine and then examined under optical microscope (40×). Gastric mucosal desquamation or atrophy (white arrows); Disruption in the region of the gastric mucosa with epithelial cell loss (yellow arrows); Well-organized glandular structures (arrowheads).

Fig. 6

BJOE administration reduces dose-dependently ulcer index in mice with gastric ulcers induced by restraint plus water immersion. Data were expressed as mean ± SD (n = 10) and analyzed with one-way ANOVA followed by LSD with SPSS (Version 20.0). The double asterisks ** stands for P < 0.01 compared with model control (gastric ulcer mice treated with normal saline). Superscripts were the protection percentage of gastric ulcer in each dosage group.

Fig. 7

Inhibition of BJOE on the incidence of gastric ulcer in rats with lesion induced by glacial acetic acid (n = 11–13). Incidence rate of gastric ulcer in each group was showed at the upside.

Fig. 8

BJOE administration reduces dose-dependently ulcer index in rats with gastric ulcers induced by pylorus ligation. Data were expressed as mean ± SD (n = 9–10) and analyzed with one-way ANOVA followed by LSD with SPSS (Version 20.0). The single asterisk * stands for P < 0.05 and the double asterisks **P < 0.01 compared with model control (gastric ulcer rats treated with normal saline). Superscripts were the protection percentage of gastric ulcer in each dosage group.

Fig. 9

Slices of the rat stomach which is subjected to the gastric ulcer induced by pyloric ligation. Samples are from rats with gastric ulcer treated with saline (A), BJOE 0.5 and 1.0 ml/kg (B, C) and cimetidine 140 mg/kg (D), respectively. The slices are stained with hematoxylin and eosine and then examined under optical microscope (40×). Inflammation and polymorphonuclear infiltrate (white arrows); Gastric mucosal desquamation (black arrows); Local disruption of the gastric mucosa (yellow arrows).