Gastroprotective Effect of Microencapsulated Myrtus communis Essential Oil against Ethanol/HCl-Induced Acute Gastric Lesions

Abstract

Myrtus communis L. essential oil (EO), mainly composed of myrtenyl acetate (30.6%), linalool (14.9%), α-pinene (11.10%) and 1,8-cineole or eucalyptol (9.9%), was microencapsulated with maltodextrin by emulsification and spray-drying, reaching a yield and efficiency of 43.7 and 48.7%, respectively. The microencapsulated myrtle EO (MMEO) was then evaluated regarding its gastroprotective activity in a model of ethanol/HCl-induced acute gastric ulcer in Wistar rats. Pretreatment with MMEO induced a remarkable inhibition of gastric lesions and acidity, correlated to high healing and protection percentages. Moreover, it exerted a potent anti-inflammatory effect on the gastric mucosa, counteracting EtOH-induced gastric lipoperoxidation and preventing the depletion of the antioxidant enzyme activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Taken together, the gastroprotective action of encapsulated MMEO may be multi-factorial, and ascribable, at least in parts, to its anti-inflammatory and antioxidant properties.

Keywords: Myrtus communis; anti-inflammatory; essential oil; gastroprotective activity; microencapsulation; spray drying.

Figure 1

GC-MS chromatogram of Myrtus communis essential oil.

Figure 2

Photomicrographs showing mucosal surface of rat stomach, (A) stomach from control rat, (B) Stomach from rat treated with EtOH/HCl. Arrows indicate hemorrhage sites. (C–E) Stomach from rat treated with 250, 500 and 1000 mg/kg of MMEO, respectively + EtOH/HCl. (F) rat treated with 20 mg/Kg of famotidine + EtOH/HCl. Bar: 1 cm.

Figure 3

Histological findings of rat gastric mucosa. (A) stomach from control rat. (B) Stomach from rat treated with EtOH/HCl. Exacerbation of necrosis of surface mucus cells and glands, hemorrhage in mucosal layer and edema of submucosal layer were observed. (C–E) Stomach from rat treated with 250, 500 and 1000 mg/kg of MMEO, respectively + EtOH/HCl. Dose dependent reduced injuries were observed. (F) Rat treated with 20 mg/Kg of famotidine + EtOH/HCl. No obvious injuries are recognized in mucosal layer. Bar: 100 µm. M: mucosal layer; SM: submucosal layer.

Figure 4

Principal component analysis (PCA) of the oral pre-treatment with microencapsulated M. communis essential oil (MMEO) showing the correlation between essential oil components and anti-inflammatory parameters. The first two components (PCs) contributed 98.41% to cumulative variance, with PC1 (F1 axis) and PC2 (F2 axis) explaining 72.85 and 25.56% of the total variance.

Figure 5

The effect of oral pre-treatment of ulcerated rat with microencapsulated M. communis essential oil (250, 500 and 1000 mg/kg MMEO) and famotidine, on nitric oxide (NO) production in gastric homogenate. Values are the means of three replicates and standard deviation. Values with different superscripts (a, b, c and d) are significantly different at p < 0.05.

Figure 6

Effect of oral pre-treatment with microencapsulated M. communis essential oil (MMEO, 250, 500 and 1000 mg/Kg) on MDA concentration (A), and superoxide dismutase (SOD) (B), catalase (CAT) (C) and glutathione peroxidase (GP_X) (D) activities. Values are the means ± SD of three independent assays. Values with different superscripts (a–e) are significantly different at p < 0.05 as compared to control group.