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. 2006 Jul 21;12(27):4318-24.
doi: 10.3748/wjg.v12.i27.4318.

Reversing gastric mucosal alterations during ethanol-induced chronic gastritis in rats by oral administration of Opuntia ficus-indica mucilage

Affiliations

Reversing gastric mucosal alterations during ethanol-induced chronic gastritis in rats by oral administration of Opuntia ficus-indica mucilage

Ricardo Vázquez-Ramírez et al. World J Gastroenterol. .

Abstract

Aim: To study the effect of mucilage obtained from cladodes of Opuntia ficus-indica (Cactaceae) on the healing of ethanol-induced gastritis in rats.

Methods: Chronic gastric mucosa injury was treated with mucilage (5 mg/kg per day) after it was induced by ethanol. Lipid composition, activity of 5'-nucleotidase (a membrane-associated ectoenzyme) and cytosolic activities of lactate and alcohol dehydrogenases in the plasma membrane of gastric mucosa were determined. Histological studies of gastric samples from the experimental groups were included.

Results: Ethanol elicited the histological profile of gastritis characterized by loss of the surface epithelium and infiltration of polymorphonuclear leukocytes. Phosphatidylcholine (PC) decreased and cholesterol content increased in plasma membranes of the gastric mucosa. In addition, cytosolic activity increased while the activity of alcohol dehydrogenases decreased. The administration of mucilage promptly corrected these enzymatic changes. In fact, mucilage readily accelerated restoration of the ethanol-induced histological alterations and the disturbances in plasma membranes of gastric mucosa, showing a univocal anti-inflammatory effect. The activity of 5'-nucleotidase correlated with the changes in lipid composition and the fluidity of gastric mucosal plasma membranes.

Conclusion: The beneficial action of mucilage seems correlated with stabilization of plasma membranes of damaged gastric mucosa. Molecular interactions between mucilage monosaccharides and membrane phospholipids, mainly PC and phosphatidylethanolamine (PE), may be the relevant features responsible for changing activities of membrane-attached proteins during the healing process after chronic gastric mucosal damage.

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Figures

Figure 1
Figure 1
Representative micrographs of gastric mucosa of rats with gastritis and treated with mucilage. A: control animals; B: animals subjected to gastritis (T0); C: animals 24 h after ethanol withdrawal. In micrographs B and C, the presence of PMN infiltrate is shown by large arrows in the insets; D: histological profile of the spontaneous recovery of gastric mucosa 72 h after ethanol withdrawal (arrows: PMN); E: histological profile corresponding to similar conditions after treated with mucilage (3 doses).
Figure 2
Figure 2
Total phospholipids and cholesterol in plasma membranes of mucilage-treated rats with gastritis (A) and the phosphatidylcholine (PC)/phosphatidylethanolamine (PE) methylation ratio (B) and cholesterol (chol)/total phospholipids (total phosp) ratio (C). In all cases mean ± SE, n = 5. Animals subjected to gastritis are represented by empty symbols while those treated with mucilage are represented by solid symbols. bP < 0.01 vs healthy animal control. dP < 0.01 vs animals with gastritis not treated with mucilage.
Figure 3
Figure 3
Effects of gastritis and mucilage from O. ficus-indica on cytoplasmic specific ADH and LDH activities. The results are expressed as mean ± SE of five individual observations per experimental group for the alcohol (ADH) and lactate (LDH) dehydrogenases in the cytosolic fraction. Statistical significance is shown in Figure 2.
Figure 4
Figure 4
Activity of 5’-nucleotidase and its relation with the cholesterol/ phospholipid ratio in plasma membranes of mucilage-treated rats with gastritis. Left panel represents the mean ± SE of five individual observations per experimental group for 5’-nucleotidase activity. The correlation between activity of this enzyme and the PC/PE ratio or the cholesterol (chol)/phospholipid (phos) ratio is shown in the right panel of Figure 2. Statistical significance is indicated in the left panel of Figure 2.

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