The therapeutic potential of Salvia aegyptiaca extracts in ethanol-induced gastric ulcer: insights into macroscopic, histopathological, and biochemical mechanisms

Abstract

Background/aim: This study explores the antiulcer activity of different doses of Salvia aegyptiaca (SAE) methanol (ME) and decocted extracts (DE) on ethanol-induced gastric ulcers in rats.

Materials and methods: Female Wistar rats weighing 180-200 g were divided into five groups: control, omeprazole (positive control), and extract-treated (100, 200, and 400 mg/kg). Ulcers were induced with absolute ethanol 30 min after treatment with the extracts. The experiment was followed by macroscopic and histopathological examination. In vitro tests were also conducted to assess lipid peroxidation, catalase activity, mucus content, glutathione, and protein levels.

Results: The study found that 100% ethanol caused significant damage, including colour and mucus loss, petechiae, haemorrhages, and oedema. However, pretreatment with ME SAE or DE SAE at doses of all three levels reduced the ethanol-induced damage. Histopathological analysis revealed reduced signs of haemorrhagic lesions, infiltration, and oedema in rats treated with ME SAE or DE SAE at doses of 100 or 200 mg/kg, whereas the 400 mg/kg dose provided complete protection. Comparable to the use of omeprazole, ingestion of DE SAE at doses of 100, 200, or 400 mg/kg demonstrated substantial protection against stomach ulcers produced by ethanol, with a range of 76%-84%. Both SAE extracts induced a dose-dependent increase in glutathione levels, with DE SAE showing a significant rise at 200 and 400 mg/kg.

Conclusion: The SAE extracts demonstrated a significant decrease in gastric lipid peroxidation, outperforming the effect of omeprazole.

Keywords: Salvia aegyptiaca; antioxidant enzyme; gastric ulcer; lipid peroxidation.

Figure 1

The effect of SAE on the visual characteristics of the stomach mucosa in gastric ulcers caused by ethanol. 1: control, 2: ethanol 100%, 3: omeprazole 5 mg/kg, (4–6): ME SAE at 100, 200, and 400 mg/kg doses, respectively, (7–9): DE SAE at 100, 200, and 400 mg/kg doses, respectively.

Figure 2

Histological assessment of the preventive effect of SAE against ethanol-induced GU at 100× magnification. Red arrows indicate damage to the epithelial barrier, and black arrows indicate infiltration of inflammatory cells.

Figure 3

The impact of SAE on the stomach mucosa in ethanol-induced GU. ME: methanolic extract, DE: decocted extract. Results are represented as average % ± SEM, # indicates p ≤ 0.05 vs omeprazole, and ns means not significant.

Figure 4

The impact of SAE on stomach mucus content. ME: methanolic extract, DE: decocted extract. Results are represented as average % ± SEM. ** indicates p < 0.001, and *** indicates p < 0.002 vs. CMC 1.5%. $ indicates p ≤ 0.05 vs. 400 mg/kg, and ns means not significant.

Figure 5

The impact of SAE on protein concentration. ME: methanolic extract, DE: decocted extract. Results are represented as an average % ± SEM. $$ indicates p ≤ 0.001 vs. 100 mg/kg, ### indicates p ≤ 0.0002 vs. omeprazole, and ns means not significant.

Figure 6

The effect of SAE on CAT activity. ME: methanolic extract, DE: decocted extract. Results are represented as average % ± SEM. **** indicates p ≤ 0.0001 vs. CMC 1.5%, $$$ indicates p ≤ 0.0002 vs. 100 mg/kg, # indicates p ≤ 0.05 vs. omeprazole, and ns means not significant.

Figure 7

The effect of SAE on GSH level. ME: methanolic extract, DE: decocted extract. Results are represented as average % ± SEM. * indicates p ≤ 0.05 vs. CMC 1.5%, and ns means not significant.

Figure 8

The effect of SAE on lipid peroxidation. ME: methanolic extract, DE: decocted extract. Results are represented as average % ± SEM. **** indicates p ≤ 0.0001 vs CMC 1.5%, #### indicates p ≤ 0.05 vs. omeprazole, and ns means not significant.