Effects of β-Glucan Pretreatment on Acetylsalicylic Acid-Induced Gastric Damage: An Experimental Study in Rats

BACKGROUND: NSAIDs have been found to induce gastrointestinal tract damage. Recently, it has been suggested that this might be mediated by lipid peroxidation. OBJECTIVE: The aim of this study was to assess the potential protective effects of beta-glucan against acetylsalicylic acid (ASA)-induced gastric damage by means of its antioxidant capacity in an experimental rat model. METHODS: Thirty-two male Wistar albino rats (200-250 g) were randomized into 4 groups consisting of 8 rats each. The beta-glucan group received 50 mg/kg beta-glucan once a day for 10 days and 30 minutes before anesthesia. The ASA group received saline once a day for 10 days and 300 mg/kg (20 mg/mL) ASA as a single dose, 4 hours before anesthesia. The ASA+beta-glucan group was administered 50 mg/kg beta-glucan once a day for 10 days and 30 minutes before anesthesia. Additionally, 300 mg/kg (20 mg/mL) ASA was administered as a single dose, 4 hours before anesthesia. The control group received saline once a day for 10 days and 30 minutes before anesthesia. All medications were administered by intragastric gavage. The stomach from each rat was dissected and divided into 2 parts for histologic and biochemical analysis. Gastric tissue malondialdehyde (MDA), nitric oxide (NO) levels, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were determined for oxidative parameter analysis. RESULTS: The gastroprotective and antioxidant effects of beta-glucan appeared to attenuate the ASA-induced gastric tissue damage. Compared with the control group, MDA and NO levels and CAT and GSH-Px activities were significantly increased in the stomachs of ASA-treated rats (MDA, 4.12 [0.44] to 13.41 [1.05] mu mol/L; NO, 8.04 [7.25-9.10] vs 30.35 [22.34-37.95] mu mol/g protein; CAT, 0.050 [0.004] to 0.083 [0.003] k/g protein; GSH-Px, 0.57 [0.42-0.66] to 1.55 [1.19-1.76] U/L; all, P < 0.001), whereas SOD activity was significantly decreased in the same group (291 [29] to 124 [61 U/mL; P < 0.001). In the ASA+beta-glucan group, MDA and NO levels and CAT and GSH-Px activities were found to be significantly lower, while SOD activity was found to be significantly higher, in comparison with the ASA-treated group (all, P < 0.001). CONCLUSION: beta-Glucan appeared to attenuate the gastric damage caused by ASA in these rats. (Curr Ther Res Clin Exp. 2010;71:369-383) (C) 2010 Elsevier HS Journals, Inc.