Effects of β-glucan pretreatment on acetylsalicylic acid-induced gastric damage: An experimental study in rats

Orhan Veli Ozkan; Oktay Hasan Ozturk; Mehmet Aydin; Nigar Yilmaz; Ibrahim Yetim; Ahmet Nacar; Suleyman Oktar; Sadik Sogut

doi:10.1016/S0011-393X(10)80003-7

Effects of β-glucan pretreatment on acetylsalicylic acid-induced gastric damage: An experimental study in rats

Curr Ther Res Clin Exp. 2010 Dec;71(6):369-83. doi: 10.1016/S0011-393X(10)80003-7.

Authors

Orhan Veli Ozkan¹, Oktay Hasan Ozturk², Mehmet Aydin³, Nigar Yilmaz², Ibrahim Yetim¹, Ahmet Nacar⁴, Suleyman Oktar⁵, Sadik Sogut²

Affiliations

¹ Department of General Surgery, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
² Department of Biochemistry, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
³ Department of Physiology, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
⁴ Department of Histology and Embryology, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
⁵ Department of Pharmacology, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.

Abstract

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 β-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 β-glucan group received 50 mg/kg β-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+β-glucan group was administered 50 mg/kg β-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 β-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] μmol/L; NO, 8.04 [7.25-9.10] vs 30.35 [22.34-37.95] μmol/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 [6] U/mL; P < 0.001). In the ASA+β-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: β-Glucan appeared to attenuate the gastric damage caused by ASA in these rats.

Keywords: acetylsalicylic acid; gastric damage; lipid peroxidation; β-glucan.