title: Effects of β-glucan pretreatment on acetylsalicylic acid-induced gastric damage: An experimental study in rats.
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).
  
  
  CONCLUSIONS
  β-Glucan appeared to attenuate the gastric damage caused by ASA in these rats.
authors.affiliation: Department of General Surgery, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
authors.forename: Orhan Veli
authors.initials: OV
authors.lastname: Ozkan
authors.affiliation: Department of Biochemistry, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
authors.forename: Oktay Hasan
authors.initials: OH
authors.lastname: Ozturk
authors.affiliation: Department of Physiology, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
authors.forename: Mehmet
authors.initials: M
authors.lastname: Aydin
authors.affiliation: Department of Biochemistry, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
authors.forename: Nigar
authors.initials: N
authors.lastname: Yilmaz
authors.affiliation: Department of General Surgery, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
authors.forename: Ibrahim
authors.initials: I
authors.lastname: Yetim
authors.affiliation: Department of Histology and Embryology, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
authors.forename: Ahmet
authors.initials: A
authors.lastname: Nacar
authors.affiliation: Department of Pharmacology, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
authors.forename: Suleyman
authors.initials: S
authors.lastname: Oktar
authors.affiliation: Department of Biochemistry, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
authors.forename: Sadik
authors.initials: S
authors.lastname: Sogut
keywords: acetylsalicylic acid; gastric damage; lipid peroxidation; β-glucan