MODULATORY ROLE OF N-ACETYL-CYSTEINE ON GASTRIC MUCOSAL LESION AND HAEMATO-BIOCHEMICAL CHANGES IN ALBINO WISTAR RATS SUBJECTED TO INDOMETHACIN TREATMENT

Abstract

Gastric ulcer is caused by multifaceted etiological factors such as environmental and
indiscriminate use of non-steroidal anti-inflammatory drugs (NSAIDs) such as
Indomethacin. N-acetyl-cysteine (NAC) is an antioxidant that protects the lipid biomembrane
against oxidative stress. This study investigated the effect of NAC on
gastric mucosal lesion and haemato-biochemical changes in albino Wistar rats
subjected to indomethacin treatment. Twenty (20) adult male rats, were divided into
five (5) groups; Group I (Control): Were administered with distilled water/kg/Bdw,
Group II: Indomethacin 40 mg/kg in 0.5 % carboxymethylcellulose (Ulcer group),
Group III: Received 2.5 ml/kg of 0.5% CMC, Group IV: Received NAC 500
mg/kg/Bdw orally + Indomethacin (500 mg/kg), Group V: Received Ranitidine 50
mg/kg/Bdw + Indomethacin (40 mg/kg). All treatment lasted for 7 days. Three hours
after last treatment, rats were humanely sacrificed. The stomach and blood samples
were collected for physical and biochemical analysis. Data was analysed using
ANOVA and p < 0.05 was considered significant. The P index of NAC in
indomethacin induced ulcer is found to be 75 %. A significant increase (p < 0.05) in
final body weight was observed in Indomethacin group, when compared to the control,
CMC and Ranitidine + Indomethacin groups. A significant (p < 0.05) increase in
inducible nitric oxide synthase (INOS) concentration was observed in all treatment
group, when compared to the control. In conclusion, we surmise that acute
administration of Indomethacin increased body weight of rats, which was decreased by
CMC and Ranitidine treatments, while NAC treatment failed to improve haematobiochemical
changes in adult Wister rats.