Effect of Helicobacter pylori on cyclooxygenase-2 and inducible nitric oxide synthase in patients with gastric precancerous lesions and its clinical significance.

Abstract

The aim of this study was to investigate the effect of Helicobacter pylori (Hp) on cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) levels in patients with gastric precancerous lesions and its clinical significance. A total of 114 patients with gastric precancerous lesions, 57 whom were positive for Hp (observation group) and 57 of whom were negative for Hp (control group), were selected for the study. The mRNA levels of COX-2 and iNOS in the gastric precancerous lesion tissue from the two groups of patients were analyzed through the reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The protein expression levels of COX-2 and iNOS were analyzed using western blotting and an iNOS kit, respectively. In addition, normal human gastric mucosal GES-1 cells were cultured in vitro and stimulated by Hp for 3, 6, 9 and 12 h. The variations in the mRNA and protein levels of COX-2 and iNOS were then analyzed via RT-qPCR and western blotting. Compared with the control group, the mRNA levels of COX-2 and iNOS in the gastric tissue from the observation group were significantly increased (P<0.05). Furthermore, the expression level of COX-2 and iNOS protein in the gastric tissue from the observation group was significantly higher than that in the tissue from the control group (P<0.05). In vitro analysis showed that the COX-2 and iNOS mRNA and protein levels were significantly increased in the Hp-stimulated normal human gastric mucosal GES-1 cells compared with those in the unstimulated cells. Furthermore, the effect was time-dependent (P<0.05). In conclusion, COX-2 and iNOS are the main inflammatory markers. Hp can induce high expression levels of COX-2 and iNOS in gastric precancerous lesion tissue, which may be associated with the occurrence and development of gastric precancerous lesions.