[Mechanism of exacerbation of colonic damage in experimental colitis treated with celecoxib].

OBJECTIVE: To assess the mechanism of exacerbation of colonic damage in rat colitis model induced by trinitrobenzene sulfonic acid (TNBS) treated with celecoxib (a selective COX-2 inhibitor). METHODS: The rats were randomized into four groups. Group 1 and Group 2 were study groups. Group 3 and Group 4 were control groups. Colitis was induced by intracolonic administration of TNBS (25 g/L) in a vehicle of 50% ethanol (0.25 mL) of study groups. The rats of study groups were treated orally, beginning 3 h before induction of colitis and continuing twice per day thereafter for up to 7 d, with celecoxib (1.25 mg/kg, Group 1) and distilled water (1 mL/0.3 kg, Group 2) respectively. In control experiments, the rats of Group 4 were treated orally with celecoxib (1.25 mg/kg) twice per day for up to 7 d. Group 3 rats were healthy control rats. All the rats that survived until the end of the experiment (d 7) were killed and the severity of colonic inflammation was assessed. The COX-2 protein expression in colon tissues was examined by immunohistochemistry. RESULTS: The colonic damage of Group 1 was exacerbated as compared with Group 2. The inflammatory index of colon tissues of Group 1 (8.5+/-2.5) was significantly reduced, as compared with Group 2 (13.5+/-1.9, P<0.05). The levels of COX-2 protein expression was decreased significantly in Group 1 (3.7 x 10(-2)+/-9.5 x 10(-3)) as compared with Group 2 (11.4 x 10(-2)+/-3.8 x 10(-2), P<0.05). The positive rate of COX-2 expression in neural cells of the myenteric plexus in Group 1 (30%) was decreased as compared with Group 2 (90%, P<0.05). No difference was found in the inflammatory index, the levels of COX-2 protein expression and the positive rate of COX-2 expression in neural cells of the myenteric plexus of Group 3 and Group 4. CONCLUSION: Selective COX-2 inhibitor-celecoxib could decrease the expression of COX-2 in intestinal tissue, attenuate the inflammatory index of colon tissues of experimental colitis induced by TNBS. But the application of celecoxib resulted in exacerbation of colonic damage. These adverse events are probably relevant to the suppression of COX-2 expression in the neural cells of the myenteric plexus, leading to decrease of intestinal contractivity and peristalsis, enteroparalysis, megacolon and death of the rat.

[Distribution of Helicobacter pylori in stomach before and after the administration of Lansoprazole].

OBJECTIVE: To investigate the effect of the acid inhibitor-Lansoprazole on the distribution of Helicobacter pylori (H.pylori) in stomach. METHODS: Biopsy specimens were taken from the duodenal ulcer patients who underwent gastroscopy before and after the treatment of Lansoprazole. The biopsy specimens were taken from the lesser curvature of the antrum and the greater curvature of the corpus respectively. H&E and Warthin-Starry staining were used for detecting the changing of active gastritis and the positive rate of H.pylori. RESULTS: (1)The positive rates of H.pylori before treatment, 4 weeks after treatment and 3 months after treatment, in the lesser curvature of the antrum were 93.02%, 58.14%, and 86.05%, respectively. The positive rate and density of H.pylori 4 weeks after treatment were greatly decreased compared with those before treatment (P<0.001) and also lower than those 3 months after treatment (P<0.05). (2) The positive rate of H.pylori before treatment, 4 weeks after treatment and 3 months after treatment in greater curvature had differences without statistical significance. However, the density of H.pylori 4 weeks after treatment was increased compared with that before treatment. CONCLUSION: Lansoprazole can change the colonization site of H.pylori in the stomach, decrease the positive rate and the density of H.pylori in lesser curvature of the antrum, but increase the density of H.pylori in the greater curvature of the corpus. This effect is most obvious in one month after treatment. Active gastritis is related to H.pylori.

[Persistent intestinal motility disorder after transient intestinal nematode infection in rats].

OBJECTIVE: To investigate the intestinal motor function (distal colonic manometry and gastrointestinal transit time) after T. spiralis infection in rats. METHODS: Sprague-Dawley rats were infected by administering T. spiralis larvae. Rats were studied on 14, 42, and 56 days post-infection (PI). Age matched non-infected animals served as controls. All rats underwent colonic manometry and gastrointestinal transit time test. RESULTS: (1) The small intestinal inflammation became the most severe on day 14 PI, and returned to normal on day 56. (2) The distal colonic manometry showed significantly active motility in acute infected rats either at rest or upon balloon stimulating. (3) Rat colonic motility parameters were not different from those of the control rats either at rest or upon small volume (1mL) balloon stimulating on day 42 and day 56 PI. But when the balloon was inflated with 2 mL of air, the colonic activity increased significantly compared with that of the control. (4) Gastrointestinal transit time was slower in acute and PI rats than that in the control group. CONCLUSION: Intestinal motility function was abnormal persistently after transient intestinal nematode infection in rats either in distal colonic manometry or in gastrointestinal transit time.

[The value of autofluorescence spectrum analysis of gastric juice in diagnosing gastric carcinoma: a preliminary result].

OBJECTIVE: To reveal the difference of autofluorescence spectrums of gastric juice derived from malignancy and benignancy for screening and diagnosis of gastric carcinoma. METHOD: Gastric juice from 202 patients with different gastric diseases were collected, then detected their autofluorescence spectrums (the excitation wavelength is 288 nm, whereas the range of emission wavelength is 300 - 800 nm) after diluted by 1:10. The diagnostic model for gastric cancer was made by Classification and Regression Trees V2.0 software. RESULTS: There were three peaks (the emission wavelength were 320 - 360 nm, 576 nm and 670 - 690 nm respectively) in the autofluorescence spectrums of all patients, though the intensity of the first peak (with the emission wavelength of 320 - 360 nm) were enhanced distinctively in malignance than those in benignancy. The diagnostic model's sensitivity and specificity of prior probability were 91.4% and 83.2% respectively, whereas the sensitivity and specificity of posterior probability were 85.7% and 82.6%. CONCLUSION: Detection of autofluorescence spectrum of gastric juice has great prospect in the diagnosis and screening gastric carcinoma.