ABSTRACT
<p><b>OBJECTIVE</b>To study the influence of SGHWJN particles on inflammation and the mediators of inflammation in esophageal tissues of rat with reflux esophagitis.</p><p><b>METHOD</b>Fifty SD rats were randomly divided into 5 groups, namely, a control group, a sham-operated group, a model group, a SGHWJN particles group and a PPI group. Reflux esophagitis was induced by adopting partial pyloric ligation plus cardiomyotomy. One week later, the rats were orally administered twice daily for 28 days. Pathological changes of esophagus mucous membrane were evaluated by using HE staining and Harry S. Cooper's method in every groups. MDA and SOD contents in esophageal tissues were measured by colorimetric method. Expression of TNF-alpha in esophageal tissues were examined by real-time fluorescent quantitative reverse transcriptase polymerase chain reaction (RT-FQ-PCR) with SYBR Green.</p><p><b>RESULT</b>Model group, esophageal inflammation scores, expression of TNF-alpha in esophageal tissues and MDA contents compared with the normal group and sham operation group were significantly higher (P < 0.05). SOD contents in the esophageal tissues of the model group was significantly lower than that of control group and sham-operated group (P < 0.05). SGHWJN particles group and PPI group of esophageal tissue inflammation scores, expression of TNF-a in esophageal tissues and MDA levels than those in model group decreased significantly (P < 0.05). SOD content was significantly higher than that of model group (P < 0.05), SGHWJN particles group and PPI group showed no statistically significant difference between the above-mentioned indicators. The above-mentioned indicators showed no statistically significant difference between the normal group and sham-operated group. MDA content and expression of TNF-alpha in esophageal tissue was positively correlated with inflammatory scores of model group (r = 0.813). Model group esophageal tissue SOD content and inflammation scores were negatively correlated (r = -0.847). Esophageal tissue SOD levels were negatively correlated with MDA levels (r = -0.863).</p><p><b>CONCLUSION</b>SGHWJN particles can effectively inhibit inflammation in rat with reflux esophagitis through regulating TNF-alpha, SOD and MDA.</p>
Subject(s)
Animals , Female , Humans , Male , Rats , Disease Models, Animal , Drugs, Chinese Herbal , Esophagitis, Peptic , Drug Therapy , Genetics , Allergy and Immunology , Esophagus , Allergy and Immunology , Gene Expression , Inflammation Mediators , Allergy and Immunology , Rats, Sprague-Dawley , Tumor Necrosis Factor-alpha , Genetics , Allergy and ImmunologyABSTRACT
Objective To detect the expressions of interleukin-17(IL-17) and interleukin-23(IL-23) in esophageal tissues of rats with reflux esophagitis(RE) and explore the role of IL-23/IL-17 axis in the pathogenesis of RE.Methods Thirty SD rats were randomly divided into 3 groups,namely,control group,sham-operated group and model group.RE was induced by adopting partial pyloric ligation plus cardiomyotomy.Then rats in each group were fasted for 24 h but had free access to water.They were fed 24 h after operation.Four weeks later,rats were killed and pathological changes of esophagus mucous membrane were observed by HE staining in each group.The expressions of IL-23p19 and IL-17 mRNA in esophageal tissues were examined by real-time fluorescent quantitative reverse transcriptase polymerase chain reaction(RT-FQ-PCR).IL-17 protein content in esophageal tissues was measured by ELISA.Results After four weeks,compared with control group,model group had significant pathological changes of esophagus mucous membrane.Expressions of IL-23p19 and IL-17 mRNA in the esophageal tissues of model group were significantly higher than those of the other two groups;the content of IL-17 protein was significant higher in model group than in the other two groups.There were no significant differences between control group and sham-operated group.Conclusion IL-23/IL-17 axis is an important cellular factor involved in the pathogenesis of RE and may be involved in the chronic inflammation of RE.