环氧合酶-2在反流性食管炎大鼠食管组织中表达的实验研究

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背景:环氧合酶(COX)-2在炎症、肿瘤等的发生、发展过程中发挥重要作用,但其在反流性食管炎(RE)中的作用尚未明确。目的:研究COX-2在混合性RE大鼠食管组织中的表达,探讨COX-2的表达与RE的关系。方法:采用贲门肌切开术加十二指肠半结扎术建立混合性RE大鼠模型。22只健康Sprague-Dawley大鼠随机分为RE模型组(n=12)和假手术组(n=10),于术前和术后1周测定食管下段和胃液pH值。处死大鼠,分别应用放射免疫测定和免疫组化方法检测食管组织中前列腺素(PG)E2的含量和COX-2的表达,光镜观察食管组织的形态学改变。结果:RE模型组术后食管下段pH值显著低于假手术组(P<0.05),胃液pH值则显著高于假手术组(P<0.05);食管组织PGE2含量亦较假手术组显著增高(P<0.001),COX-2表达均为阳性,假手术组食管组织中无COX-2表达。光镜观察显示RE模型组食管黏膜病理损害明显。结论:COX-2高表达和PGE2含量增高参与了混合性RE的发生、发展过程,COX-2可能通过升高PGE2含量而在RE的发病中起重要作用。 BACKGROUND Cyclooxygenase (COX) -2 plays an important role in the development and progression of inflammation and tumor, but its role in reflux esophagitis (RE) has not been clarified. Objective: To investigate the expression of COX-2 in esophageal tissue of mixed RE rats and to explore the relationship between COX-2 expression and RE. Methods: A mixed RE rat model was established by cardiomyotomy and duodenal ligation. Twenty-two healthy Sprague-Dawley rats were randomly divided into RE model group (n = 12) and sham operation group (n = 10). The lower esophageal and gastric fluid pH values ​​were measured preoperatively and one week after surgery. The rats were sacrificed and the contents of prostaglandin (PG) E2 and the expression of COX-2 in esophageal tissues were detected by radioimmunoassay and immunohistochemistry respectively. Morphological changes of esophageal tissues were observed under light microscope. Results: The pH value of esophageal lower segment in RE model group was significantly lower than that in sham operation group (P <0.05), while the pH value in gastric juice group was significantly higher than that in sham operation group (P <0.05). The content of PGE2 in esophageal tissue was also significantly increased (P <0.001). The expression of COX-2 in the sham-operation group was no expression of COX-2 in the esophageal tissue. Light microscope observation showed that the pathological changes of esophageal mucosa in RE model group were obvious. CONCLUSION: COX-2 overexpression and increased PGE2 content are involved in the development and progression of mixed RE. COX-2 may play an important role in the pathogenesis of RE by increasing PGE2 content.
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