磷酸铝凝胶、康复新液对溶血卵磷脂相关反流性食管炎模型大鼠食管组织学和IL-8、PGE2的影响

目的探讨磷酸铝凝胶、康复新液对溶血卵磷脂相关反流性食管炎模型大鼠食管组织学结构和组织IL-8、PGE2含量的影
响及其可能的作用机制。方法60只SD大鼠，随机分为磷酸铝组（n=10）、康复新组（n=10）、磷酸铝+康复新组（n=10）、模型组
（n=20）、对照组（n=10），采用食管灌注1.5 mg/L溶血卵磷脂+0.1 mol/L HCI（含0.5%胃蛋白酶）方法制备溶血卵磷脂相关反流性
食管炎模型，对照组灌注液为等量生理盐水，连续14 d，处死10只模型组大鼠和全部对照组大鼠并取出完整食管，剩余4组大鼠
分别予磷酸铝凝胶、康复新液、磷酸铝凝胶+康复新液、生理盐水经食管灌注干预治疗14 d，处死所有大鼠并取出完整食管，分别
检测食管组织一般形态学、超微形态学和放免法检测组织IL-8、PGE2含量。结果模型制备结束时模型组与对照组组织形态学
比较：模型组一般形态学表现为粘膜及粘膜下层大量炎症细胞浸润，上皮细胞空泡变性、糜烂甚至溃疡形成，超微结构改变表现
为粘膜上皮细胞呈大片脱落，对照组的一般形态学和超微结构均正常。治疗结束时各治疗组和模型组比较：各治疗组食管的一
般形态学、超微结构显示粘膜损伤程度较轻，粘膜损伤指数、食管组织IL-8、PGE2含量均较模型组低（P<0.05）。磷酸铝+康复新
组分别与磷酸铝组、康复新组比较：食管组织的一般形态学、超微结构显示粘膜损伤程度均较轻，粘膜损伤指数、IL-8、PGE2含
量均低（P<0.05）。结论康复新液、磷酸铝凝胶对溶血卵磷脂与盐酸联合灌注所致反流性食管炎模型大鼠的食管组织具有保护
作用，其机制可能与其降低IL-8、PGE2水平、阻止炎症发生及发展有关，溶血卵磷脂与盐酸在十二指肠胃食管反流中作为混合
反流物引起GERD，其致病机制可能与上调食管组织的IL-8、PGE2的含量相关。

Effect of aluminum phosphate gel and Kangfuxin on esophageal pathology and IL-8 and PGE2 expressions in a rat model of reflux esophagitis

Objective To explore the effect of aluminum phosphate gel and Kangfuxin on esophageal pathology and expressions
of interleukin-8 (IL-8) and prostaglandin E2 (PGE2) in rats with reflux esophagitis and explore the possible mechanisms.
Method Sixty SD rats were randomized into aluminum phosphate gel group (n=10), Kangfuxin group (n=10), aluminum
phosphate gel+Kangfuxin group (n=10), model group (n=20), and control group (n=10). Except for those in the control group,
all the rats were subjected to infusion of diluted lysolecithin with hydrochloric acid in the esophagus for 14 days. Ten rats in
the model group and those in the control group were sacrificed to examine the pathological changes and contents of IL-8 and
PGE2 in the esophagus using optical and electron microscopes and radioimmunoassay. The next day the rest rats were given
corresponding treatments (saline in model group) administered into the esophagus on a daily basis for 14 days, after which
esophageal pathologies and IL-8 and PGE2 contents were examined. Results The model rats showed obvious esophageal
pathologies including inflammatory cell infiltration, vacuolar degeneration of the epithelial cells, esophageal erosion and even
ulceration, with severe detachment of the epithelial cells. The rats in all the intervention groups showed lessened esophageal
pathologies and lowered esophageal IL-8 and PGE2 contents compared with those in the model group. Esophageal mucosal
injury index and IL-8 and PGE2 contents were all significantly lower in rats receiving combined treatment with aluminum
phosphate and Kangfuxin than in those receiving either of the treatments (P<0.05). Conclusion Both Kangfuxin and aluminum
phosphate gel are effective in the treatment for reflux esophagitis induced by lysolecithin and hydrochloric acid, and their
therapeutic effects are achieved possibly by reducing IL-8 and PGE2 levels in the esophagus.