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目的探讨甘遂对重症急性胰腺炎(SAP)大鼠胰腺组织环氧合酶-2(COX-2)表达的影响及意义。方法将SD大鼠随机分为假手术组(S组)、SAP组、甘遂治疗组(K组),每组40只。建立SAP模型后K组立即给予甘遂灌胃(200 mg/kg体重),每8 h 1次。各组动物在术后2、6、12、24 h检测胰腺组织的COX-2 mRNA和蛋白表达、血浆TXB2和6-Keto-PGF1α水平、胰腺光镜和电镜检查。结果SAP组COX-2 mRNA和蛋白表达、血检查B2(TXB2)、6-酮-前列腺素F1α(6-Keto- PGF1α)水平及TXB2/PGF1α比值均显著高于S组(P<0.01)。K组6,12 h COX-2 mRNA表达显著低于SAP组(P<0.05);6、12、24h COX-2蛋白表达、TXB2及TXB2/PGF1α比值均显著低于SAP组(P<0.01)。TXB2/PGF1α比值与COX-2蛋白表达呈显著正相关(r=0.851,P<0.01)。K组胰腺组织损害较SAP组减轻,微血管内血栓较SAP组明显减少。结论SAP时有COX-2的高表达,甘遂可以下调COX-2的表达,减轻炎症反应,并可能通过纠正TXA2和PGI2之间的失衡改善胰腺微循环。
Objective To investigate the effect of kansui on the expression of cyclooxygenase-2 (COX-2) in pancreas of rats with severe acute pancreatitis (SAP) and its significance. Methods SD rats were randomly divided into sham operation group (S group), SAP group, and Ganzi treatment group (K group), 40 rats in each group. After the establishment of the SAP model, the K group was immediately given gavage (200 mg/kg body weight), once every 8 h. The levels of COX-2 mRNA and protein in pancreatic tissue, plasma TXB2 and 6-Keto-PGF1α levels, pancreatic light microscopy and electron microscopy were detected at 2, 6, 12 and 24 h after operation. Results The expression of COX-2 mRNA and protein, blood test B2 (TXB2), 6-keto-PGF1α and TXB2/PGF1α in SAP group were significantly higher than those in S group (P<0.01). The expression of COX-2 mRNA was significantly lower in K group than that in SAP group at 6 and 12 h (P<0.05), and the COX-2 protein expression, TXB2 and TXB2/PGF1α ratio were significantly lower than those in SAP group at 6, 12, and 24 h (P<0.01). . The ratio of TXB2/PGF1α was positively correlated with the expression of COX-2 protein (r=0.851, P<0.01). The damage of pancreatic tissue in group K was less than that in SAP group, and the micro-vessel thrombus was significantly reduced compared with SAP group. Conclusions There is a high expression of COX-2 in SAP. Ganzi can down-regulate the expression of COX-2 and reduce the inflammatory response, and may improve the pancreas microcirculation by correcting the imbalance between TXA2 and PGI2.