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目的 比较特异性环氧合酶 2 (COX 2 )抑制剂西乐葆与传统非甾体抗炎药 (NSAIDs)对胃黏膜的损害。方法 分别以西乐葆、吲哚美辛复制大鼠NSAIDs性胃黏膜损伤模型 (n =8) ;以无水乙醇复制胃黏膜急性损伤模型 ,再以西乐葆灌胃 (n =8)。观察各组胃黏膜 6 酮 前列腺素F1α(6 keto PGF1α)、血栓素B2 (TXB2 )水平、损伤指数 (LI)及光镜、扫描电镜下的变化。结果 吲哚美辛组胃黏膜损害明显 (LI :13.38± 2 .0 6 ) ,6 keto PGF1α、TXB2 明显下降 (P <0 .0 1) ,抑制率分别为 81.6 %,81.8%,LI与 6 keto PGF1α、TXB2 水平呈负相关。西乐葆组 6 keto PGF1α、TXB2 无明显抑制 (P >0 .0 5 ) ,对健康胃黏膜无损害 (LI :0 ) ,但可加重乙醇诱导的胃损伤 (LI :37.19± 3.34比 19.90± 2 .2 8,P <0 .0 1)。结论 COX 1活性抑制是NSAIDs胃病的主要机制 ;特异性COX 2抑制剂西乐葆不造成健康鼠胃黏膜损伤 ,有较高的胃肠道安全性 ,但可加重原有胃损伤。
Objective To compare the gastric mucosal damage of the specific cyclooxygenase 2 (COX 2) inhibitor Celebrex and traditional non-steroidal anti-inflammatory drugs (NSAIDs). Methods Rats with NSAIDs gastric mucosa injury were induced by celecoxib and indomethacin, respectively. Acute gastric mucosa injury model was established by ethanol injection and celecoxib was given into the stomach (n = 8). The changes of 6 keto PGF1α, TXB2, injury index (LI) and light microscope and scanning electron microscope were observed in each group. Results The indometacin group had obvious gastric mucosal damage (LI: 13.38 ± 2.06), 6 keto PGF1α and TXB2 decreased significantly (P <0.01), and the inhibitory rates were 81.6% and 81.8% keto PGF1α, TXB2 levels was negatively correlated. Celebrex showed no significant inhibition on 6 keto PGF1α and TXB2 (P> 0.05), and no damage to healthy gastric mucosa (LI: 0), but could aggravate ethanol-induced gastric injury (LI: 37.19 ± 3.34 vs 19.90 ± 2 .2 8, P <0. 0 1). Conclusion COX-1 activity inhibition is the main mechanism of NSAIDs gastric diseases. Celebrex, a specific COX 2 inhibitor, does not cause gastric mucosal injury in healthy rats, and has high gastrointestinal tract safety, but aggravates the original gastric injury.