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目的观察内毒素(ET)致兔急性肺损伤(ALI)后肺组织炎症反应指标及病理改变。探讨1,6-二磷酸果糖(FDP)对ET所致的兔ALI可能的保护性作用。方法24只大耳白兔随机分为对照组(A组)、ET致伤组(B组)、ET致伤+FDP干预组(C组),每组8只。A组仅注射生理盐水作为空白对照,B、C组经静脉一次性注射ET复制兔ALI模型,C组在ET致伤后静注FDP作干预。6h后处死动物,观察肺组织病理改变,并测定肺组织中脂质过氧化物(LPO)、血栓素B2(TXB2)、6-酮-前列腺素F1α(6-keto-PGF1α)和白介素13(IL-13)含量以及超氧化物歧化酶(SOD)活性。结果与A组相比,B组肺组织LPO和TXB2含量显著增高(P<0.05,P<0.01),SOD活性显著降低(P<0.05),6-keto-PGF1α和IL-13含量则无明显变化。C组LPO含量和SOD活性较A组无显著变化,而TXB2、6-keto-PGF1α和IL-13含量则较A组显著增加(P<0.01)。光、电镜下观察,A组肺组织结构基本正常,B组病理损害明显,C组损伤较轻。结论ALI过程中,氧化损伤、TXB2/6-keto-PGF1α比值失衡和保护性细胞因子分泌不足是导致肺组织病理损伤的重要因素。FDP可抑制氧化损伤,改善TXB2/6-keto-PGF1α平衡并促进保护性细胞因子分泌,从而在ET致兔ALI的过程中对肺组织起到一定的保护作用。
Objective To observe the lung tissue inflammation index and pathological changes after acute lung injury (ALI) induced by endotoxin (ET) in rabbits. To investigate the possible protective effect of 1,6-diphosphate (FDP) on ALI induced by ET in rabbits. Methods Twenty - four large white rabbits were randomly divided into control group (A group), ET - injured group (B group) and ET - injured group (F group) (C group). In group A, only saline was injected as a blank control group. Groups B and C were given a single intravenous injection of ET to replicate the rabbit ALI model, while group C received intravenous injection of FDP after ET injury. Six hours later, the animals were sacrificed and the pathological changes of the lung tissue were observed. The levels of LPO, TXB2, 6-keto-PGF1α and IL-13 IL-13) content and superoxide dismutase (SOD) activity. Results Compared with group A, the content of LPO and TXB2 in group B were significantly increased (P <0.05, P <0.01), the activity of SOD was significantly decreased (P <0.05), while the content of 6-keto-PGF1α and IL-13 in group B was not significantly Variety. There was no significant change in LPO content and SOD activity in group C compared with that in group A, while the content of TXB2, 6-keto-PGF1α and IL-13 in group C was significantly higher than that in group A (P <0.01). Light and electron microscopy, A group of lung tissue structure was normal, B group obvious pathological damage, C group lighter damage. Conclusion The oxidative damage, the imbalance of TXB2 / 6-keto-PGF1α ratio and the insufficient secretion of protective cytokines are the important factors that lead to the pathological damage of lung tissue in ALI. FDP can inhibit oxidative damage, improve the balance of TXB2 / 6-keto-PGF1α and promote the secretion of protective cytokines, which may play a protective role on lung tissue during ET induced rabbit ALI.