1,6-二磷酸果糖对内毒素损伤性肺组织的保护作用

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.

Protective effects of fructose-1,6-diphosphate on pulmonary tissue injured by endotoxin in rabbits

Objective To observe the pulmonary pathologic changes of endotoxin (ET)-induced acute lung injury (ALI) in rabbits and the potential protective effects of fructose-1,6-diphosphate (FDP) on the ET-induced ALI of rabbits. Methods 24 flap-eared albation rabbits were randomly assigned to 3 groups, 8 for each, as follows: control group (group A), ET-treated group (group B) and combination group (treated by ET and FDP, group C). ALI was induced by injection of ET at one time. Group A was only injected with placebo, normal saline. ET was given to the rest groups. In group C, FDP was given as an intervening measure after rabbits injured. Rabbits were sacrificed at 6h time point. The pulmonary pathologic changes were observed. Some markers of pulmonary tissues, including the content of lipid peroxide (LPO), thromboxane B2 (TXB2), 6-keto-prostaglandin F1α(6-keto-PGF1α), interleukin-13 (IL-13) and the activity of superoxide dismutase (SOD), were observed. Results Compared with group A, the contents of LPO and TXB2 of group B showed significant increase (P＜0.05, P＜0.01), the SOD activity of group B weakened obviously (P＜0.01), the contents of 6-keto-PGF1α and IL-13 showed no statistical differences. The LPO content and the SOD activity of group C were similar to those of group A, the contents of TXB2, 6-keto-PGF1α and IL-13 of group C were much higher than those of group A (P＜0.01). Estimated by light microscope and electron microscope, the structure of lung tissue of group A is basically normal, the pathologic injuries of lung tissue of group B were much more severer and that of group C were slighter. Conclusion In the progress of ET-induced ALI, the oxidative injury, imbalance of TXB2/6-keto-PGF1α ratio and the secretion deficiency of protective cytokines play important role in inducing pathologic injuries of lung tissues. FDP can inhibit oxidative injury, ameliorate TXB2/6-keto-PGF1α balance and promote the secretion of protective cytokines, which, in turn, can protect rabbits from ET-induced ALI to some extent.