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目的通过观察盐酸戊乙奎醚(Pneheydidine hydrochloride,PHCD)对大鼠急性肺损伤中过氧化物酶增殖体激活受体-γ(PPAR-γ)和细胞间粘附分子-1(ICAM-1)的影响,探讨盐酸戊乙奎醚对急性肺损伤的保护作用。方法 32只SD大鼠随机分为正常组、致伤组、预处理组和治疗各8只。制备大鼠急性肺损伤模型,使用pH=1.25的盐酸,按照1.2ml/kg的剂量注入大鼠气管,建立大鼠胃内容物误吸模型。药物干预使用PHCD,观察实验组不同组间组织中PPAR-γ和ICAM-1的表达变化。结果与正常组相比,致伤组PPAR-γ表达明显降低,ICAM-1表达明显升高(P<0.01)。与致伤组比较,预处理组PPAR-γ表达升高,ICAM-1表达降低(P<0.01)。与致伤组比较,治疗组PPAR-γ表达升高,ICAM-1表达降低(P<0.01)。与治疗组相比,预处理组PPAR-γ表达升高,ICAM-1表达降低(P<0.05)。结论盐酸戊乙奎醚对急性肺损伤具有预防和治疗作用,且于疾病发生前应用效果更明显,其机制可能与上调机体PPAR-γ的表达并且抑制ICAM-1的表达有关。
Objective To observe the effects of Pneheydidine hydrochloride (PHCD) on the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) and intercellular adhesion molecule-1 (ICAM- To investigate the protective effect of penehyclidine hydrochloride on acute lung injury. Methods Thirty-two SD rats were randomly divided into normal group, injury group, pretreatment group and treatment group. The model of acute lung injury in rats was prepared. The rat gastric trachea was infused with hydrochloric acid (pH = 1.25) according to the dosage of 1.2ml / kg to establish rat aspiration model. PHCD was used for drug intervention to observe the changes of PPAR-γ and ICAM-1 in different groups of experimental groups. Results Compared with the normal group, the expression of PPAR-γ was significantly decreased and the expression of ICAM-1 was significantly increased in the injured group (P <0.01). Compared with the injury group, the expression of PPAR-γ in pretreatment group was increased and the expression of ICAM-1 was decreased (P <0.01). Compared with the injury group, the expression of PPAR-γ in the treatment group was increased and the expression of ICAM-1 was decreased (P <0.01). Compared with the treatment group, pretreatment group PPAR-γ expression increased, ICAM-1 expression decreased (P <0.05). Conclusion Penehyclidine hydrochloride can prevent and treat acute lung injury and its effect is more obvious before the onset of the disease. The mechanism may be related to up-regulating the expression of PPAR-γ and inhibiting the expression of ICAM-1.