目的研究口服1,6二磷酸果糖(1,6-Fructose-diphosphate,FDP)对大剂量异丙肾上腺素所致大鼠脑组织损伤的保护作用,并探讨其保护作用机制.方法将Wistar大鼠随机分为3组,每组8只:(1)ISO组:给大鼠皮下注射异丙肾上腺素[isoproterenol,ISO,5 mg/(kg·d)],连续7 d;(2)FDP组:除注射异丙肾上腺素外,同时给予FDP灌胃[10 ml/(kg·d)],连续21 d;(3)对照组:给予等容积生理盐水皮下注射及灌胃.测定脑组织匀浆丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性和总抗氧化能力(T-AOC),用光镜、电镜观察脑组织形态学改变.结果ISO组、FDP组MDA含量均高于对照组,SOD活性均低于对照组,且脑组织有损害,海马神经元密度均较对照组降低,均P<0.01;但FDP组与ISO组比较,MDA含量低于ISO组,SOD活性和T-AOC均高于ISO组,均P<0.01;FDP组T-AOC与对照组接近,P>0.05,对脑组织的病理损害也较ISO组明显减轻.结论FDP可预防、治疗慢性心肌缺血坏死所致的缺血性脑组织损伤.FDP的神经保护机制可能与其抗氧化应激、抗自由基、增加细胞内能量、膜稳定等作用有关.%Abstract: Objective: To investigate whether 1,6 - Fructose - Diphosphate (FDP) plays a neuroprotectiverole on rat cerebral tissues in the chronic myocardial ischemia model induced by large dose of isoproterenol (ISO).Methods: 24 Wistar rats were randomly divided into 3 groups ( n = 8 ): ( 1 ) Isoproterenol - treated group ( ISO group) :The rats were injected subcutaneously with isoproterenol 5 mg/( kg · d) for 7 days; (2) FDP - treated group (FDP group): Except injection of isoproterenol, the rats were treated by FDP 10 ml/( kg · d) perfused into stomachs for 21 days; (3) Control group: without any special treatment. At the end of the experiment, the content of MDA, SOD activity and total anti - oxidation capacity ( T - AOC) of the brain tissue were examined. The brain tissue sam-ples were checked under light and electric microscopes. Results: It was found that the content of MDA was reduced and both the activities of SOD and T - AOC were enhanced after chronic myocardial ischemia in FDP group as com-pared with ISO group (P <0.01 ). The abnormalities of the neuropathology were also alleviated in the FDP- treated group. Conclusions:FDP has a certain protective effect on brain tissue damage induced by isoproterenol. This effect may relate to its antioxidant properties, reducing the lipoperoxidized reaction, improving cellular energy metabolism and stabilizing biomembrane.
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