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目的观察丹酚酸A(SAA)对Zucker糖尿病肥胖(ZDF)大鼠视网膜病变的干预作用,探讨SAA可能的作用机制。方法取7~8周龄雄性ZDF大鼠32只,Purina#5008饲料饲喂4周后,按血糖平均分为模型对照组,SAA高、低剂量组与二甲双胍(Met)组,每组8只。另取同龄雄性ZL大鼠8只作为正常对照。SAA低、高剂量组每日尾静脉注射SAA 0.5 mg/kg、1 mg/kg,Met组每日经口灌胃Met 200 mg/kg,连续给药12周,观察ZDF大鼠白内障发生率和视网膜病理学改变,并检测血糖血脂、糖化血红蛋白(Hb A1c)和血清白介素1(IL-1)、IL-6、氧化性低密度脂蛋白(ox-LDL)、丙二醛(MDA)含量和脂蛋白相关磷脂酶A2(Lp-PLA2)的活性,以及尿液中转铁蛋白(TRF)、视黄醇结合蛋白(RBP)的含量。结果模型对照组大鼠血糖、血脂及Hb A1c均上升,糖尿病性白内障发病率68.75%,视网膜基底增厚和微血管病变,血清IL-1、IL-6、ox-LDL和MDA含量和Lp-PLA2活性显著升高,尿液中TRF和RBP含量亦显著升高。给予SAA后,ZDF大鼠白内障发病率降低,视网膜病理学形态有不同程度的改善,血清IL-1、IL-6、ox-LDL、MDA含量和Lp-PLA2活性下降,尿液中TRF、RBP含量亦下降。结论 SAA能改善ZDF大鼠糖尿病视网膜病变,降低白内障发生率,其作用途径可能与抑制慢性炎症、防止脂质过氧化和降低Lp-PLA2活性有关。
Objective To observe the effect of salvianolic acid A (SAA) on retinopathy in Zucker diabetic and obese rats (ZDF) and to explore the possible mechanism of SAA. Methods 32 male ZDF rats aged 7-8 weeks were fed with Purina # 5008 for 4 weeks. The rats were divided into model control group, SAA high and low dose groups and metformin group according to the average blood glucose level, with 8 rats in each group . Another same age male ZL rats 8 as a normal control. SAA low and high dose groups were injected daily with SAA 0.5 mg / kg, 1 mg / kg, Met group daily oral gavage Met 200 mg / kg, continuous administration for 12 weeks to observe the incidence of cataract in ZDF rats and Retinal pathological changes, and the levels of blood glucose, Hb A1c, IL-1, IL-6, ox-LDL and MDA Lipoprotein-associated phospholipase A2 (Lp-PLA2) activity, urinary transferrin (TRF), retinol binding protein (RBP) content. Results The levels of blood glucose, blood lipids and Hb A1c were increased in model control group, the incidence of diabetic cataract was 68.75%, the thickness of retinal basement and microvascular disease, the levels of IL-1, IL-6, oxLDL and MDA, Activity was significantly increased, urinary TRF and RBP content also significantly increased. Serum levels of IL-1, IL-6, ox-LDL, MDA and Lp-PLA2 decreased after administration of SAA in ZDF rats. The levels of TRF, RBP The content also dropped. Conclusions SAA can improve diabetic retinopathy and reduce the incidence of cataract in ZDF rats. Its mechanism may be related to inhibiting chronic inflammation, preventing lipid peroxidation and decreasing Lp-PLA2 activity.