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目的观察木犀草素对糖尿病脑梗死大鼠SOD、MDA及NO的影响。方法将实验大鼠随机分为正常对照组(Normal Control,NC)、糖尿病组(Diabetes Mellitus,DM)、糖尿病脑梗死组(Diabetes Mellitus Cerebral Infarction,DMCI)、木犀草素高剂量组(Luteolin-H)、木犀草素中剂量组(Luteolin-M)、木犀草素低剂量组(Luteolin-L)共6组,每组10只。DM模型制备成功后,不同剂量Luteolin灌胃,使用线栓法制备DMCI模型。检测大鼠血糖,进行神经功能缺损评分,检测大鼠血浆及脑组织的SOD、MDA、NO水平。结果 Luteolin各剂量组大鼠血糖显著下降,差异有统计学意义(FH=74.55,FM=42.48,FL=17.36,P<0.01);Luteolin可降低DMCI大鼠神经功能缺损评分,差异有统计学意义(FH=9.093,FM=7.881,FL=5.312,P<0.05);Luteolin各剂量组大鼠血浆SOD明显升高,差异有统计学意义(FH=188.809,FM=120.871,FL=99.141,P<0.01),MDA(FH=125.65,FM=103.48,FL=101.98,P<0.01)和NO(FH=92.468,FM=35.58,FL=6.492,P<0.05)明显降低,差异有统计学意义。Luteolin各剂量组大鼠脑组织SOD明显升高,差异有统计学意义(FH=125.292,FM=51.367,FL=12.997,P<0.01),MDA(FH=226.18,FM=125.14,FL=56.882,P<0.01)和NO(FH=217.993,FM=92.84,FL=22.173,P<0.05)明显降低,差异有统计学意义。结论 Luteolin可降低DM大鼠血糖,可改善DMCI大鼠的神经功能缺损,可缓解DMCI大鼠的氧化应激反应以及NO过高所引起的神经细胞和其他组织损伤,起重要的保护作用。
Objective To observe the effects of luteolin on SOD, MDA and NO in diabetic rats with cerebral infarction. Methods The experimental rats were randomly divided into normal control group (NC), diabetic group (DM), diabetic mellitus cerebral infarction group (DMCI), high dose luteolin group (Luteolin-H ), Luteolin-M and Luteolin-L were divided into 6 groups (n = 10 in each group). DM model was successfully prepared, different doses of Luteolin gavage, the use of thread method DMCI model. The blood glucose of rats was measured and the neurological impairment was evaluated. The levels of SOD, MDA and NO in plasma and brain of rats were detected. Results Luteolin could significantly decrease the blood glucose of rats in each dose group (FH = 74.55, FM = 42.48, FL = 17.36, P <0.01). Luteolin decreased the neurological deficit score in DMCI rats (FH = 9.093, FM = 7.881, FL = 5.312, P <0.05). The plasma SOD in each dose group of Luteolin increased significantly (FH = 188.809, FM = 120.871, FL = 99.141, P < 0.01). The levels of MDA (FH = 125.65, FM = 103.48, FL = 101.98, P <0.01) and NO (FH = 92.468, FM = 35.58, FL = 6.492, P <0.05) decreased significantly with statistical significance. The levels of SOD in brain tissue of rats in Luteolin group were significantly higher than those in Luteolin group (FH = 125.292, FM = 51.367, FL = 12.997, P <0.01) P <0.01) and NO (FH = 217.993, FM = 92.84, FL = 22.173, P <0.05). The difference was statistically significant. Conclusion Luteolin can decrease the blood glucose in DM rats and improve the neurological deficits in DMCI rats. It can relieve the oxidative stress in DMCI rats and the damage of nerve cells and other tissues caused by NO excess.