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目的通过分别给予大鼠不同铁含量的饮食,观察长期运动和不同铁含量饮食对大鼠海马中一氧化氮(NO)含量及一氧化氮合酶(NOS)活力的影响。方法采用刚断乳雌性SD大鼠105只,随机分为3组:ID组(低铁含量12 mg/kg)、CN组(标准铁含量45 mg/kg)和SU组(高铁含量1 000 mg/kg),用相应的铁含量饲料喂养1个月后,每组取15只大鼠,测定海马NO含量及NOS诱导型NOS(i NOS)和结构型NOS(c NOS)活力。其余的大鼠每组再进一步分为运动组和静息组,运动组大鼠进入游泳期(运动强度为120 min/d,5 d/周,持续1个月);静息组除不进行运动外,其余处理与相应的运动组相同。在末次运动后,所有大鼠禁食24 h,戊巴比妥钠麻醉下取全脑,冰上快速分离出海马,测定NO含量及i NOS、c NOS活力。结果 1大鼠在3种不同铁含量饮食1个月后,与标准铁组对比,海马高铁组NO含量、c NOS活力差异均无统计学意义(P>0.05);低铁组NO含量和c NOS活力均降低(P<0.05),而高铁组和低铁组i NOS活力差异均无统计学意义(P>0.05)。2高铁含量饮食时,与静息组比,运动组NO含量(t=2.262,P<0.05)和c NOS活力(t=5.651,P<0.01)均升高,而i NOS活力升高但差异无统计学意义(t=0.622,P>0.05)。标准铁含量饮食时,与静息组对比,运动组NO含量(t=2.935,P<0.01),c NOS活力(t=5.257,P<0.01)显著升高,i NOS活力(t=1.001,P>0.05)。低铁含量饮食时,与静息组对比,运动组NO含量升高(t=2.731,P<0.05)、i NOS活力(t=6.118,P<0.01)、c NOS活力(t=8.423,P<0.01)升高。结论饮食铁缺乏可使海马中c NOS活力降低,NO合成减少。不同铁含量饮食下长期运动均会引起海马中c NOS活力升高,NO合成增多。而在饮食铁缺乏的情况下,长期运动会使i NOS活力升高,对机体造成毒性作用。
OBJECTIVE: To observe the effects of long-term exercise and different iron content diet on nitric oxide (NO) content and nitric oxide synthase (NOS) activity in hippocampus of rats by giving different dietary iron content in rats. Methods 105 female SD rats were randomly divided into three groups: ID group (low iron content 12 mg / kg), CN group (standard iron content 45 mg / kg) and SU group (high iron content 1000 mg / kg). After fed with the corresponding iron content for 1 month, 15 rats in each group were taken to measure the NO content in hippocampus and the activity of NOS-induced NOS (iNOS) and constitutive NOS (cNOS). The remaining rats were further divided into exercise group and rest group in each group. Rats in exercise group entered swimming period (exercise intensity was 120 min / d for 5 d / week for 1 month) Exercise, the rest of the treatment and the corresponding exercise group the same. After the last exercise, all rats were fasted for 24 h, the whole brain was anesthetized with sodium pentobarbital, and the hippocampus was quickly isolated on ice to determine NO content and iNOS, cNOS activity. Results Compared with the standard iron group, there was no significant difference in NO content and cNOS activity in hippocampus (P> 0.05) after 1 month of 3 different iron content diet. NOS activity decreased (P <0.05), while there was no significant difference in iNOS activity between high-iron group and low-iron group (P> 0.05). Compared with the rest group, NO content (t = 2.262, P <0.05) and cNOS activity (t = 5.651, P <0.01) increased in high-iron diet group, No statistical significance (t = 0.622, P> 0.05). Compared with resting group, NO content in exercise group (t = 2.935, P <0.01) and cNOS activity (t = 5.257, P <0.01) P> 0.05). Compared with resting group, NO content in exercise group (t = 2.731, P <0.05), iNOS activity (t = 6.118, P <0.01) and cNOS activity (t = 8.423, P <0.01) increased. Conclusions Dietary iron deficiency can decrease c NOS activity and decrease NO synthesis in hippocampus. Long-term exercise under different iron content diet will cause increased c NOS activity in the hippocampus, NO synthesis increased. In the absence of dietary iron deficiency, prolonged exercise increases iNOS activity and causes toxic effects on the body.