高压氧治疗STZ大鼠糖尿病性心肌病变作用机理的研究

来源 :中国临床医学 | 被引量 : 0次 | 上传用户:zhongli2511
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目的 :检测经高压氧治疗 (HBOT)的有糖尿病性心肌病变的STZ(链脲佐菌素 )大鼠血浆细胞因子水平 ,探讨高压氧治疗糖尿病性心肌病变的作用机理。方法 :STZ糖尿病大鼠造模成功 3个月、电镜证实有糖尿病性心肌病变后 ,随机分为三组 :(1)HBOT组 (n =30 ) :每天接受 0 .15MPa、HBOT 1h ,连续 2 0d。 (2 )糖尿病对照组 (n =32 ) :不做治疗。 (3)正常对照组 (n =2 0 ) :腹腔注射生理盐水的无糖尿病的正常大鼠。分别在疗程 5d、10d、2 0d后处死三组大鼠 ,测定三组大鼠血清NGF、IGF - 1、TGF - β、NO和MMP - 1水平。结果 :HBO治疗 10d后 ,HBOT组心肌病变明显好于同期糖尿病对照组 ,低于正常对照组 ;血清NGF、NO水平稍有增高 ,但与对照组间无显著差异。HBOT 2 0d后 ,血清NGF和NO水平显著高于糖尿病对照组 (均P <0 .0 1) ,治疗组血IGF - 1水平显著高于DM组 (P =0 .0 0 0 84 ) ,但仍低于正常对照组 (P =0 .0 0 15 3) ;血清MMP - 1、TGF - β水平较糖尿病组明显降低 (P <0 .0 5 )。结论 :HBOT改善STZ大鼠糖尿病性心肌病变的机理可能与促进NGF、IGF - 1合成和血清NO增加、抑制MMP- 1和TGF - β有关 Objective: To detect the levels of plasma cytokines in rats with diabetic cardiomyopathy induced by hyperbaric oxygen (HBOT) and to investigate the mechanism of hyperbaric oxygen therapy in diabetic cardiomyopathy. Methods: The model of STZ diabetic rats was successfully established for 3 months. Electron microscopy confirmed diabetic cardiomyopathy and then randomly divided into three groups: (1) HBOT group (n = 30) 0d. (2) Diabetic control group (n = 32): No treatment. (3) Normal control group (n = 20): normal rats without diabetes mellitus injected with normal saline. Three groups of rats were killed after 5 days, 10 days and 20 days of treatment, respectively. The levels of serum NGF, IGF - 1, TGF - β, NO and MMP - 1 in the three groups were measured. Results: After 10 days HBO treatment, the cardiomyopathy in HBOT group was significantly better than that in the control group and lower than that in the normal control group. Serum NGF and NO levels were slightly increased, but no significant difference compared with the control group. Serum levels of NGF and NO were significantly higher than those of the diabetic control group (all P <0.01) after HBOT 20d. The level of IGF - 1 in the treatment group was significantly higher than that in the DM group (P = 0.000084) (P = 0.0153). The levels of serum MMP - 1 and TGF - β in diabetic group were significantly lower than those in diabetic group (P <0.05). Conclusion: The mechanism of HBOT in improving diabetic cardiomyopathy in STZ rats may be related to the promotion of the synthesis of NGF, IGF - 1 and the increase of serum NO, and the inhibition of MMP - 1 and TGF - β
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