氨基胍对糖尿病大鼠心肌损伤的拮抗作用

目的：研究氨基胍（AG）对糖尿病大鼠心肌保护作用的机制。 方法：用透射电镜观察AG对链脲佐菌素诱导的糖尿病大鼠心肌形态学改变的影响，并测定心肌组织内超氧化物歧化酶(SOD)、一氧化氮合酶(NOS)、诱导型一氧化氮合酶(iNOS)的活性及丙二醛(MDA)含量，采用Western blotting法检测ONOO-标志物-硝基酪氨酸(NT)蛋白质在心肌组织中的含量。 结果：电镜下可见模型组大鼠心肌细胞核周围水肿，部分肌节断裂消失，Z线模糊或消失，心肌细胞线粒体部分嵴部分膜断裂或消失；SOD含量变化无统计学差异，NOS、iNOS活性，MDA和NT蛋白质含量大于对照组。AG组心肌组织形态学病变较轻，心肌细胞线粒体嵴部分消失，肌纤维排列较整齐，仅见少量脂滴沉着；AG治疗组NOS、iNOS活性及MDA含量低于模型组；NT含量低于模型组。 结论：AG可能通过抗脂质过氧化作用和降低ONOO^-水平而对糖尿病心肌产生保护作用。

Antagonistic effect of aminoguanidine on diabitic myocardial damage in rats

AIM: To investigate the mechanism of the antagonistic effect of aminoguanidine (AG) on diabitic myocardial damage in rats. METHODS: Morphology of myocardium in diabetic group and AG group were observed under transmission electron microscope (TEM). Activity of superoxide dismutase (SOD), nitric oxide synthase (NOS), inducible nitric oxide synthase (iNOS) and contents of malondialdehyde (MDA) were detected biochemically in myocardial homogenate. Nitrotyrosine (NT), which is the sign of peroxynitrite anion (ONOO-), was detected using Western blotting. RESULTS: Under TEM, there was edema around nucleus of cadiocytes, part of inocommaes were breaked and Z lines were ambiguity, and part of costulaes and membranes of mitochondrion in cadiocytes were breaked or disappeared. The activity of NOS, iNOS and the content of MDA and NT increased in diabetic group as compared to control. The pathological changes of myocardium induced by diabetes were reversed in AG group, only part of costulaes of mitochondrion of cadiocytes disappeared, inocommaes were in order on the whole and only some lipid droplets deposited. The activity of NOS, iNOS and the content of MDA and NT in AG group decreased as compared to diabetic group. CONCLUSION: The protective effect of AG on diabitic myocardium may be through anti-lipid peroxidation and decreasing the content of ONOO-.