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为探讨二甲基硫脲（ＤＭＴＵ）保护心肌细胞抗过氧化氢（Ｈ２Ｏ２）损伤。３２瓶培养乳鼠心肌细胞随机分４组，每组８瓶：（１）对照组；（２）Ｈ２Ｏ２（５ｍｍｏｌ）组；（３）ＤＭＴＵ（２０ｍｍｏｌ）组；（４）Ｈ２Ｏ２（５ｍｍｏｌ）＋ＤＭＴＵ（２０ｍｍｏｌ）组。在３７℃、５％ＣＯ２的ＭＥＭ培养４小时。结果发现：（１）与对照组比，Ｈ２Ｏ２组乳酸脱氢酶（ＬＤＨ，Ｕ／１００ｍｌ）释放多（２８２．３８±４７．２８比７７．２５±１８．２５，Ｐ＜０．０１）、ＴＢＡ反应物（ＴＢＡＲＳ，ｎｍｏｌ／ｍｇＰｒ．）产生多（２．２５±０．５３比０．７９±０．３６，Ｐ＜０．０１）；（２）与Ｈ２Ｏ２组比，Ｈ２Ｏ２＋ＤＭ－ＴＵ组ＬＤＨ释放少（９９．２５±４１．８８比２８２．３８±４７．２８，Ｐ＜０．０１）；ＴＢＡＲＳ产生少（０．５９±０．１８比２．２５±０．５３，Ｐ＜０．０１）；此外，我们还发现ＤＭＴＵ组超氧化物歧化酶（ＳＯＤ，μｇ／ｍｇＰｒ．）比对照组高（８．４９±３．６５比１．９２±１．４０，Ｐ＜０．０１）。ＤＭＴＵ能保护心肌细胞抗Ｈ２Ｏ２损伤，机制与灭活羟自由基（·ＯＨ）、保护ＳＯＤ活性有关
To investigate dimethylthiourea (DMTU) protects cardiomyocytes against hydrogen peroxide (H2O2) injury. Thirty-two bottles of neonatal rat cardiomyocytes were randomly divided into 4 groups with 8 bottles in each group: (1) control group; (2) H2O2 (5 mmol) group; (3) DMTU 20 mmol) group. Incubate at 37 ° C in 5% CO2 in MEM for 4 hours. The results showed that: (1) Lactate dehydrogenase (LDH, U / 100ml) released more in the H2O2 group than in the control group (282.38 ± 47.28 vs. 77.25 ± 18.25, P <0.01) (2.25 ± 0.53 vs 0.79 ± 0.36, P <0.01); (2) Compared with H2O2 group, H2O2 + DM-TU group had more LDH (99.25 ± 41.88 vs. 282.38 ± 47.28, P <0.01), and less TBARS (0.59 ± 0.18 vs. 2.25 ± 0.53, P <0. In addition, we also found that the superoxide dismutase (SOD, μg / mgPr.) In DMTU group was higher than that in control group (8.49 ± 3.65 vs 1.92 ± 1.40, P <0.01) . DMTU can protect cardiomyocytes against H2O2 injury, the mechanism of inactivation of hydroxyl radicals (· OH), the protection of SOD activity