Department of Applied Chemistry, Tokyo Metropolitan University, Minami-Osawa, Hachioji, Tokyo, Japan.
Mol Pharm. 2012 Oct 1;9(10):2956-9. doi: 10.1021/mp300147v. Epub 2012 Aug 28.
Mice lacking manganese-superoxide dismutase (Mn-SOD) activity exhibit typical pathology of dilated cardiomyopathy (DCM). In the present study, the structure-activity relationship between the water-soluble manganese (Mn) porphyrin with SOD activity and the in vivo pharmaceutical effect on DCM is reported. The Mn-SOD-deficient mice were treated with Mn-porphyrins for 3 weeks. The treatment of a Mn-porphyrin, MnM2Py(2)P, suppressed the progression of cardiac dilation. These results suggest that the Mn-porphyrin MnM2Py(2)P treatment is proposed as a potential therapy for DCM.
缺乏锰超氧化物歧化酶（Mn-SOD）活性的小鼠表现出扩张型心肌病（DCM）的典型病理。在本研究中，报道了具有 SOD 活性的水溶性锰（Mn）卟啉与 DCM 体内药物作用之间的构效关系。用 Mn-卟啉处理 Mn-SOD 缺乏的小鼠 3 周。MnM2Py(2)P 这种 Mn-卟啉治疗抑制了心脏扩张的进展。这些结果表明，Mn-卟啉 MnM2Py(2)P 治疗可能是治疗 DCM 的一种方法。
