Читать книгу Recent Advances in Dialysis Therapy in Japan - Группа авторов - Страница 70

To elucidate the mechanism of cognitive impairment development in CKD, we conducted the following experiment using 5/6 nephrectomized CKD mice. Eight weeks after model development, a water maze test was performed to compare the learning function of sham-operated control mice with that of CKD mice. Then, brains were collected from the mice and analyzed pathologically and immunohistochemically. Accumulation of 8-hydroxydeoxyguanosine (8-OHdG) and the appearance of pyknotic cells were observed in the hippocampus of the brains of CKD mice, which also showed a marked decrease in learning function in the water maze test. Meanwhile, CKD mice treated with the antioxidant tempol showed almost no 8-OHdG accumulation or pyknotic cells in the hippocampus and achieved a level of performance similar to that of control mice in the water maze test (Fig. 6) [17]. These results suggest the involvement of CKD-induced oxidative stress as the primary cause of neuronal cell damage and decreased learning function in CKD.