@phdthesis{oai:nagasaki-u.repo.nii.ac.jp:00027438, author = {井上, 大}, month = {Mar}, note = {Peritoneal fibrosis is a serious complication of long-term peritoneal dialysis, attributable to inflammation and mitochondrial dysfunction. Mitochonic acid-5 (MA-5), an indole-3-acetic acid derivative, improves mitochondrial dysfunction and has therapeutic potential against various diseases including kidney diseases. However, whether MA-5 is effective against peritoneal fibrosis remains unclear. Therefore, we investigated the effect of MA-5 using a peritoneal fibrosis mouse model. Peritoneal fibrosis was induced in C57BL/6 mice via intraperitoneal injection of chlorhexidine gluconate (CG) every other day for 3 weeks. MA-5 was administered daily by oral gavage. The mice were divided into control, MA-5, CG, and CG + MA-5 groups. Following treatment, immunohistochemical analyses were performed. Fibrotic thickening of the parietal peritoneum induced by CG was substantially attenuated by MA-5. The number of α-smooth muscle actin-positive myofibroblasts, transforming growth factor β-positive cells, F4/80-positive macrophages, monocyte chemotactic protein 1-positive cells, and 4-hydroxy-2-nonenal-positive cells was considerably decreased. In addition, reduced ATP5a1-positive and uncoupling protein 2-positive cells in the CG group were notably increased by MA-5. MA-5 may ameliorate peritoneal fibrosis by suppressing macrophage infiltration and oxidative stress, thus restoring mitochondrial function. Overall, MA-5 has therapeutic potential against peritoneal fibrosis., 長崎大学学位論文 学位記番号:博(医歯薬)甲第1434号 学位授与年月日:令和4年3月18日, Author: Hiro Inoue, Kenta Torigoe, Miki Torigoe, Kumiko Muta, Yoko Obata, Takehiro Suzuki, Chitose Suzuki, Takaaki Abe, Takehiko Koji, Hiroshi Mukae & Tomoya Nishino, Citation: Medical Molecular Morphology, 55(1), pp. 27–40; 2022, Nagasaki University (長崎大学), 博士(医学) (2022-03-18)}, school = {Nagasaki University (長崎大学)}, title = {Mitochonic acid-5 ameliorates chlorhexidine gluconate-induced peritoneal fibrosis in mice}, year = {2022} }