@article{oai:nagasaki-u.repo.nii.ac.jp:00007799,
 author = {Nakazawa, Masayuki and Obata, Yoko and Nishino, Tomoya and Abe, Shinichi and Nakazawa, Yuka and Abe, Katsushige and Furusu, Akira and Miyazaki, Masanobu and Koji, Takehiko and Kohno, Shigeru},
 issue = {2},
 journal = {ACTA HISTOCHEMICA ET CYTOCHEMICA},
 month = {Apr},
 note = {013LeptinThe isJapana hormoneSociety mainlyof Histochemistryproduced byandwhite adipose cells, and regulates body fat and food intake by acting on hypothalamus. Leptin receptor is expressed not only in the hypothalamus but in a variety of peripheral tissues, suggesting that leptin has pleiotropic functions. In this study, we investigated the effect of leptin on the progression of peritoneal fibrosis induced by intraperitoneal injection of chlorhexidine gluconate (CG) every other day for 2 or 3 weeks in mice. This study was conducted in male C57BL/6 mice and leptin-deficient ob/ob mice. Peritoneal fluid, blood, and peritoneal tissues were collected 15 or 22 days after CG injection. CG injection increased the level of leptin in serum and peritoneal fluid with thickening of submesothelial compact zone in wild type mice, but CG-injected ob/ob mice attenuate peritoneal fibrosis, and markedly reduced the number of myofibroblasts, infiltrating macrophages, and blood vessels in the thickened submesothelial area. The 2-week leptin administration induced a more thickened peritoneum in the CG-injected C57BL/6 mice than in the PBS group. Our results indicate that an upregulation of leptin appears to play a role in fibrosis and inflammation during peritoneal injury, and reducing leptin may be a therapeutically potential for peritoneal fibrosis., ACTA HISTOCHEMICA ET CYTOCHEMICA, 46(2), pp,75-84; 2013},
 pages = {75--84},
 title = {Involvement of Leptin in the Progression of Experimentally Induced Peritoneal Fibrosis in Mice},
 volume = {46},
 year = {2013}
}