title: Chondroitin sulfate prevents peritoneal fibrosis in mice by suppressing NF-κB activation.
abstract: Long-term peritoneal dialysis causes peritoneal fibrosis, and previous reports suggest that inflammation plays a critical role in peritoneal fibrosis. Chondroitin sulfate (CS) suppresses the inflammatory response by preventing activation of nuclear factor (NF)-κB. We examined the effect of CS on the peritoneal fibrosis induced by chlorhexidine gluconate (CG) in mice. CS or water was administered daily. We divided mice into four groups: administered vehicle and water (control); administered vehicle and CS (CS); administered CG and water (CG); and administered CG and CS (CG+CS). Morphologic changes were assessed by Masson's trichrome staining. Inflammation- and fibrosis-associated factors were assessed by immunohistochemistry. Activation of NF-κB was examined by southwestern histochemistry. CS administration suppressed the progression of submesothelial thickening. The numbers of inflammation- and fibrosis-associated factors -positive cells were significantly decreased in the CG+CS group, compared to the CG group. Based on SWH, the CG+CS group contained significantly fewer NF-κB-activated cells than the CG group. Our results indicate that CS suppresses peritoneal fibrosis via suppression of NF-κB activation. These results suggest that CS has therapeutic potential for peritoneal fibrosis.
authors.affiliation: Department of Nephrology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki, Japan.|Department of infectious disease, Unit of molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
authors.forename: Shinichi
authors.initials: S
authors.lastname: Abe
authors.affiliation: Department of Nephrology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki, Japan. yobata@nagasaki-u.ac.jp.|Medical Education Development Center, Nagasaki University Hospital, Nagasaki, Japan. yobata@nagasaki-u.ac.jp.
authors.forename: Yoko
authors.initials: Y
authors.lastname: Obata
authors.affiliation: Department of Nephrology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki, Japan.
authors.forename: Satoru
authors.initials: S
authors.lastname: Oka
authors.affiliation: Unit of Basic Medical Science, Department of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
authors.forename: Takehiko
authors.initials: T
authors.lastname: Koji
authors.affiliation: Department of Nephrology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki, Japan.
authors.forename: Tomoya
authors.initials: T
authors.lastname: Nishino
authors.affiliation: Department of infectious disease, Unit of molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
authors.forename: Koichi
authors.initials: K
authors.lastname: Izumikawa
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D018932:Chemokine CCL2 / Q000378:metabolism; D002809:Chondroitin Sulfates / Q000494:pharmacology / Q000627:therapeutic use*; D007150:Immunohistochemistry; D053583:Interleukin-1beta / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008813:Mice, Inbred ICR; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism*; D056627:Peritoneal Fibrosis / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control; D010641:Phenotype; D010766:Phosphorylation; D051785:Smad Proteins / Q000378:metabolism; D013194:Staining and Labeling
chemical_list: C558396:Acta2 protein, mouse; D000199:Actins; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D053583:Interleukin-1beta; D016328:NF-kappa B; D051785:Smad Proteins; D002809:Chondroitin Sulfates; D020928:Mitogen-Activated Protein Kinases
keywords: Chlorhexidine gluconate; Chondroitin sulfate; Mitogen-activated protein kinase; NF-κB; Peritoneal fibrosis