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Poly-γ-Glutamic Acid Attenuates Angiogenesis and Inflammation in Experimental Colitis
Author(s) -
Munkhtugs Davaatseren,
Jin-Taek Hwang,
Jae Ho Park,
Myung-Sunny Kim,
Shuaiyu Wang,
Mi Jeong Sung
Publication year - 2013
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/2013/982383
Subject(s) - angiogenesis , colitis , inflammation , inflammatory bowel disease , ulcerative colitis , medicine , immunology , pharmacology , database , algorithm , disease , mathematics , computer science
Poly- γ -glutamic acid ( γ -PGA), naturally secreted from various strains of Bacillus , has anti-inflammatory activity. In inflammatory bowel disease (IBD), inflammation is promoted and sustained by angiogenesis; however, the role played by γ -PGA in this condition is unclear. Therefore, we evaluated γ -PGA effects on angiogenesis and inflammation in a dextran sulfate sodium- (DSS-) induced mouse colitis model. Experimental colitis was induced in male C57BL/6 mice by administering 3% DSS. Disease activity index (DAI), histopathological scores, microvascular density, myeloperoxidase activity, and VEGF-A and VEGFR2 expression were compared among control mice, DSS-treated mice, and mice receiving 3% DSS along with γ -PGA at 50 mg/kg body weight per day or 3% DSS with γ -PGA at 200 mg/kg body weight per day. We found that γ -PGA significantly attenuated weight loss, DAI, and colon shortening. γ -PGA also significantly reduced histopathological evidence of injury. Moreover, γ -PGA significantly attenuated DSS-induced blood vessel densities. Furthermore, γ -PGA attenuated DSS-induced expression of VEGF-A and its receptor, VEGFR2. In addition, γ -PGA treatment led to reduced recruitment of leukocytes to the inflamed colon. Therefore, our results indicate that γ -PGA has potential application in conditions marked by inflammatory-driven angiogenesis and mucosal inflammation.

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