title: Camel milk inhibits inflammatory angiogenesis via downregulation of proangiogenic and proinflammatory cytokines in mice.
abstract: Camel milk has traditionally been used to treat cancer, but this practice awaits scientific scrutiny, in particular its role in tumor angiogenesis, the key step involved in tumor growth and metastasis. We aimed to investigate the effects of camel milk on key components of inflammatory angiogenesis in sponge implant angiogenesis model. Polyester-polyurethane sponges, used as a framework for fibrovascular tissue growth, were implanted in Swiss albino mice and camel milk (25, 50 and 100 mg/kg/day) was administered for 14 days through installed cannula. The implants collected at day 14 post-implantation were processed for the assessment of hemoglobin (Hb), myeloperoxidase (MPO), N-acetylglucosaminidase (NAG), and collagen, which were used as indices for angiogenesis, neutrophil, and macrophage accumulation and extracellular matrix deposition, respectively. Relevant inflammatory, angiogenic, and fibrogenic cytokines were also determined. Camel milk treatment attenuated the main components of the fibrovascular tissue, wet weight, vascularization (Hb content), macrophage recruitment (NAG activity), collagen deposition and the levels of vascular endothelial growth factor (VEGF), interleukin (IL)-1β, IL-6, IL-17, tumor necrosis factor-α, and transforming growth factor-β. A regulatory function of camel milk on multiple parameters of the main components of inflammatory angiogenesis has been revealed, giving insight into the potential therapeutic benefit underlying the anti-cancer actions of camel milk.
authors: Department of Physiology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
authors: Abdulqader A
authors: AA
authors: Alhaider
authors: Abdel Galil M
authors: AG
authors: Abdel Gader
authors: Nawaf
authors: N
authors: Almeshaal
authors: Sarita
authors: S
authors: Saraswati
mesh_terms: D000118:Acetylglucosaminidase / Q000032:analysis; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000818:Animals; D002162:Camelus; D018890:Chemoprevention; D003094:Collagen / Q000032:analysis; D016207:Cytokines / Q000032:analysis; D004195:Disease Models, Animal; D006454:Hemoglobins / Q000032:analysis; D007249:Inflammation / Q000276:immunology; D020381:Interleukin-17 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D007774:Lactation; D008264:Macrophages / Q000276:immunology; D008297:Male; D051379:Mice; D008892:Milk / Q000378:metabolism*; D009369:Neoplasms / Q000188:drug therapy*; D009389:Neovascularization, Pathologic / Q000188:drug therapy*; D009504:Neutrophils / Q000276:immunology; D009195:Peroxidase / Q000032:analysis; D011091:Polyesters; D011140:Polyurethanes; D016212:Transforming Growth Factor beta / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis
chemical_list: D020533:Angiogenesis Inhibitors; D016207:Cytokines; D006454:Hemoglobins; C508600:IL6 protein, human; D020381:Interleukin-17; D053583:Interleukin-1beta; D015850:Interleukin-6; D011091:Polyesters; D011140:Polyurethanes; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D003094:Collagen; D009195:Peroxidase; D000118:Acetylglucosaminidase
keywords: CD31; Camel milk; VEGF; angiogenesis; microvessel density