Ganglioside GM1 effects on the expression of nerve growth factor (NGF), Trk-A receptor, proinflammatory cytokines and on autoimmune diabetes onset in non-obese diabetic (NOD) mice
| Autor: | Conceição Aparecida Vilella, Karla Priscila Vieira, Carina Malaguti, Ana Rachel de Almeida e Silva Lima Zollner, Ricardo de Lima Zollner |
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| Rok vydání: | 2007 |
| Předmět: |
Male
medicine.medical_specialty medicine.medical_treatment Immunology Nerve Tissue Proteins Nod G(M1) Ganglioside S100 Calcium Binding Protein beta Subunit Biochemistry Proinflammatory cytokine Islets of Langerhans Mice Mice Inbred NOD Internal medicine Diabetes mellitus Glial Fibrillary Acidic Protein Nerve Growth Factor medicine Immunology and Allergy Animals Humans Nerve Growth Factors Age of Onset Receptor trkA Molecular Biology NOD mice Type 1 diabetes Ganglioside business.industry S100 Proteins Hematology medicine.disease Nerve growth factor Endocrinology Cytokine Diabetes Mellitus Type 1 Cytokines Female Schwann Cells business Spleen |
| Zdroj: | Cytokine. 42(1) |
| ISSN: | 1096-0023 |
| Popis: | NOD (non-obese diabetic) mice develop type 1 diabetes mellitus spontaneously and with a strong similarity to the human disease. Differentiation and function of pancreas beta cells are regulated by a variety of hormones and growth factors, including the nerve growth factor (NGF). Gangliosides have multiple immunomodulatory activities with immunosuppressive properties, decreasing lymphoproliferative responses and modulating cytokine production. In the present study, serum, pancreas islets and spleen mononuclear cells from NOD mice treated with monosialic ganglioside GM1 (100 mg/kg/day) and the group control which received saline solution were isolated to investigate the proinflammatory cytokines (IL-1beta, IFN-gamma, IL-12, TNF-alpha), NGF and its high-affinity receptor TrkA, peri-islet Schwann cells components (GFAP, S100-beta) expression and the relationship with diabetes onset and morphological aspects. Our results suggest that GM1 administration to female NOD mice beginning at the 4th week of life is able to reduce the index of inflammatory infiltrate and consequently the expression of diabetes, modulating the expression of proinflammatory cytokines (IL-12, IFN-gamma, TNF-alpha and IL-1beta). Furthermore, GM1 increases GFAP, S-100beta and NGF in pancreas islets, factors involved in beta cell survival. |
| Databáze: | OpenAIRE |
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