Burke Susan J, Karlstad Michael D, Conley Caroline P, Reel Danielle, Whelan Jay, Collier J Jason
Department of Nutrition, University of Tennessee, Knoxville, TN, USA.
Department of Nutrition, University of Tennessee, Knoxville, TN, USA; Department of Surgery, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN, USA.
Nutr Res. 2015 Apr;35(4):328-36. doi: 10.1016/j.nutres.2014.12.003. Epub 2014 Dec 27.
Type 1 diabetes mellitus results from autoimmune-mediated destruction of pancreatic islet β-cells, a process associated with inflammatory signals. We hypothesized that dietary supplementation with botanicals known to contain anti-inflammatory properties would prevent losses in functional β-cell mass in nonobese diabetic (NOD) mice, a rodent model of autoimmune-mediated islet inflammation that spontaneously develops diabetes. Female NOD mice, a model of spontaneous autoimmune diabetes, were fed a diet supplemented with herbal extracts (1.916 g total botanical extracts per 1 kg of diet) over a 12-week period. The mice consumed isocaloric matched diets without (controls) and with polyherbal supplementation (PHS) ad libitum starting at a prediabetic stage (age 6 weeks) for 12 weeks. Control mice developed hyperglycemia (>180 mg/dL) within 16 weeks (n = 9). By contrast, mice receiving the PHS diet did not develop hyperglycemia by 18 weeks (n = 8). Insulin-positive cell mass within pancreatic islets was 31.9% greater in PHS mice relative to controls. We also detected a 26% decrease in CD3(+) lymphocytic infiltration in PHS mice relative to mice consuming a control diet. In vitro assays revealed reduced β-cell expression of the chemokines CCL2 and CXCL10 after overnight PHS addition to the culture media. We conclude that dietary PHS delays initiation of autoimmune-mediated β-cell destruction and subsequent onset of diabetes mellitus by diminishing islet inflammatory responses.
1型糖尿病是由自身免疫介导的胰岛β细胞破坏所致,这一过程与炎症信号相关。我们推测,膳食补充已知具有抗炎特性的植物药可预防非肥胖糖尿病(NOD)小鼠功能性β细胞量的损失,NOD小鼠是一种自身免疫介导的胰岛炎症啮齿动物模型,可自发发展为糖尿病。雌性NOD小鼠作为自发自身免疫性糖尿病模型,在12周内喂食补充了草药提取物的饮食(每1千克饮食中含有1.916克总植物提取物)。小鼠从糖尿病前期阶段(6周龄)开始随意食用等热量匹配饮食,一组不补充(对照组),另一组补充多草药制剂(PHS),持续12周。对照组小鼠在16周内出现高血糖(>180mg/dL)(n = 9)。相比之下,接受PHS饮食的小鼠在18周时未出现高血糖(n = 8)。与对照组相比,PHS小鼠胰岛内胰岛素阳性细胞量多31.9%。我们还检测到,与食用对照饮食的小鼠相比,PHS小鼠的CD3(+)淋巴细胞浸润减少了26%。体外试验显示,在培养基中添加过夜的PHS后,趋化因子CCL2和CXCL10的β细胞表达降低。我们得出结论,膳食PHS通过减少胰岛炎症反应,延迟了自身免疫介导的β细胞破坏的起始及随后糖尿病的发生。