Jang Sun-Mi, Yee Sung-Tae, Choi Jina, Choi Myung-Sook, Do Gyeong-Min, Jeon Seon-Min, Yeo Jiyoung, Kim Myung-Joo, Seo Kwon-Il, Lee Mi-Kyung
Department of Nutrition Education, Graduate School of Education, Sunchon National University, Suncheon 540-742, Republic of Korea.
Int Immunopharmacol. 2009 Jan;9(1):113-9. doi: 10.1016/j.intimp.2008.10.013. Epub 2008 Nov 20.
This study investigated the effects of ursolic acid on immunoregulation and pancreatic beta-cell function in type 1 diabetes fed a high-fat diet for 4 weeks. Male mice were divided into non-diabetic, diabetic control, and diabetic-ursolic acid (0.05%, w/w) groups, which were fed a high-fat (37% calories from fat). Diabetes was induced by injection of streptozotocin (200 mg/kg B.W., i.p.). Ursolic acid significantly improved blood glucose levels, glucose intolerance, and insulin sensitivity compared to the diabetic group. The plasma insulin and C-peptide concentrations were significantly higher in the diabetic-ursolic acid group than in the diabetic group. Ursolic acid significantly elevated the insulin levels with preservation of insulin staining of beta-cells in the pancreas. In splenocytes, concanavalin (Con) A-induced T-cell proliferation was significantly higher in the diabetic-ursolic acid group compared to the diabetic group, but liposaccharide (LPS)-induced B-cell proliferation did not differ between groups. Ursolic acid enhanced IL-2 and IFN-gamma production in response to Con A stimulation, whereas it inhibited TNF-alpha production in response to LPS stimulation. In this study, neither streptozotocin nor ursolic acid had effects on lymphocyte subsets. These results indicate that ursolic acid exhibits potential anti-diabetic and immunomodulatory properties by increasing insulin levels with preservation of pancreatic beta-cells and modulating blood glucose levels, T-cell proliferation and cytokines production by lymphocytes in type 1 diabetic mice fed a high-fat diet.
本研究调查了熊果酸对高脂饮食喂养4周的1型糖尿病小鼠免疫调节和胰岛β细胞功能的影响。将雄性小鼠分为非糖尿病组、糖尿病对照组和糖尿病-熊果酸（0.05%，w/w）组，给予高脂饮食（37%的热量来自脂肪）。通过腹腔注射链脲佐菌素（200 mg/kg体重）诱导糖尿病。与糖尿病组相比，熊果酸显著改善了血糖水平、葡萄糖耐量和胰岛素敏感性。糖尿病-熊果酸组的血浆胰岛素和C肽浓度显著高于糖尿病组。熊果酸显著提高了胰岛素水平，同时保留了胰腺中β细胞的胰岛素染色。在脾细胞中，与糖尿病组相比，糖尿病-熊果酸组中刀豆球蛋白A（Con A）诱导的T细胞增殖显著更高，但脂多糖（LPS）诱导的B细胞增殖在两组之间没有差异。熊果酸增强了对Con A刺激的IL-2和IFN-γ产生，而抑制了对LPS刺激的TNF-α产生。在本研究中，链脲佐菌素和熊果酸均对淋巴细胞亚群没有影响。这些结果表明，熊果酸通过提高胰岛素水平、保留胰腺β细胞以及调节高脂饮食喂养的1型糖尿病小鼠的血糖水平、T细胞增殖和淋巴细胞产生的细胞因子，表现出潜在的抗糖尿病和免疫调节特性。
