目的 研究黄刺多糖对代谢综合征小鼠糖脂代谢的作用及可能的作用机制。方法 将小鼠随机分为对照组、模型组，黄刺多糖低、高剂量(150、600 mg·kg^-1)组，二甲双胍(150 mg·kg^-1)组，黄刺多糖(600 mg·kg^-1)+Z-Gug[法尼醇X受体（FXR）拮抗剂，150 mg·kg^-1]组，除对照组外，其他组通过30%果糖溶液构建代谢综合征小鼠模型，连续给药4周，其中黄刺多糖和二甲双胍ig给药，Z-Gug ip给药；其余组ig 0.9%氯化钠溶液。检测小鼠尾动脉收缩压；自动分析仪检测小鼠生化指标；分离并称量脂肪质量，计算体脂比；血糖仪测量空腹血糖水平；试剂盒检测血清空腹胰岛素、丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）及胆汁酸水平，并计算胰岛素指数（IRI）；苏木素-伊红（HE）染色分析肝脏和肠组织病理损伤；Western blotting检测肠组织FXR/FGF15相关蛋白表达。结果 与对照组相比，模型组体脂比、空腹血糖、空腹胰岛素、IRI显著增加（P<0.05）,ALT、AST、胆汁酸、收缩压、低密度脂蛋白、三酰甘油、总胆固醇水平显著增加（P<0.05），肠组织中FXR和FGF15蛋白表达、血清高密度脂蛋白水平显著降低（P<0.05）；肝组织结构模糊，细胞肿胀，排列紊乱；小肠绒毛肿胀、萎缩及脱落现象。与模型组相比，黄刺多糖组和二甲双胍组体脂比、空腹血糖、空腹胰岛素、IRI显著降低（P<0.05）,ALT、AST、胆汁酸、收缩压、低密度脂蛋白、三酰甘油、胆固醇水平显著降低（P<0.05），肠组织中FXR、FGF15蛋白表达、血清高密度脂蛋白显著增加（P<0.05），肝脏及小肠病理损伤明显减轻，且黄刺多糖作用呈剂量相关性；Z-Gug逆转了黄刺多糖对代谢综合征小鼠糖脂代谢的改善作用（P<0.05）。结论 黄刺多糖通过上调FXR/FGF15信号通路改善代谢综合征小鼠糖脂代谢。

Objective To study the effect of Rosa xanthina polysaccharide（RXP） on glycolipid metabolism in mice with metabolic syndrome and the possible mechanism of action. Methods Mice were randomly divided into the control group, the model group, the low-dose(150 mg·kg^-1) and high-dose(600 mg·kg^-1) RXP groups, the metformin(150 mg·kg^-1) group, and the high-dose RXP(600 mg·kg^-1) + Z-Gug [farnesoid X receptor（FXR） antagonist, 150 mg·kg^-1] group. Except for the control group, the metabolic syndrome mouse model was established by 30% fructose solution, and the drugs were administered continuously for four weeks. RXP and metformin were ig administered, while Z-Gug was ip administered. The remaining groups were ig administered 0.9% sodium chloride solution. The systolic blood pressure of the tail artery in mice was detected. The biochemical indicators of mice were detected by the automatic analyzer; Separate and weigh the fat mass, and analyze the body fat ratio; The blood glucose meter measures the fasting blood glucose level. The kit detects fasting insulin, alanine aminotransferase（ALT）, aspartate aminotransferase（AST） and bile acids. Hematoxylin-eosin（HE） staining was used to analyze the pathological damage of liver and intestinal tissues; Western blotting was used to detect the expression of FXR/FGF15-related proteins in intestinal tissues. Results Compared with the control group, the model group showed significant increases in body fat ratio, fasting blood glucose, fasting insulin, and IRI（P＜0.05）, as well as significant increases in ALT, AST, bile acid, systolic blood pressure, low-density lipoprotein, triglyceride, and cholesterol levels（P＜0.05）, and significant decreases in FXR and FGF15 protein expression in intestinal tissue and high-density lipoprotein levels in serum（P＜0.05）. The liver tissue structure was blurred, cells were swollen, and the arrangement was disordered; the small intestinal villi were swollen, atrophied, and shed. Compared with the model group, the RXP groups and the metformin group showed significant decreases in body fat ratio, fasting blood glucose, fasting insulin, and IRI（P＜0.05）, as well as significant decreases in ALT, AST, bile acid, systolic blood pressure, low-density lipoprotein, triglyceride, and cholesterol levels（P＜0.05）, and significant increases in FXR and FGF15 protein expression in intestinal tissue and high-density lipoprotein levels in serum（P＜0.05）. The pathological damage of liver and small intestine was significantly alleviated, and the effect of RXP was dose-dependent. Z-Gug reversed the improvement of glucose and lipid metabolism in metabolic syndrome mice by RXP（P＜0.05）. Conclusion RXP upregulates the FXR/FGF15 signaling pathway and improves glucose and lipid metabolisms in metabolic syndrome mice.

R285.5

广西自然科学基金项目(2024GXNSFAA010460); 山西省基础研究计划项目(202203021212058)