目的 研究黃刺多糖對(duì)代謝綜合征小鼠糖脂代謝的作用及可能的作用機(jī)制。方法 將小鼠隨機(jī)分為對(duì)照組、模型組，黃刺多糖低、高劑量(150、600 mg·kg^-1)組，二甲雙胍(150 mg·kg^-1)組，黃刺多糖(600 mg·kg^-1)+Z-Gug[法尼醇X受體（FXR）拮抗劑，150 mg·kg^-1]組，除對(duì)照組外，其他組通過(guò)30%果糖溶液構(gòu)建代謝綜合征小鼠模型，連續(xù)給藥4周，其中黃刺多糖和二甲雙胍ig給藥，Z-Gug ip給藥；其余組ig 0.9%氯化鈉溶液。檢測(cè)小鼠尾動(dòng)脈收縮壓；自動(dòng)分析儀檢測(cè)小鼠生化指標(biāo)；分離并稱(chēng)量脂肪質(zhì)量，計(jì)算體脂比；血糖儀測(cè)量空腹血糖水平；試劑盒檢測(cè)血清空腹胰島素、丙氨酸氨基轉(zhuǎn)移酶（ALT）、天冬氨酸氨基轉(zhuǎn)移酶（AST）及膽汁酸水平，并計(jì)算胰島素指數(shù)（IRI）；蘇木素-伊紅（HE）染色分析肝臟和腸組織病理?yè)p傷；Western blotting檢測(cè)腸組織FXR/FGF15相關(guān)蛋白表達(dá)。結(jié)果 與對(duì)照組相比，模型組體脂比、空腹血糖、空腹胰島素、IRI顯著增加（P<0.05）,ALT、AST、膽汁酸、收縮壓、低密度脂蛋白、三酰甘油、總膽固醇水平顯著增加（P<0.05），腸組織中FXR和FGF15蛋白表達(dá)、血清高密度脂蛋白水平顯著降低（P<0.05）；肝組織結(jié)構(gòu)模糊，細(xì)胞腫脹，排列紊亂；小腸絨毛腫脹、萎縮及脫落現(xiàn)象。與模型組相比，黃刺多糖組和二甲雙胍組體脂比、空腹血糖、空腹胰島素、IRI顯著降低（P<0.05）,ALT、AST、膽汁酸、收縮壓、低密度脂蛋白、三酰甘油、膽固醇水平顯著降低（P<0.05），腸組織中FXR、FGF15蛋白表達(dá)、血清高密度脂蛋白顯著增加（P<0.05），肝臟及小腸病理?yè)p傷明顯減輕，且黃刺多糖作用呈劑量相關(guān)性；Z-Gug逆轉(zhuǎn)了黃刺多糖對(duì)代謝綜合征小鼠糖脂代謝的改善作用（P<0.05）。結(jié)論 黃刺多糖通過(guò)上調(diào)FXR/FGF15信號(hào)通路改善代謝綜合征小鼠糖脂代謝。

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

廣西自然科學(xué)基金項(xiàng)目(2024GXNSFAA010460); 山西省基礎(chǔ)研究計(jì)劃項(xiàng)目(202203021212058)