胰島素阻抗所引起的血壓增高、血脂異常、糖代謝失調為造成代謝症候群的主要發病機制。在胰島素調控的組織中，肝臟為主要調控醣類及脂質代謝的組織。研究指出，香椿對於治療代謝症候群有益，然而香椿對肝臟代謝調控的功能仍然不明瞭。本研究中，使用了二維電泳及西方墨點法來探討香椿醇萃物對高隻飼料餵食小鼠的影響。並分別使用線粒體膜電位及油紅染色來判斷抗氧化活性及降低脂質堆積的效果。經由2D及mass的鑑定，發現了餵食香椿醇萃物的HFD小鼠相較於HFD小鼠，在氧化壓力相關蛋白及脂質代謝相關蛋白的表現上有顯著的差異。HFD上调山梨醇脱氢酶（SDH），UDP-葡萄糖的脱氢酶（UDGH），谷氨酸脱氢酶（GDH）蛋白表达的建议，HFD增加的小鼠肝脏糖异生。在另一方面，HFD + TSL-E抑制糖原异生增加，GDH的蛋白的表达下降，磷酸烯醇式丙酮酸羧2（PCK2）证实了，恢复的SDH，UDGH HFD。虽然HFD70 kDa的热休克蛋白（HSP70），过氧化氢酶（CAT），HSPd1增加和减少过氧化物酶（PRDX6）蛋白的表达，HFD+ TSL-E增加PRDX6和恢复HSP70，Hspd1和猫的蛋白表达，表示，TSL-E表现出抗氧化活性。 Luciferase report assay的結果顯示香椿醇萃物具有活化PPARα及PPARγ，且在動物實驗種也發現香椿純萃物會增加HFD小鼠肝臟PPARα及PPARγ的表現。
在HFD小鼠中，餵食香椿醇萃物會降低氧化壓力及抑制多元醇路徑(polyol pathway) 的活化，且會經由活化PPARα及PPARγ改善血脂異常

The major pathogenesis of metabolic syndrome is the development of insulin resistance, which promotes the elevation of blood pressure, dyslipidemia, and dysregulation of glucose metabolism. Among the target tissues of insulin, liver is the principal regulator of glucose and lipid metabolism by controlling hepatic glucose production, glycogen storage and lipogenesis. Toona sinnesis (TS) has been reported to be beneficial for metabolic syndrome, however the effect of TS on liver metabolism is not clear. In the present study, proteomics analysis and Western blot were used to investigate the effect of TSL-E on the high-fat diet (HFD) fed mice. The anti-oxidation activity and lipid lowering effect were investigated by measurement of mitochondria membrane potential (MMP) and Oil-red-O staining. Using the 2D-gel proteomic analysis followed by mass spectrometry identification, we found a clear distinction in differential expression of oxidative stress, glucose metabolism and lipid metabolism related proteins responding TSL-E. HFD up regulated sorbitol dehydrogenase (SDH), UDP-6 glucose dehydrogenase (UDGH), glutamate dehydrogenase (GDH) proteins expression suggested that HFD increased gluconeogenesis in liver of mice. In the other hand, HFD+TSL-E inhibited the increasing of gluconeogenesis in HFD by restored SDH, UDGH, GDH protein expression that were confirmed by decreased of phosphoenolpyruvate carboxykinase 2 (PCK2). While HFD increased heat shock protein 70 kda (HSP70), Catalase (Cat), HSPd1 and decreased peroxiredoxin 6 (Prdx6) proteins expression, HFD+TSL-E increased Prdx6 and restored HSP70, Hspd1 and Cat proteins expression, indicated that TSL-E exhibited anti-oxidant activity. TSL-E also shown high peroxisome proliferator-activated receptor alpha/gamma (PPARalpha/gamma)-dependent luciferase activity that confirmed by increased the expression of PPARalpha/gamma in liver of HFD mice treated with TSL-E. In conclusion, TSL-E improved the dyslipidemia of high fat diet mice through activation of PPARalpha/gamma, reduction of oxidative stress and decreasing gluconeogenesis by inhibition of the activation of the polyol pathway

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