Astragaloside IV (AST) is a major bioactive compound of Radix Astragali with medical and health benefits. Previous studies have found that AST can reduce the body weights of high-fat diet fed mice. However, the effect of AST on fat metabolism of ageing mice is unclear. In this study, naturally ageing mice were administered intragastrically with AST at 30 mg/kg/day (ageing + AST-L group) and 90 mg/kg/day (ageing + AST-H group) for 16–20 months. Adult (4 months old) and ageing mice were given 1% sodium carboxyl methylcellulose as vehicle. Energy metabolism-related biological parameters of living mice were examined. Moreover, mRNA and protein levels of key enzymes/proteins involved in triglyceride (TG) lipolysis, fatty acid β-oxidation (FAO), ketone body (KB) production and mitochondrial respiratory chain were also examined after sacrifice. Results demonstrated that treatment with AST significantly reduced body weight, white fat and liver/body weight ratio of ageing mice, significantly reduced serum/hepatic TG levels, respiratory quotient, promoted fatty acid mobilization in white adipose tissue, mitochondrial FAO and KB production and mitochondrial biosynthesis/functions in the liver of ageing mice. AST also up-regulated the expression of phosphorylated AMP-activated protein kinase, acetyl-CoA carboxylase, acetyl-coenzyme A synthetase, carnitine palmitoyltransferase 1a/1b, enoyl coenzyme A hydratase-short chain, acyl-CoA dehydrogenase medium chain and mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase-2 involved in fat metabolism. These results indicated that mitochondrial activity could be the target of AST to treat abnormal fat metabolism during ageing.

中文翻译：

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黄芪甲苷通过靶向线粒体活性改善衰老小鼠肝脏中的脂肪代谢

黄芪甲苷 (AST) 是黄芪的主要生物活性化合物具有医疗和健康益处。以前的研究发现，AST可以减轻高脂饮食喂养的小鼠的体重。然而，AST对衰老小鼠脂肪代谢的影响尚不清楚。在这项研究中，自然衰老的小鼠以 30 mg/kg/天（老化 + AST-L 组）和 90 mg/kg/天（老化 + AST-H 组）的 AST 灌胃给药 16-20 个月。成年（4 个月大）和老年小鼠被给予 1% 羧甲基纤维素钠作为载体。检查了活小鼠的能量代谢相关生物学参数。此外，在处死后还检测了参与甘油三酯 (TG) 脂解、脂肪酸 β-氧化 (FAO)、酮体 (KB) 产生和线粒体呼吸链的关键酶/蛋白质的 mRNA 和蛋白质水平。结果表明，用 AST 治疗可显着减轻体重，衰老小鼠的白色脂肪和肝脏/体重比，显着降低血清/肝脏 TG 水平，呼吸商，促进白色脂肪组织中的脂肪酸动员，促进衰老小鼠肝脏中线粒体FAO 和 KB 的产生以及线粒体生物合成/功能。AST 还上调磷酸化 AMP 活化蛋白激酶、乙酰辅酶 A 羧化酶、乙酰辅酶 A 合成酶、肉碱棕榈酰转移酶 1a/1b、烯酰辅酶 A 水合酶-短链、酰基辅酶 A 脱氢酶中链和线粒体 3- 的表达。 hydroxy-3-methylglutaryl-CoA synthase-2 参与脂肪代谢。这些结果表明，线粒体活性可能是 AST 治疗衰老过程中脂肪代谢异常的靶点。呼吸商，促进白色脂肪组织中的脂肪酸动员，线粒体FAO和KB的产生以及衰老小鼠肝脏中的线粒体生物合成/功能。AST 还上调磷酸化 AMP 活化蛋白激酶、乙酰辅酶 A 羧化酶、乙酰辅酶 A 合成酶、肉碱棕榈酰转移酶 1a/1b、烯酰辅酶 A 水合酶-短链、酰基辅酶 A 脱氢酶中链和线粒体 3- 的表达。 hydroxy-3-methylglutaryl-CoA synthase-2 参与脂肪代谢。这些结果表明，线粒体活性可能是 AST 治疗衰老过程中脂肪代谢异常的靶点。呼吸商，促进白色脂肪组织中的脂肪酸动员，线粒体FAO和KB的产生以及衰老小鼠肝脏中的线粒体生物合成/功能。AST 还上调磷酸化 AMP 活化蛋白激酶、乙酰辅酶 A 羧化酶、乙酰辅酶 A 合成酶、肉碱棕榈酰转移酶 1a/1b、烯酰辅酶 A 水合酶-短链、酰基辅酶 A 脱氢酶中链和线粒体 3- 的表达。 hydroxy-3-methylglutaryl-CoA synthase-2 参与脂肪代谢。这些结果表明，线粒体活性可能是 AST 治疗衰老过程中脂肪代谢异常的靶点。AST 还上调磷酸化 AMP 活化蛋白激酶、乙酰辅酶 A 羧化酶、乙酰辅酶 A 合成酶、肉碱棕榈酰转移酶 1a/1b、烯酰辅酶 A 水合酶-短链、酰基辅酶 A 脱氢酶中链和线粒体 3- 的表达。 hydroxy-3-methylglutaryl-CoA synthase-2 参与脂肪代谢。这些结果表明，线粒体活性可能是 AST 治疗衰老过程中脂肪代谢异常的靶点。AST 还上调磷酸化 AMP 活化蛋白激酶、乙酰辅酶 A 羧化酶、乙酰辅酶 A 合成酶、肉碱棕榈酰转移酶 1a/1b、烯酰辅酶 A 水合酶-短链、酰基辅酶 A 脱氢酶中链和线粒体 3- 的表达。 hydroxy-3-methylglutaryl-CoA synthase-2 参与脂肪代谢。这些结果表明，线粒体活性可能是 AST 治疗衰老过程中脂肪代谢异常的靶点。