Abstract：
BACKGROUND: Diabetes mellitus (DM) is a chronic metabolic disease characterized by hyperglycemia, and its increasing prevalence is a global concern. Early diagnostic markers and therapeutic targets are essential for DM prevention and treatment. Pueraria, derived from kudzu root, is used clinically for various symptoms, and its active compound, Puerarin, shows promise in improving insulin resistance and reducing inflammation.
OBJECTIVE: This study aims to evaluate the protective effects of metformin and Puerarin at different doses in an STZ-induced DM mouse model. The intricate metabolites within the serum of STZ-induced diabetic mice were subjected to thorough investigation, thus elucidating the intricate mechanism through which Puerarin demonstrates notable efficacy in the treatment of diabetes.
METHODS: An STZ-induced DM mouse model is established. Mice are treated with metformin and puerarin at varying doses. Physiological, biochemical, and histomorphological assessments are performed. Metabolomics analysis is carried out on serum samples from control, DM, metformin, and medium-dose Puerarin groups. Western blot and qRT-PCR technologies are used to validate the mechanisms.
RESULTS: The DM mouse model replicates abnormal blood glucose, insulin levels, physiological, biochemical irregularities, as well as liver and pancreas damage. Treatment with metformin and Puerarin restores these abnormalities, reduces organ injury, and modulates AMPK, PPARγ, mTOR, and NF-κB protein and mRNA expression. Puerarin activates the AMPK-mTOR and PPARγ-NF-κB signaling pathways, regulating insulin signaling, glucolipid metabolism, and mitigating inflammatory damage.
CONCLUSIONS: This study demonstrates that Puerarin has the potential to treat diabetes by modulating key signaling pathways. The focus was on the finding that Puerarin has been shown to improve insulin signaling, glucolipid metabolism and attenuate inflammatory damage through the modulation of the AMPK-mTOR and PPARγ-NF-κB pathways. The discovery of Puerarin\'s favorable protective effect and extremely complex mechanism highlights its prospect in the treatment of diabetes and provides theoretical support for its comprehensive development and utilization.
OBJECTIVE: This study aims to evaluate the protective effects of metformin and Puerarin at different doses in an STZ-induced DM mouse model. The intricate metabolites within the serum of STZ-induced diabetic mice were subjected to thorough investigation, thus elucidating the intricate mechanism through which Puerarin demonstrates notable efficacy in the treatment of diabetes.
METHODS: An STZ-induced DM mouse model is established. Mice are treated with metformin and puerarin at varying doses. Physiological, biochemical, and histomorphological assessments are performed. Metabolomics analysis is carried out on serum samples from control, DM, metformin, and medium-dose Puerarin groups. Western blot and qRT-PCR technologies are used to validate the mechanisms.
RESULTS: The DM mouse model replicates abnormal blood glucose, insulin levels, physiological, biochemical irregularities, as well as liver and pancreas damage. Treatment with metformin and Puerarin restores these abnormalities, reduces organ injury, and modulates AMPK, PPARγ, mTOR, and NF-κB protein and mRNA expression. Puerarin activates the AMPK-mTOR and PPARγ-NF-κB signaling pathways, regulating insulin signaling, glucolipid metabolism, and mitigating inflammatory damage.
CONCLUSIONS: This study demonstrates that Puerarin has the potential to treat diabetes by modulating key signaling pathways. The focus was on the finding that Puerarin has been shown to improve insulin signaling, glucolipid metabolism and attenuate inflammatory damage through the modulation of the AMPK-mTOR and PPARγ-NF-κB pathways. The discovery of Puerarin\'s favorable protective effect and extremely complex mechanism highlights its prospect in the treatment of diabetes and provides theoretical support for its comprehensive development and utilization.
摘要：
背景：糖尿病（DM）是一种以高血糖为特征的慢性代谢性疾病，其日益流行是一个全球关注的问题。早期诊断标记物和治疗靶点对于DM的预防和治疗至关重要。葛根,来源于葛根,临床上用于各种症状，和它的活性化合物，葛根素,显示出改善胰岛素抵抗和减少炎症的希望。
目的：本研究旨在评估不同剂量的二甲双胍和葛根素对STZ诱导的DM小鼠模型的保护作用。对STZ诱导的糖尿病小鼠血清中复杂的代谢物进行了彻底的研究，从而阐明了葛根素在糖尿病治疗中表现出显著疗效的复杂机制。
方法：建立STZ诱导的DM小鼠模型。用不同剂量的二甲双胍和葛根素治疗小鼠。生理学,生物化学，并进行组织形态学评估。对来自对照的血清样品进行代谢组学分析，DM,二甲双胍,和中剂量葛根素组。使用蛋白质印迹和qRT-PCR技术来验证机制。
结果：DM小鼠模型复制血糖异常，胰岛素水平，生理,生化不规则，还有肝脏和胰腺的损伤.二甲双胍和葛根素治疗可恢复这些异常，减少器官损伤，并调制AMPK，PPARγ,mTOR,NF-κB蛋白和mRNA表达。葛根素激活AMPK-mTOR和PPARγ-NF-κB信号通路,调节胰岛素信号，糖脂代谢，减轻炎症损伤。
结论：本研究表明葛根素具有通过调节关键信号通路治疗糖尿病的潜力。重点是发现葛根素已被证明可以改善胰岛素信号，糖脂代谢和通过调节AMPK-mTOR和PPARγ-NF-κB途径减轻炎症损伤。葛根素具有良好的保护作用和极其复杂的机制,突出了其在糖尿病治疗中的应用前景,为其综合开发利用提供了理论支持。
目的：本研究旨在评估不同剂量的二甲双胍和葛根素对STZ诱导的DM小鼠模型的保护作用。对STZ诱导的糖尿病小鼠血清中复杂的代谢物进行了彻底的研究，从而阐明了葛根素在糖尿病治疗中表现出显著疗效的复杂机制。
方法：建立STZ诱导的DM小鼠模型。用不同剂量的二甲双胍和葛根素治疗小鼠。生理学,生物化学，并进行组织形态学评估。对来自对照的血清样品进行代谢组学分析，DM,二甲双胍,和中剂量葛根素组。使用蛋白质印迹和qRT-PCR技术来验证机制。
结果：DM小鼠模型复制血糖异常，胰岛素水平，生理,生化不规则，还有肝脏和胰腺的损伤.二甲双胍和葛根素治疗可恢复这些异常，减少器官损伤，并调制AMPK，PPARγ,mTOR,NF-κB蛋白和mRNA表达。葛根素激活AMPK-mTOR和PPARγ-NF-κB信号通路,调节胰岛素信号，糖脂代谢，减轻炎症损伤。
结论：本研究表明葛根素具有通过调节关键信号通路治疗糖尿病的潜力。重点是发现葛根素已被证明可以改善胰岛素信号，糖脂代谢和通过调节AMPK-mTOR和PPARγ-NF-κB途径减轻炎症损伤。葛根素具有良好的保护作用和极其复杂的机制,突出了其在糖尿病治疗中的应用前景,为其综合开发利用提供了理论支持。
