多草药提取物通过降低MAPK/JNK通路的调节,调节Nrf-2/Keap-1表达,并刺激胰岛素信号传递来改善aloxan诱导的糖尿病大鼠中的糖代谢控制
Bilal Aslam1, Asif Hussain1,2, Muhammad Naeem Faisal1
1Institute of Physiology and Pharmacology, University of Agriculture, Faisalabad-38040, Faisalabad, Punjab, Pakistan.
Iranian journal of basic medical sciences
|January 18, 2024
概括
这种多草药提取物在老鼠模型中显示出显著的抗氧化和抗糖尿病作用. 它有效调节参与葡萄糖调节和氧化应激的关键信号通路,提供一种潜在的自然治疗方法.
科学领域:
- 药理学和毒理学 药理学和毒理学
- 生物化学 生物化学
- 草药是一种草药.
背景情况:
- 糖尿病是一种全球性健康问题,其特点是高血糖和氧化应激.
- 多草药提取物由于协同作用,为开发新型抗糖尿病疗法提供了有希望的途径.
- 卡西亚absus,Gymnema sylvestre,Nigella sativa和Piper nigrum是传统上使用的具有已知的药用功能的草药.
研究的目的:
- 评估多草本提取物 (PHE) 的抗氧化和抗糖尿病潜力,其中包括Cassia absus,Gymnema sylvestre,Nigella sativa和Piper nigrum.
- 在Wistar大鼠的阿洛素诱导糖尿病模型中研究PHE作用的潜在分子机制.
- 通过急性口服毒性研究来评估PHE的安全性.
主要方法:
- 在体外:HPLC特征,DPPH激素清除试验和α-氨酶抑制试验.
- 在体内:阿洛诱导的糖尿病大鼠接受了PHE (200,400,600毫克/公斤) 或glibenclamide (10毫克/公斤) 治疗六周.
- 分析包括生物化学标记,氧化应激参数,基因病理学和关键信号通路的基因表达 (RT-qPCR).
主要成果:
- PHE表现出显著的DPPH清除 (IC50: 1.60 mg/ml) 和α-氨酶抑制 (IC50: 0.82 mg/ml),表明抗氧化和抗糖尿病特性.
- 在糖尿病大鼠中,PHE没有显示出高达2000mg/kg的毒性,并且剂量取决于改善的血糖控制,胰岛素水平和HbA1c.
- PHE调节MAPK/JNK,Nrf-2/Keap-1和胰岛素信号通路,减少胰腺组织中的氧化应激和炎症.
结论:
- 多草药提取物具有显著的抗氧化和抗糖尿病活性.
- PHE通过调节关键的细胞信号通路,包括MAPK/JNK,Nrf-2/Keap-1和胰岛素信号来发挥其治疗作用.
- 这项研究支持PHE作为治疗糖尿病的天然治疗剂的潜力.
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