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希尔苏丁通过Keap1/Nrf2通路减轻了糖尿病病中的氧化应激和自

Yao Zhang¹, Bing Yang¹, Miao Tan¹

¹The First Affiliated Hospital of Hebei University of Chinese Medicine, Hebei, 050200, China.

Journal of pharmacological sciences

|April 27, 2025

概括

希尔苏丁证明了糖尿病病 (DKD) 的治疗潜力. 这种天然化合物通过减少氧化应激,增强自和激活Nrf2通路来保护脏.

科学领域:

药理学和病学药理学和病学
自然产品研究自然产品研究
细胞和分子生物学细胞和分子生物学

背景情况:

糖尿病病 (DKD) 是糖尿病的一个主要并发症,导致逐渐的损伤.
目前对DKD的治疗方法存在局限性,需要探索新型治疗剂.
希尔苏丁是一种生物活性类化合物,在各种生物活动中表现出潜力.

研究的目的:

研究hirsutine对糖尿病病 (DKD) 的治疗作用.
在DKD模型中阐明hirsutine的脏保护机制.

主要方法:

在使用高脂肪饮食和链毒素的老鼠中诱导了DKD;高葡萄糖刺激的HK-2细胞被用作体外模型.
评估功能,纤维化标志物 (维门丁,原四,α-SMA),氧化应激 (ROS,MDA,SOD,GSH) 和与自相关的蛋白质 (贝克林1,LC3I/II,P62).
评估了Nrf2信号通路的激活及其下游目标.

主要成果:

希尔苏丁治疗显著改善了DKD大鼠的功能,并减少了纤维化.
希尔苏丁通过降低活性氧物种 (ROS) 和恶性甲酸 (MDA) 水平来减轻氧化应激,同时增加超氧化解酶 (SOD) 和谷氨酸 (GSH) 活性.
希尔苏丁促进了自,并激活了Keap1/Nrf2通路,导致Nrf2水平增加和抗氧化酶的上调.

结论:

希尔苏丁在糖尿病病 (DKD) 中表现出显著的保护作用.
治疗机制包括减轻氧化应激,促进自和调节Keap1/Nrf2信号通路.
希尔苏丁代表了 DKD 管理的有前途的治疗候选人.

关键词:

自自是一种自的过程.糖尿病脏疾病糖尿病脏疾病她的日常生活.凯普1/Nrf2 在线观看氧化应激是一种氧化应激.

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