Yang Ah Young, Kim Jung-Yeon, Gwon Mi-Gyeong, Kim Kiryeong, Kwon Hyun Hee, Leem Jaechan, Kim Sung-Woo
Department of Immunology, School of Medicine, Daegu Catholic University, Daegu, Republic of Korea.
Department of Internal Medicine, School of Medicine, Daegu Catholic University, Daegu, Republic of Korea.
Redox Rep. 2025 Dec;30(1):2500271. doi: 10.1080/13510002.2025.2500271. Epub 2025 May 5.
Renal fibrosis is a key factor in the progression of chronic kidney disease (CKD), and current treatments remain inadequate. In this study, we investigated the therapeutic effects of cynaroside (Cyn), a natural flavonoid, in a mouse model of renal fibrosis induced by unilateral ureteral obstruction. Cyn treatment significantly ameliorated tubular injury and interstitial fibrosis while improving renal function. Mechanistically, Cyn inhibited the expression of fibrosis-related proteins and suppressed Smad2/3 phosphorylation. Additionally, Cyn reduced myofibroblast accumulation by inhibiting epithelial-mesenchymal transition, as indicated by increased E-cadherin expression and decreased levels of mesenchymal markers. Cyn also reduced oxidative stress by downregulating the prooxidant enzyme NADPH oxidase 4 and restoring antioxidant enzymes. Furthermore, Cyn attenuated ferroptosis by regulating key proteins, including acyl-CoA synthetase long-chain family member 4, transferrin receptor 1, and glutathione peroxidase 4, while also restoring glutathione levels. Cyn alleviated endoplasmic reticulum stress, as evidenced by the downregulation of key markers such as glucose-regulated protein 78 and activating transcription factor 6, and reduced inflammation, as confirmed by decreased macrophage infiltration and lower cytokine production. Overall, Cyn demonstrated broad protective effects against renal fibrosis by modulating oxidative stress, ferroptosis, ER stress, and inflammation, positioning it as a potential therapeutic agent for CKD management.
肾纤维化是慢性肾脏病(CKD)进展的关键因素,目前的治疗方法仍然不足。在本研究中,我们研究了天然黄酮类化合物木犀草苷(Cyn)对单侧输尿管梗阻诱导的肾纤维化小鼠模型的治疗作用。Cyn治疗显著改善了肾小管损伤和间质纤维化,同时改善了肾功能。机制上,Cyn抑制纤维化相关蛋白的表达并抑制Smad2/3磷酸化。此外,Cyn通过抑制上皮-间质转化减少肌成纤维细胞积累,表现为E-钙黏蛋白表达增加和间充质标志物水平降低。Cyn还通过下调促氧化酶NADPH氧化酶4和恢复抗氧化酶来降低氧化应激。此外,Cyn通过调节关键蛋白,包括酰基辅酶A合成酶长链家族成员4、转铁蛋白受体1和谷胱甘肽过氧化物酶4,减轻铁死亡,同时还恢复了谷胱甘肽水平。Cyn减轻了内质网应激,表现为葡萄糖调节蛋白78和激活转录因子6等关键标志物的下调,并减少了炎症,巨噬细胞浸润减少和细胞因子产生降低证实了这一点。总体而言,Cyn通过调节氧化应激、铁死亡、内质网应激和炎症,对肾纤维化表现出广泛的保护作用,使其成为CKD治疗的潜在药物。