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Abstract Title:The flavonoid fisetin ameliorates renal fibrosis by inhibiting SMAD3输尿管中的磷酸化，氧化损伤和炎症在小鼠中阻塞了肾脏。
摘要来源：
肾脏Res Clin。 2023年5月； 42（3）：325-339。 EPUB 2023 3月22日PMID： 37098680 Han
Article Affiliation:Ha Young Ju
Abstract:BACKGROUND: Renal fibrosis is characterized by the accumulation of extracellular matrix and inflammatory cells and kidney dysfunction, which is a major pathway in the progression of chronic kidney disease (CKD).积累的证据表明氧化应激在IN中起着关键作用CKD通过促炎和纤维化信号通路的ITIAT和进展。 fisetin（3,3,4,7-四氢氟氟氟酮）具有生物学活性，包括抗氧化剂，抗炎和抗衰老作用。 Therefore, we evaluated the antifibrotic effects of fisetin on unilateral ureteral obstruction (UUO)-induced kidneys.
METHODS: C57BL/6 female mice were subjected to right UUO and intraperitoneally injected every other day with fisetin (25 mg/kg/一天）或手术前1小时到手术后7天的车辆。 Kidney samples were analyzed for renal fibrosis (α-smooth muscle actin [α-SMA] expression, collagen deposition, and transforming growth factor [TGF]β1/SMAD3 signaling pathway), oxidative damage (4-HNE and 8-OHdG expression), inflammation (proinflammatory cytokine/chemokine, macrophage, and neutrophil infiltration), and apoptosis （Tunel染色）。培养的人近端小管细胞用Fiset处理in before TGF-βto confirm the TGF-βdownstream pathway (SMAD2/3 phosphorylation).
RESULTS: We found that fisetin treatment protected against renal fibrosis by inhibiting the phosphorylation of SMAD3, oxidative damage, inflammation, apoptotic cell death, and阻塞肾脏中纤维化的M2巨噬细胞的积累。 In cultured human proximal tubular cells, fisetin treatment inhibited TGF-β1-induced phosphorylation of SMAD3 and SMAD2.
CONCLUSION: Fisetin alleviates kidney fibrosis to protect against UUO-induced renal fibrosis, and could be a novel therapeutic阻塞性肾病的药物。