Abstract：
METHODS: Isorhamnetin is a natural flavonoid with various pharmacological activities, which can be widely and continuously ingested by humans and animals through their daily diet. The aim of this study is to explore the benefits and molecular mechanisms of isorhamnetin on oocyte maturation.
RESULTS: Oocytes are incubated with isorhamnetin (5, 10, 20, and 30 µM) for 44 h. Isorhamnetin (10 µM) increases the polar body extrusion rate of oocytes. Furthermore, isorhamnetin alleviates oxidative stress by inhibiting reactive oxygen species levels and stimulating SOD2 protein expression. The changes in intracellular mitochondrial autophagy and apoptosis-related proteins (Bcl-2, Bax/Bcl-2, and C-Casp3) indicate that isorhamnetin inhibits oocyte apoptosis. Isorhamnetin inhibits endoplasmic reticulum stress by reducing the protein expression of CHOP and GRP78 and improving the normal distribution rate of endoplasmic reticulum. Mechanistic studies show that isorhamnetin activates the PI3K/Akt signaling pathway.
CONCLUSIONS: Isorhamnetin promotes oocyte maturation by inhibiting oxidative stress, mitochondrial dysregulation, apoptosis, and endoplasmic reticulum stress, which have important potential for improving oocyte quality and treating female infertility.
RESULTS: Oocytes are incubated with isorhamnetin (5, 10, 20, and 30 µM) for 44 h. Isorhamnetin (10 µM) increases the polar body extrusion rate of oocytes. Furthermore, isorhamnetin alleviates oxidative stress by inhibiting reactive oxygen species levels and stimulating SOD2 protein expression. The changes in intracellular mitochondrial autophagy and apoptosis-related proteins (Bcl-2, Bax/Bcl-2, and C-Casp3) indicate that isorhamnetin inhibits oocyte apoptosis. Isorhamnetin inhibits endoplasmic reticulum stress by reducing the protein expression of CHOP and GRP78 and improving the normal distribution rate of endoplasmic reticulum. Mechanistic studies show that isorhamnetin activates the PI3K/Akt signaling pathway.
CONCLUSIONS: Isorhamnetin promotes oocyte maturation by inhibiting oxidative stress, mitochondrial dysregulation, apoptosis, and endoplasmic reticulum stress, which have important potential for improving oocyte quality and treating female infertility.
摘要：
方法：异鼠李素是一种具有多种药理活性的天然黄酮类化合物，人类和动物可以通过日常饮食广泛和持续地摄入。本研究的目的是探讨异鼠李素对卵母细胞成熟的益处和分子机制。
结果：将卵母细胞与异鼠李素（5、10、20和30µM）一起孵育44小时。异鼠李素（10µM）增加了卵母细胞的极体挤出速率。此外，异鼠李素通过抑制活性氧水平和刺激SOD2蛋白表达来减轻氧化应激。细胞内线粒体自噬和凋亡相关蛋白（Bcl-2，Bax/Bcl-2和C-Casp3）的变化表明异鼠李素抑制卵母细胞凋亡。异鼠李素通过降低CHOP和GRP78的蛋白表达和提高内质网的正态分布率来抑制内质网应激。机制研究表明，异鼠李素激活PI3K/Akt信号通路。
结论：异鼠李素通过抑制氧化应激促进卵母细胞成熟,线粒体失调,凋亡，和内质网应激，这对于改善卵母细胞质量和治疗女性不孕症具有重要的潜力。
结果：将卵母细胞与异鼠李素（5、10、20和30µM）一起孵育44小时。异鼠李素（10µM）增加了卵母细胞的极体挤出速率。此外，异鼠李素通过抑制活性氧水平和刺激SOD2蛋白表达来减轻氧化应激。细胞内线粒体自噬和凋亡相关蛋白（Bcl-2，Bax/Bcl-2和C-Casp3）的变化表明异鼠李素抑制卵母细胞凋亡。异鼠李素通过降低CHOP和GRP78的蛋白表达和提高内质网的正态分布率来抑制内质网应激。机制研究表明，异鼠李素激活PI3K/Akt信号通路。
结论：异鼠李素通过抑制氧化应激促进卵母细胞成熟,线粒体失调,凋亡，和内质网应激，这对于改善卵母细胞质量和治疗女性不孕症具有重要的潜力。
