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首页> 外文期刊>Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research >Phycocyanin may suppress d-galactose-induced human lens epithelial cell apoptosis through mitochondrial and unfolded protein response pathways
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Phycocyanin may suppress d-galactose-induced human lens epithelial cell apoptosis through mitochondrial and unfolded protein response pathways

机译:藻蓝蛋白可能通过线粒体和未折叠的蛋白反应途径抑制d-半乳糖诱导的人晶状体上皮细胞凋亡

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Apoptosis of lens epithelial cell (LEC) plays an important role in cataract formation, and its prevention may be one of the therapeutic strategies in treating cataract. This study used human lens epithelial cell (hLEC) line SRA01/04 to investigate the protective effect and mechanism of phycocyanin on glactose-induced apoptosis in hLEC. hLECs were cultured in D/F 12-10% FBS medium containing 125mM d-galactose with or without phycocyanin. Cell viability was assessed by methylthiazol tetrazolium (MTT) assay. Cell apoptosis was elevated with Wright-Giemsa staining, AO/EB double staining, and DNA fragmentation assay. Mitochondrial apoptosis-associated molecules and unfolded protein response-associated molecules from cultured SRA01/04 cells were quantified using protein blot analysis. The results demonstrated that phycocyanin suppressed SRA01/04 cells' morphologic changes and apoptosis induced by d-galactose, inhibited the expression and activation of caspase 3, alternated the Bax/Bcl-2 ratio, and down-regulated the level of p53, GRP78, and CHOP in d-galactose-treated SRA01/04 cells. These results suggest that phycocyanin might suppress d-galactose-induced hLEC apoptosis through two pathways: mitochondrial pathway, involving p53 and Bcl-2 family protein expression, and unfolded protein response pathway, involving GRP78 and CHOP expression.
机译:晶状体上皮细胞(LEC)的凋亡在白内障形成中起重要作用,其预防可能是治疗白内障的治疗策略之一。本研究使用人晶状体上皮细胞(hLEC)系SRA01 / 04来研究藻蓝蛋白对乳糖诱导的hLEC细胞凋亡的保护作用及其机制。将hLECs在含有125mM d-半乳糖的D / F 12-10%FBS培养基中培养或不培养藻蓝蛋白。通过甲基噻唑四唑(MTT)测定法评估细胞活力。 Wright-Giemsa染色,AO / EB双重染色和DNA片段测定法可提高细胞凋亡。使用蛋白印迹分析定量来自培养的SRA01 / 04细胞的线粒体凋亡相关分子和未折叠的蛋白反应相关分子。结果表明,藻蓝蛋白抑制了SRA01 / 04细胞的形态变化和d-半乳糖诱导的凋亡,抑制了caspase 3的表达和激活,改变了Bax / Bcl-2的比例,并下调了p53,GRP78, d-半乳糖处理的SRA01 / 04细胞中的CHOP和CHOP。这些结果表明,藻蓝蛋白可能通过两个途径抑制d-半乳糖诱导的hLEC细胞凋亡:线粒体途径(涉及p53和Bcl-2家族蛋白表达)和未折叠的蛋白应答途径(涉及GRP78和CHOP表达)。

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