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柿子叶中的类黄酮(FPL)通过 NF-κB 通路减轻 MC3T3-E1 细胞中 H2O2 诱导的细胞凋亡。

Flavonoids from persimmon (Diospyros kaki) leaves (FPL) attenuate H2O2-induced apoptosis in MC3T3-E1 cells via the NF-κB pathway.

机构信息

Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, P.R. China+86-029-82668463.

出版信息

Food Funct. 2014 Mar;5(3):471-9. doi: 10.1039/c3fo60522a.

Abstract

The leaves of persimmon (Diospyros kaki L.) have long been used in Chinese medicine for the treatment of paralysis, frostbite, burns, and to stop bleeding. Flavonoids of persimmon leaves (FPL) are known for their antioxidant activity in murine osteoblast MC3T3-E1 cells, but their mechanisms in osteoblast cells injured by oxidative stress are unknown. In this study, the effects of FPL on oxidative damage were investigated by addressing their potential therapeutic or toxic effects on H2O2-stimulated MC3T3-E1 cells. MC3T3-E1 cells were pretreated with FPL (1.25, 2.5 and 5 μg mL(-1)) for 24 h and were then exposed to 250 μM H2O2 for an additional 6 h. FPL pre-incubated with MC3T3-E1 cells did not present any cytotoxicity, instead they increased cell viability and ΔΨm in a dose-dependent manner when challenged with H2O2. Treatment with this pro-incubated FPL also significantly suppressed the production of MDA and NO and the activity of iNOS. The mRNA expression of iNOS, COX-2, Bax, Bcl-2, and caspase-3 and the protein expression of NF-κB/p65 showed that FPL significantly inhibited apoptosis in H2O2-stimulated MC3T3-E1 cells. These results suggest that the molecular mechanism of FPL in anti-apoptosis was associated with the suppression of the translocation of NF-κB/p65 into the nucleus. The protective effect of FPL could provide a promising approach for the treatment of osteoporosis.

摘要

柿子叶(Diospyros kaki L.)长期以来一直被用于中医治疗瘫痪、冻伤、烧伤和止血。柿子叶中的类黄酮以其在鼠成骨细胞 MC3T3-E1 细胞中的抗氧化活性而闻名,但它们在氧化应激损伤的成骨细胞中的机制尚不清楚。在这项研究中,通过研究 FPL 对 H2O2 刺激的 MC3T3-E1 细胞的潜在治疗或毒性作用,研究了 FPL 对氧化损伤的影响。将 MC3T3-E1 细胞用 FPL(1.25、2.5 和 5 μg mL(-1))预处理 24 h,然后再用 250 μM H2O2 处理 6 h。用 FPL 预孵育的 MC3T3-E1 细胞没有表现出任何细胞毒性,相反,当用 H2O2 处理时,它们以剂量依赖性的方式增加细胞活力和 ΔΨm。用这种预孵育的 FPL 处理还显著抑制 MDA 和 NO 的产生以及 iNOS 的活性。iNOS、COX-2、Bax、Bcl-2 和 caspase-3 的 mRNA 表达以及 NF-κB/p65 的蛋白表达表明,FPL 显著抑制了 H2O2 刺激的 MC3T3-E1 细胞中的凋亡。这些结果表明,FPL 抗细胞凋亡的分子机制与抑制 NF-κB/p65 向核内易位有关。FPL 的保护作用可能为骨质疏松症的治疗提供一种有前途的方法。

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