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龙须菜水提物可预防 H₂O₂诱导的 DNA 损伤、生长抑制和细胞周期停滞。

Aqueous extracts of the edible Gracilaria tenuistipitata are protective against H₂O₂-induced DNA damage, growth inhibition, and cell cycle arrest.

机构信息

Department of Seafood Science, National Kaohsiung Marine University, Kaohsiung 811, Taiwan.

出版信息

Molecules. 2012 Jun 13;17(6):7241-54. doi: 10.3390/molecules17067241.

DOI:10.3390/molecules17067241
PMID:22695230
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6268842/
Abstract

Potential antioxidant properties of an aqueous extract of the edible red seaweed Gracilaria tenuistipitata (AEGT) against oxidative DNA damage were evaluated. The AEGT revealed several antioxidant molecules, including phenolics, flavonoids and ascorbic acid. In a cell-free assay, the extract exhibited 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity that significantly reduced H₂O₂-induced plasmid DNA breaks in a dose-response manner (P < 0.001). The AEGT also suppressed H₂O₂-induced oxidative DNA damage in H1299 cells by reducing the percentage of damaged DNA in a dose-response manner (P < 0.001) as measured by a modified alkaline comet-nuclear extract (comet-NE) assay. The MTT assay results showed that AEGT confers significant protection against H₂O₂-induced cytotoxicity and that AEGT itself is not cytotoxic (P < 0.001). Moreover, H₂O₂-induced cell cycle G2/M arrest was significantly released when cells were co-treated with different concentrations of AEGT (P < 0.001). Taken together, these findings suggest that edible red algae Gracilaria water extract can prevent H₂O₂-induced oxidative DNA damage and its related cellular responses.

摘要

评估了可食用红藻龙须菜(AEGT)水提物的潜在抗氧化特性,以对抗氧化 DNA 损伤。AEGT 显示出几种抗氧化分子,包括酚类、类黄酮和抗坏血酸。在无细胞测定中,该提取物表现出 1,1-二苯基-2-苦基肼(DPPH)自由基清除活性,可显著降低 H₂O₂诱导的质粒 DNA 断裂,呈剂量反应方式(P < 0.001)。AEGT 还通过降低改良碱性彗星核提取物(彗星-NE)测定中损伤 DNA 的百分比,以剂量反应方式抑制 H1299 细胞中 H₂O₂诱导的氧化 DNA 损伤(P < 0.001)。MTT 测定结果表明,AEGT 对 H₂O₂诱导的细胞毒性具有显著的保护作用,并且 AEGT 本身没有细胞毒性(P < 0.001)。此外,当用不同浓度的 AEGT 共同处理细胞时,H₂O₂诱导的细胞周期 G2/M 阻滞显著释放(P < 0.001)。总之,这些发现表明可食用红藻龙须菜水提物可以预防 H₂O₂诱导的氧化 DNA 损伤及其相关的细胞反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/7236cc9ded4d/molecules-17-07241-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/5b50d936dc2e/molecules-17-07241-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/792516296144/molecules-17-07241-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/b989fe21d130/molecules-17-07241-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/e62b9f7e8b40/molecules-17-07241-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/7236cc9ded4d/molecules-17-07241-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/5b50d936dc2e/molecules-17-07241-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/792516296144/molecules-17-07241-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/b989fe21d130/molecules-17-07241-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/e62b9f7e8b40/molecules-17-07241-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9702/6268842/7236cc9ded4d/molecules-17-07241-g005.jpg

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