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龙须菜提取物在体内诱导艾氏腹水癌细胞凋亡并抑制肿瘤。

Gracilaria edulis extract induces apoptosis and inhibits tumor in Ehrlich ascites tumor cells in vivo.

机构信息

Medical University of the Americas, Charlestown, Nevis, West Indies.

出版信息

BMC Complement Altern Med. 2013 Nov 25;13:331. doi: 10.1186/1472-6882-13-331.

DOI:10.1186/1472-6882-13-331
PMID:24274337
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4222716/
Abstract

BACKGROUND

Marine environment is inestimable for their chemical and biological diversity and therefore is an extraordinary resource for the discovery of new anticancer drugs. Recent development in elucidation of the mechanism and therapeutic action of natural products helped to evaluate for their potential activity.

METHODS

We evaluated Gracilaria edulis J. Ag (Brown algae), for its antitumor potential against the Ehrlich ascites tumor (EAT) in vivo and in vitro. Cytotoxicity evaluation of Ethanol Extract of Gracilaria edulis (EEGE) using EAT cells showed significant activity. In vitro studies indicated that EEGE cytotoxicity to EAT cells is mediated through its ability to produce reactive oxygen species (ROS) and therefore decreasing intracellular glutathione (GSH) levels may be attributed to oxidative stress.

RESULTS

Apoptotic parameters including Annexin-V positive cells, increased levels of DNA fragmentation and increased caspase-2, caspase-3 and caspase-9 activities indicated the mechanism might be by inducing apoptosis. Intraperitoneally administration of EEGE to EAT-bearing mice helped to increase the lifespan of the animals significantly inhibited tumor growth and increased survival of mice. Extensive hematology, biochemistry and histopathological analysis of liver and kidney indicated that daily doses of EEGE up to 300 mg/kg for 35 days are well tolerated and did not cause hematotoxicity nor renal or hepatotoxicity.

CONCLUSION

Comprehensive antitumor analysis in animal model and in Ehrlich Ascites Tumor cells was done including biochemical, and pathological evaluations indicate antitumor activity of the extract and non toxic in vivo. It was evident that the mechanism explains the apoptotic activity of the algae extract.

摘要

背景

海洋环境拥有丰富的化学和生物多样性,是发现新型抗癌药物的宝贵资源。近年来,天然产物作用机制和治疗作用的阐明取得了新的进展,有助于评估其潜在的活性。

方法

我们评估了江蓠(红藻)的抗肿瘤潜力,对体内和体外艾氏腹水瘤(EAT)进行了评估。江蓠乙醇提取物(EEGE)对 EAT 细胞的细胞毒性评估显示出显著的活性。体外研究表明,EEGE 对 EAT 细胞的细胞毒性是通过其产生活性氧(ROS)的能力介导的,因此,细胞内谷胱甘肽(GSH)水平的降低可能归因于氧化应激。

结果

包括 Annexin-V 阳性细胞在内的凋亡参数增加、DNA 片段水平增加以及 caspase-2、caspase-3 和 caspase-9 活性增加表明,机制可能是通过诱导细胞凋亡。EEGE 腹腔注射给 EAT 荷瘤小鼠,显著提高了动物的寿命,抑制了肿瘤生长,提高了小鼠的存活率。对肝和肾的广泛血液学、生物化学和组织病理学分析表明,每天给予 EEGE 高达 300mg/kg,连续 35 天,耐受性良好,不会引起血液毒性或肾或肝毒性。

结论

在动物模型和艾氏腹水瘤细胞中进行了全面的抗肿瘤分析,包括生化和病理评估,表明提取物具有抗肿瘤活性,且在体内无毒性。很明显,该机制解释了藻类提取物的凋亡活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/7905cf5b6e0e/1472-6882-13-331-10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/2276bf63431c/1472-6882-13-331-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/d5d3213b4875/1472-6882-13-331-2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/4ff0ec50fe97/1472-6882-13-331-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/dc40c2e1cb0c/1472-6882-13-331-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/9e871967e3a5/1472-6882-13-331-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/44b0af1b9f7b/1472-6882-13-331-8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/beebc8657506/1472-6882-13-331-9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/7905cf5b6e0e/1472-6882-13-331-10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/2276bf63431c/1472-6882-13-331-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/d5d3213b4875/1472-6882-13-331-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/dbeb21b5574c/1472-6882-13-331-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/fbfe926c270d/1472-6882-13-331-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/4ff0ec50fe97/1472-6882-13-331-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/dc40c2e1cb0c/1472-6882-13-331-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/9e871967e3a5/1472-6882-13-331-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/44b0af1b9f7b/1472-6882-13-331-8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c1b/4222716/beebc8657506/1472-6882-13-331-9.jpg
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