虾青素对秀丽隐杆线虫衰老的改善作用及机制研究
The aging improvement effects and mechanism of astaxanthin on Caenorhabditis elegans
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摘要: 通过寿命实验、氧化应激、热应激实验研究虾青素(Astaxanthin)对秀丽隐杆线虫衰老和急性应激效应的改善作用并探究其作用机制。秀丽隐杆线虫分为对照组和虾青素处理组(0.8、1.2和1.6 mmol/L),首先研究不同浓度虾青素对野生型线虫寿命的影响,通过平均与最大寿命确定作用的最佳剂量;选用最佳剂量的虾青素作用于野生型和突变株线虫,采用热应激和氧化应激实验研究其可能机制。结果表明:与对照组相比,采用1.2 mmol/L虾青素饲喂秀丽隐杆线虫,野生型线虫平均寿命延长了41.79%(p<0.01),最大寿命延长了32.72%(p<0.01)。热应激及氧化应激实验中,采用1.2 mmol/L虾青素饲喂秀丽隐杆线虫,野生型线虫平均生存时间分别延长了22.54%和24.23%(p<0.01)。1.2 mmol/L虾青素可显著提高sir-2.1突变株线虫的存活时间,但对daf-2、daf-16和eat-2突变株线虫均无显著影响。综上所述,浓度为1.2 mmol/L的虾青素可显著延长野生型线虫的平均寿命和最大寿命,并显著延长其在氧化应激及热应激条件下的平均生存时间和最大生存时间。虾青素延长线虫寿命的功效可能是通过提高线虫的在热及氧化恶劣环境下的耐受能力而实现的,其作用机制可能与胰岛素信号通路及能量限制通路有关。Abstract: In this study, the mechanism of the aging improvement of astaxanthin on Caenorhabditis elegans was studied by lifespan extension analysis, oxidative stress, and heat stress analyses. Astaxanthin-treated groups ( 0.8, 1.2, and 1.6 mmol/L) were compared to the control group to explore the anti-aging effect of different concentrations in wild-type nematode and identify the optimal dose according to mean and maximum lifespan extension.The optimal dose of astaxanthin was 1.2 mmol/L, at which dose astaxanthin prolonged mean lifespan of wild type nematode by 41.79% ( p < 0.01) and increased maximum lifespan by 32.72% ( p < 0.01) .The possible mechanisms of astaxanthin 's aging effects were further studied using the1.2 mmol/L treatment to test its impact on resistance to heat and oxidative stress. The mean survival times of astaxanthin-treated wild type nematode after oxidative and heat stress were increased by 22.54% and 24.23% ( p < 0.01) , respectively. In oxidative stress and heat stress experiments, 1.2 mmol/L astaxanthin could significantly increase the survival time of the sir-2.1 mutant nematodes, but had no significant effect on daf-2, daf-16, or eat-2 mutants. The above results suggested that astaxanthin can prolong the lifespan of nematodes by increasing stress tolerance and its mechanism may be related to the insulin signaling and diet-restriction pathways.