转录组测序分析虾青素对肝癌HepG2细胞的抑制作用

目的 探讨虾青素处理肝癌细胞后的基因表达差异,并对其进行生物学信息分析。方法 虾青素处理细胞后,用TRIzol试剂提取RNA,选用Illumina TruseqTM RNA sample prep Kit方法进行文库构建、测序,最后进行差异表达基因及功能富集分析。结果 转录组测序得到对照组和处理组总的数据量分别有39 642 566和497 1 55 920条,过滤得到各组数据量所占比例分别为94.89%和93.56%,共检测到77 344个转录本,有统计学差异表达基因4 997个,其中上调的基因1 564个,下调的基因3 433个。结论 虾青素通过影响多个与代谢相关的生物学进程和信号通路,其中抑制翻译过程可能在虾青素调控肝癌的生长抑制过程中发挥主要作用。     

虾青素防治冠心病作用机制的研究进展

心血管病死亡率占我国主要疾病死因首位，其中冠心病是临床最常见死亡原因之一。虾青素因其独特结构被认为是一种适合预防及治疗冠心病的药物。本文对近年来虾青素在防治冠心病方面的研究进展，包括抗氧化、抗炎、降压、改善糖代谢、调节脂代谢和心肌梗死后保护作用作一综述。     

Effect of astaxanthin and melatonin on cell viability and DNA damage in human breast cancer cell lines

BackgroundAstaxanthin is a xanthophyll pigment found in algae and marine animals, having strong anti-oxidative, anti-tumoral, and anti-inflammatory effects. Additionally, melatonin has shown inhibitory effects on the growth of human breast cancer cells. The aim of the present study was to evaluate the effect of astaxanthin and the combined effects of astaxanthin and melatonin on breast cancer cells and the non-tumoral breast cell line.Materials and methodsThe human breast cancer cell lines, T47D and MDA-MB-231, and non-tumorigenic cell line MCF 10A were treated and compared to astaxanthin, melatonin, and co-administration of these two compounds. Cell viability, apoptosis induction, Bcl-2 protein expression, and DNA damage were measured by MTT assay, acridine orange/ethidium bromide (AO/EB) staining, immunocytochemistry, and comet assay.ResultsAstaxanthin at lower doses than melatonin reduced cell viability and Bcl2 expression, induced apoptosis and DNA damage in MDA-MB-231 and T47D. Meanwhile, the effects of astaxanthin on cell cytotoxicity, apoptosis, and DNA damage in MCF10A cells are insignificant compared to MDA-MB-231 and T47D. Moreover, the results indicated that astaxanthin in T47D cells caused more cell death compared to MDA-MB-231 cells. Astaxanthin induced cell death on breast cancer cells and without cell cytotoxicity for non-cancerous cells.ConclusionFurthermore, the presence of astaxanthin increased the function of melatonin-induced cell death in breast cancer cells.     

Effect of astaxanthin intervention on contrast-induced acute kidney injury in experimental rats

Objective To explore the protective effect and mechanism of astaxanthin (AST) on the acute kidney injury induced by iohexol in rats. Method Thirty rats were randomly divided into five groups: control group (Ctrl); iohexol group (CM); astaxanthin group (AST, 100 mg/kg), low astaxanthin dose group (LAST+CM, 50 mg/kg) and high astaxanthin dose group (HAST+CM, 100 mg/kg), 6 in each group. The rats in AST, LAST+CM, HAST+CM groups were administrated with AST by oral gavages using an intubation needle for 10 consecutive days. The rats in Ctrl and CM groups rats in Ctrl, CM groups were given with dissolvant instead in equal volume. Except for the Ctrl and AST groups, on day 8, rats were given indomethacin, L-NAME and iohexol in their femoral vein under chloral hydrate anesthesia to build a contrast induced-nephropathy (CIN) model. At the end of the experiment (72 h after CIN induction), all rats were sacrificed. The Scr level, BUN level, renal histology, renal tissue activities in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), Glutathione (GSH) and level of malondialdehyde ( MDA ) were performed. Apoptosis of renal cells was detected by Bcl-2, Bax and Caspase-3 p17 with Western blot. Results Compared with Ctrl group, the levels of Scr, BUN were significantly increased in CM group (all P＜0.01); while compared with CM group, the indicators were decreased in treatment groups (P＜0.01). Renal tubular structure damage, medulla congestion, loss of brush border, vacuolar degeneration, apoptosis and proteinaceous casts were observed in the CM group, and the renal injury scores were higher compared with Ctrl group (P＜0.05), however, administrated with AST could significantly improve the changes (P＜0.05). Oxidative stress indicators showed that MDA level were increased while SOD, GPx, GSH activities were significantly decreased at CM group (all P＜0.05), and the indicators above were ameliorated in treatment groups (all P＜0.05). Western blot showed that the expression of Bcl-2 was down-regulated while the Bax, Caspase 3 p17 was up-regulated respectively at CM group (P＜0.05), while the HAST+CM group could prevent the changes. Conclusions Iohexol can results in oxidative stress increased in kidney, which activate Caspase-3 p17 signal path, down-regulated Bcl-2 expression, up-regulated Bax expression respectively, and lead to cell apoptosis. AST can ameliorate the changes, especially with high AST dose, which suggest that the possible protection mechanism is by ameliorating oxidative stress and inhibiting apoptosis pathways.     

Electrophoretic karyotype of the astaxanthin-producing yeast Phaffia rhodozyma

The electrophoretic karyotype of three different strains of Phaffia rhodozyma was determined by contour-clamped homogeneous electric field (CHEF)-gel electrophoresis. Significant differences in electrophoretic karyotyping patterns were found among the three strains studied. Between nine and 17 bands were observed. The size of these bands, based on their migration relative to the chromosomal DNA of Schizosaccharomyces pombe, Hansenula wingei was estimated to be between 0.48 and 3.1 Mb.     

虾青素体内抗肿瘤及其免疫调节作用的实验研究

目的研究虾青素体内抗肿瘤作用和免疫调节作用。方法利用小鼠移植性肿瘤实验观察虾青素对其体内肿瘤细胞生长和免疫器官胸腺、脾脏的影响，并通过ANAE法检测虾青素对T细胞阳性率的影响。结果虾青素对S180肉瘤生长有一定抑制作用，各剂量组均可以提高免疫器官脏器指数，与模型组比具有显著性差异（P〈0.01）；能够提高S180荷瘤小鼠T淋巴细胞的百分数。结论虾青素有抗肿瘤和增强免疫功能作用。     

虾青素对兔骨性关节炎软骨细胞增殖与凋亡影响的研究

目的通过观察虾青素对新西兰兔骨性关节炎模型的软骨细胞增殖与凋亡基因表达的影响,初步探索其干预软骨细胞代谢的作用机制。方法取5月龄新西兰兔骨性关节炎模型的膝关节软骨建立软骨细胞体外培养体系,分别采用MTT法、TUNEL法、免疫组化法对细胞增殖、凋亡及细胞周期调控基因Bax、Bcl-2、Caspase-3、p53 mRNA的表达进行检测。结果不同剂量组虾青素可显著促进软骨细胞体外增殖,并可通过减弱软骨细胞Bax、Caspase-3、p53 mRNA的表达,增强Bcl-2 mRNA的表达来减缓软骨细胞凋亡进程。结论虾青素可有效调控兔骨性关节炎软骨细胞代谢,增强细胞活性,延缓凋亡,具有研发成为骨性关节炎治疗药物的潜能。     

Protective effects of astaxanthin on subarachnoid hemorrhage-induced early brain injury: Reduction of cerebral vasospasm and improvement of neuron survival and mitochondrial function

The purpose of this study was to evaluate the neuroprotective effects of astaxanthin on early brain injury (EBI) caused by subarachnoid hemorrhage (SAH) in rats and to explore possible molecular mechanisms. Experimental SAH model was introduced in adult male SD rats by injecting autologous arterial blood into the prechiasmatic cistern. Astaxanthin (75?mg/kg bodyweight) or olive oil was administered by oral gavage at 3?h after SAH. Our results showed that astaxanthin attenuated SAH-induced cerebral vasospasm and reduced neuronal apoptosis. Astaxanthin inhibited mitochondria-associated neuron apoptosis in the prefrontal cortex after SAH: increased mitochondrial membrane potential, decreased Bax/Bcl-2 ratio, inhibited cytochrome C release in cytoplasm, and suppressed caspase-3 enzyme activity. Furthermore, the cerebral expression levels of synaptic proteins (Synapsin-1, postsynaptic density-95 and growth-associated protein-43) and nerve growth and neuronal differentiation factors (brain-derived neurotropic factor and purine-rich binding protein-alpha) were reduced following SAH. Astaxanthin partly restored their expression. In conclusion, our current work demonstrates that astaxanthin attenuates SAH-induced EBI, possibly by improving neuronal survival and mitochondrial function.