2种紫草中紫草素提取工艺优化及含量比较

优化微波提取2种紫草中紫草素的工艺条件,并对紫草素的含量进行比较。采用单因素和正交试验,研究提取溶剂、提取温度、提取时间和料液比对微波法提取2种紫草中紫草素的影响,优选最佳提取工艺条件并比较紫草素含量。结果表明,微波提取软紫草的紫草素得率高于硬紫草,最佳工艺条件为:提取溶剂90%乙醇、提取温度80℃、提取时间9 min、料液比1︰12(g/mL),此条件下紫草素含量为2.49%。软紫草中紫草素含量高于硬紫草,所选软紫草最佳提取工艺稳定可行、重现性好、色素得率高。     

Modification of shikonin with reactive UV-absorbent and its dyeing and functional properties for silk北大核心CSCD

为提高天然染料染色织物的功能性并实现同浴染整,文章采用水溶性、反应性抗紫外剂改性的紫草素和未改性紫草素对蚕丝织物进行染色,研究了染浴pH值对织物染色性能及抗紫外性能的影响,探究了部分织物的抗菌性能。结果表明,紫草素及改性紫草素染色织物的色深值和颜色特征值受染浴pH值影响,染色织物均呈现一系列由紫红色至蓝紫色色光。当染浴pH值为9.0时,改性前、后紫草素染色织物的K/S值均较高,改性紫草素染色织物的耐皂洗色牢度和耐摩擦色牢度不低于改性前,抗紫外性能和抗菌性能均高于改性前。     

荧光光谱法研究紫草素与牛血清白蛋白的相互作用

采用荧光光谱法研究了紫草素和牛血清白蛋白的相互作用. 实验结果表明,紫草素对牛血清白蛋白的荧光有明显的猝灭作用,其方式为静态猝灭,紫草素与牛血清白蛋白之间发生了分子内非辐射能量转移;紫草素和牛血清白蛋白的结合位点数为1,结合位置距离212位色氨酸残基1.92 nm;温度为22和36℃时,紫草素对牛血清白蛋白荧光的猝灭常数分别为6.96′104和5.91′104 mol/L. 热力学分析表明,紫草素与蛋白之间的结合以静电作用力为主. 同时,紫草素分子含有多个羟基,它们之间还存在氢键作用力.     

Shikonin Derivatives Inhibit Inflammation Processes and Modulate MAPK Signaling in Human Healthy and Osteoarthritis Chondrocytes

Osteoarthritis (OA) is the most common joint disorder and is characterized by the degeneration of articular cartilage. To develop new therapeutic approaches, we investigated the effect of shikonin derivatives on inflammation, MMP expression, and the regulation of MAPK signaling in human healthy (HC) and OA chondrocytes (pCH-OA). Viability was analyzed using the CellTiter-Glo^® Assay. Inflammatory processes were investigated using a proteome profiler™ assay. Furthermore, we analyzed the effects of the shikonin derivatives by protein expression analysis of the phosphorylation pattern and the corresponding downstream gene regulation using RT-qPCR. Both HC and pCH-OA showed a dose-dependent decrease in viability after treatment. The strongest effects were found for shikonin with IC₅₀ values of 1.2 ± 0.1 µM. Shikonin counteracts the inflammatory response by massively reducing the expression of the pro-inflammatory mediators. The phosphorylation level of ERK changed slightly. pJNK and pp38 showed a significant increase, and the downstream targets c/EBPs and MEF2c may play a role in the cartilage homeostasis. STAT3 phosphorylation decreased significantly and has a chondroprotective function through the regulation of cyclin D1 and Sox9. Our results demonstrate for the first time that shikonin derivatives have extensive effects on the inflammatory processes, MAPKs, and IL6/STAT3 downstream regulation in healthy and OA chondrocytes.     

Nec-1 Enhances Shikonin-Induced Apoptosis in Leukemia Cells by Inhibition of RIP-1 and ERK1/2

Necrostatin-1 (Nec-1) inhibits necroptosis by allosterically inhibiting the kinase activity of receptor-interacting protein 1 (RIP1), which plays a critical role in necroptosis. RIP1 is a crucial adaptor kinase involved in the activation of NF-κB, production of reactive oxygen species (ROS) and the phosphorylation of mitogen activated protein kinases (MAPKs). NF-κB, ROS and MAPKs all play important roles in apoptotic signaling. Nec-1 was regarded as having no effect on apoptosis. Here, we report that Nec-1 increased the rate of nuclear condensation and caspases activation induced by a low concentration of shikonin (SHK) in HL60, K562 and primary leukemia cells. siRNA-mediated knockdown of RIP1 significantly enhanced shikonin-induced apoptosis in K562 and HL60 cells. Shikonin treatment alone could slightly inhibit the phosphorylation of ERK1/2 in leukemia cells, and the inhibitory effect on ERK1/2 was significantly augmented by Nec-1. We also found that Nec-1 could inhibit NF-κB p65 translocation to the nucleus at a later stage of SHK treatment. In conclusion, we found that Nec-1 can promote shikonin-induced apoptosis in leukemia cells. The mechanism by which Nec-1 sensitizes shikonin-induced apoptosis appears to be the inhibition of RIP1 kinase-dependent phosphorylation of ERK1/2. To our knowledge, this is the first study to document Nec-1 sensitizes cancer cells to apoptosis.     

紫草色素的稳定性及在羊毛上的染色性能

用无水乙醇提取紫草色素，并对其稳定性以及在羊毛上的染色性能进行了研究分析。实验结果表明：紫草色素具有良好的热稳定性及耐弱酸稳定性；较高的染色温度、弱酸性条件有利于紫草色素在羊毛纤维上获得较高的得色率；媒染剂的加入使织物呈现不同的颜色特征值，具有氧化性或还原性的媒染剂如Cr^6 、Sn^2 、Fe^2 会破坏紫草色素的结构，使织物的色光发生变化。     

反应性抗紫外剂改性天然染料紫草素北大核心CSCD

为提高紫草素水溶性和紫外线吸收性能,采用水溶性、反应性紫外线吸收剂对天然染料紫草素进行改性,本文合成了一种新型水溶性紫草素染料。通过单因素条件实验确定了改性反应的最佳条件,分析了反应机理,对反应物和产物进行了FTIR红外光谱和紫外光谱表征。结果表明,改性反应最佳条件为紫草素与抗紫外剂的近似摩尔比约1︰0.8,在pH值为9.0的碳酸钠溶液中,80℃水浴振荡40 min。改性紫草素在1 250 cm^(-1)处出现芳香醚中C—O(Φ)键的反对称伸缩振动,紫外-可见吸收光谱显示在波长288 nm处出现吸收峰,且可见光区吸光度增加。通过改性提高了紫草素的水溶性和紫外线吸收性能,用于织物染色可以提高织物的功能性和附加值。     

细胞固定化条件对紫草细胞生产紫草色素的影响

以海藻胶做包埋剂,研究了固化液构成、细胞包埋量和胞龄对紫草色素合成的影响。结果表明：固定化细胞合成紫草色素的合适固化液为含有０．１ｍｏｌ／ＬＣａＣｌ２的紫草色素生产培养基,该固化条件比较温和,并可长久保持固定化细胞活性;最适宜的细胞包埋质量分数为１０％２０％;用于细胞包埋的最佳细胞生长时间为１７ｄ。对紫草细胞固定化培养生产紫草色素过程的动力学特征进行了分析,建立了基质消耗和色素合成的动力学模型,并用该模型对实验数据进行了回归分析,实验数据与理论值之间具有比较令人满意的一致性     

植物细胞培养紫草色素特性的研究

本文研究了PH，糖浓度，温度，光照，紫外线，柠檬酸-磷酸氢二纳缓冲液，柠檬酸，维生素C，氧化剂过氧化氢．还原剂亚硫酸钠等对植物细胞培养生产的紫草色素稳定性的影响。为植物细胞大规模培养紫草色素的生产及利用提供科学依据。     

Shikonin Inhibits the Migration and Invasion of Human Glioblastoma Cells by Targeting Phosphorylated β-Catenin and Phosphorylated PI3K/Akt: A Potential Mechanism for the Anti-Glioma Efficacy of a Traditional Chinese Herbal Medicine

Shikonin is an anthraquinone derivative extracted from the root of lithospermum. Shikonin is traditionally used in the treatment of inflammatory and infectious diseases such as hepatitis. Shikonin also inhibits proliferation and induces apoptosis in various tumors. However, the effect of shikonin on gliomas has not been fully elucidated. In the present study, we aimed to investigate the effects of shikonin on the migration and invasion of human glioblastoma cells as well as the underlying mechanisms. U87 and U251 human glioblastoma cells were treated with shikonin at 2.5, 5, and 7.5 μmol/L and cell viability, migration and invasiveness were assessed with CCK8, scratch wound healing, in vitro Transwell migration, and invasion assays. The expression and activity of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) and the expression of phosphorylated β-catenin (p-β-catenin) and phosphorylated PI3K/Akt were also checked. Results showed that shikonin significantly inhibited the cell proliferation, migration, invasion, and expression of MMP-2 and MMP-9 in U87 and U251 cells. The expression of p-β-catenin showed contrary trends in two cell lines. It was significantly inhibited in U87 cells and promoted in U251 cells. Results in this work indicated that shikonin displayed an inhibitory effect on the migration and invasion of glioma cells by inhibiting the expression and activity of MMP-2 and -9. In addition, shikonin also inhibited the expression of p-PI3K and p-Akt to attenuate cell migration and invasion and MMP-2 and MMP-9 expression in both cell lines, which could be reversed by the PI3K/Akt pathway agonist, insulin-like growth factor-1 (IGF-1).