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11.
An HPLC method was developed to resolve the enantiomers of shikonin derivatives of the Lithospermi Radix. The optimum mobile
phase on a Chiracel AD column was 5% isopropanol inn-hexane with flow rate of 1 ml/min. Establishment of this method made possible to determine the ratios of shikonin/acetylshikonin
or alkanin/acetylalkanin in the same root. The correlation of the ratios of these substance pairs appeared characteristic
for the country where they were originated from. All of the Korean species showed significantly higher ratios of shikonin/acetylshikonin
and alkanin/acetylalkanin than the Chinese ones. This method would be useful to determine the origin of Lithospermi Radix. 相似文献
12.
Young Ock Kim Seung Jae Hong Sung-Vin Yim 《The Korean journal of physiology & pharmacology》2010,14(4):199-204
The potential therapeutic action of shikonin in an experimental model of rheumatoid arthritis (RA) was investigated. As a RA animal model, DBA/1J mice were immunized two times with type II collagen. After the second collagen immunization, mice were orally administered shikonin (2 mg/kg) once a day for 35 days, and the incidence, clinical score, bone mineral density (BMD), bone mineral content (BMC) and joint histopathology were evaluated. BMD in the proximal regions of the tibia largely increased in the shikonin treatment group compared with the control group. We also examined the effect of shikonin on inflammatory cytokines and cartilage protection. Shikonin treatment significantly reduced the incidence and severity of collagen-induced arthritis (CIA), markedly abrogating joint swelling and cartilage destruction. Shikonin also significantly inhibited the production of matrix metalloproteinase (MMP)-1 and up-regulated tissue inhibitors of metalloproteinase (TIMP)-1 in mice with CIA. In conclusion, shikonin exerted therapeutic effects through regulation of MMP/TIMP; these results suggest that shikonin is an outstanding candidate as a cartilage protective medicine for RA. 相似文献
13.
目的:研究紫草素对人喉癌Hep-2细胞生长的作用。方法:以不同浓度的紫草素作用于人喉癌Hep-2细胞,MTT法检测紫草素对人喉癌Hep-2细胞生长的抑制率,荧光显微镜观察人喉癌Hep-2细胞凋亡情况,流式细胞仪分析细胞周期分布及凋亡率变化,荧光定量PCR法测量人喉癌Hep-2细胞增殖诱导配体(APRIL)的表达量。结果:紫草素对人喉癌Hep-2细胞的增殖有明显抑制作用,并呈明显的量效关系和时间依赖性。紫草素主要阻滞细胞G1期向S期的发展。紫草素作用人喉癌Hep-2细胞后其APRIL mRNA表达量随时间的延长和浓度的增加而升高,48 h后各紫草素浓度组APRIL mRNA表达与空白组比较差异有统计学意义(P<0.05)。结论:紫草素可以抑制喉癌Hep-2细胞的增殖,未凋亡的人喉癌Hep-2细胞因APRIL表达升高而有增殖能力增强的潜在趋势。 相似文献
14.
Zhou W Zhang X Xiao L Ding J Liu QH Li SS 《European journal of medicinal chemistry》2011,46(8):3420-3427
We recently discovered that 5, 8-O-dimethyl acylshikonin derivatives displayed the selectivity towards MCF-7 and no toxicity to normal cells. Herein, a series of the corresponding 6-isomers of 5, 8-O-dimethyl acylshikonin derivatives were synthesized starting from shikonin. In vitro evidence of the cytotoxicities indicated that most of thecompounds were more active than or comparative to shikonin and retained the selectivity against MCF-7, MDA-MB-231 besides no toxicity in the normal cells. Also, in vivo anticancer activity of the positional isomers 5p, 6c further showed that 6-isomers of 5, 8-O-dimethyl acylshikonin derivatives were more active than their corresponding 2-isomers. Thus, we may conclude that the position of the side chain of shikonin attached to 5,8-dimethoxy -1,4-naphthoquinone is associated with the antitumor activity. 相似文献
15.
目的:考察紫草素滴丸的制备工艺,设计正交实验,确定最佳工艺条件。方法:以聚乙二醇4000为基质,二甲基硅油为冷却剂,滴制工艺为:滴制温度85℃,冷却液5~25℃梯度冷却,滴距5cm,滴速40滴/min。结果:该工艺制得的滴丸圆整度好,丸重差异小,崩解时限为21 min,符合药典规定。结论:该工艺适合紫草素滴丸的制备。 相似文献
16.
《中医科学杂志(英文)》2022,9(4):432-442
ObjectiveTo investigate the potential anti-tumor mechanisms of naphthoquinone compound shikonin (SKN) extracted from the root of Chinese herbal medicine plant lithospermum (Lithospermum erythrorhizon Sieb. & Zucc.).MethodsWe first observed that SKN treatment led to swelling and bubbles in HeLa cells that were similar to the phenotype of cell pyroptosis. Subsequently, the HeLa cells experienced a pyroptotic process with SKN, and this was then assessed using lactate dehydrogenase (LDH) release and propidium iodide (PI)/Hoechst double staining experiments. Pyroptosis is defined as gasdermin-mediated programmed necroptosis. To identify the potential pyroptosis machinery, two strategies were utilized that included a genome-wide clustered regularly interspaced short palindromic repeats (CRISPR)-associated protein 9 screening experiment and a pyroptosis reconstitution assay executed by each of the five known gasdermins (GSDMA-E). Moreover, endogenous cleavage was also detected in a panel of tumor cell lines.ResultsCompared with the control, both the LDH release and PI/Hoechst double-staining experiments suggested that SKN induced perforation and enhancement of the permeability of the cell membranes that resulted in pyroptosis in HeLa cells (P = .028 and P = .032, respectively). In addition, the reconstitution assays in human embryonic kidney 293T (HEK-293T) cells and endogenous cleavage assays in HeLa cells indicated that the pyroptosis was controlled by GSDME. In addition, we also found SKN could trigger pyroptosis in a panel of tumor cell lines in which the cellular morphologies were proportional to the GSDME expression levels. Additionally, the cleavage of GSDME was also detected, and this was indicative of a similar GSDME-mediated mechanism.ConclusionOur study not only explained the molecular mechanism of cytotoxicity of SKN to various tumor cells, but also provided additional information for the potential clinical application of natural naphthoquinone compounds against cancer. 相似文献
17.
Oxidative stress acts as the major causative factor for various age‐associated neurodegenerative diseases, triggering cognitive and memory impairments. In the present study, the underlying neuroprotective mechanism governing how shikonin acts against D-galactose (D-gal)-induced memory impairment, neuroinflammation and neuron damage was examined. The results revealed that chronic administration of D-gal [150 mg/kg intraperitoneally (i.p.)] in mice caused cognitive and memory impairments, as determined by Morris water-maze test. Shikonin treatment, however, alleviated D‐gal-induced memory impairment and reversed the D‐gal-induced neural damage and apoptosis. Furthermore, western blotting and the results of morphological analysis revealed that shikonin treatments markedly reduced D‐gal induced neuroinflammation through inhibition of astrocytosis as determined by glial fibrillary acidic protein (GFAP) detection, and downregulating other inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6. Moreover, shikonin treatment led to inhibition of the activation of nuclear factor‐κB (NF‐κB) and the phosphorylation of mitogen-activated protein kinases (MAPKs), preventing neurodegeneration. Hence, taken together, the results of the present study suggested that shikonin attenuated D‐gal-induced memory impairment, neuroinflammation and neurodegeneration, possibly via the NF‐κB/mitogen-activated protein kinase (MAPK) pathway. Our data suggest that shikonin could be a promising, endogenous and compatible antioxidant candidate for age‐associated neurodegenerative diseases, including Alzheimer's disease. 相似文献
18.
目的:为紫草和紫草制剂的抗炎机制研究及产品开发提供参考。方法:以"紫草""紫草素""制剂""抗炎""进展""zicao""shikonin""anti-inflammatory"等为关键词,在Pub Med、CNKI等多个数据库中查询建库至2017年12月31日的相关文献,对紫草、紫草素和紫草复方制剂抗炎作用的相关研究进行综述。结果与结论:共检索到相关文献128篇,其中有效文献41篇。紫草以新疆软紫草品质最佳,而滇紫草、泰山紫草等也被逐步肯定。紫草醇提物抗炎效果最优,紫草素及其衍生物的抗炎活性突出。紫草、紫草素及紫草复方制剂治疗烧烫伤、湿疹、银屑病、过敏性紫癜、关节炎、静脉炎、妇科炎症、急性肺损伤、重症急性胰腺炎伴肺损伤或肝损伤、局部脑缺血等多种疾病的实验研究正逐步深入,多认为其抗炎机制与NF-κB、IL-1β、IL-6、TNF-α、NO、CCR、COX-2、IL-22、IL-17等密切相关。紫草及紫草制剂现已广泛用于临床治疗湿疹、皮炎、妇科炎症、皮肤创面及黏膜损伤等多种炎症性疾病,其剂型多为油剂、膏剂、栓剂、喷雾剂等。如何高效发挥紫草及紫草制剂的抗炎作用,尚有待在微观层面运用生物组学技术等继续深入研究。 相似文献
19.
靛玉红紫草素对角质形成细胞株凋亡的影响 总被引:9,自引:0,他引:9
目的 观察靛玉红、紫草素对体外角质形成细胞株凋亡的影响 ,初步探讨其治疗银屑病的机制。方法 以PI法和Annexin Ⅴ法在流式细胞仪上检测靛玉红、紫草素对体外角质形成细胞凋亡的影响。结果 靛玉红在 0 .10 ,0 .2 5 ,0 .5mol/L时细胞凋亡率分别为 7.5 2 %± 0 .73 % ,19.2 2 %± 4.13 % ,3 0 .62 %± 2 .68% ;紫草素在相同浓度时分别为6.72 %± 0 .73 % ,12 .5 9%± 2 .0 5 % ,3 6.47%± 3 .11%。结论 靛玉红、紫草素可以诱导细胞凋亡 ,从而达到治疗银屑病的目的。 相似文献
20.