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Background

Flavonoids possess a rich polypharmacological profile and their biological role is linked to their oxidation state protecting DNA from oxidative stress damage. However, their bioavailability is hampered due to their poor aqueous solubility. This can be surpassed through encapsulation to supramolecular carriers as cyclodextrin (CD). A quercetin- 2HP-β-CD complex has been formerly reported by us. However, once the flavonoid is in its 2HP-β-CD encapsulated state its oxidation potential, its decomplexation mechanism, its potential to protect DNA damage from oxidative stress remained elusive. To unveil this, an array of biophysical techniques was used.

Methods

The quercetin-2HP-β-CD complex was evaluated through solubility and dissolution experiments, electrochemical and spectroelectrochemical studies (Cyclic Voltammetry), UV–Vis spectroscopy, HPLC-ESI-MS/MS and HPLC-DAD, fluorescence spectroscopy, NMR Spectroscopy, theoretical calculations (density functional theory (DFT)) and biological evaluation of the protection offered against H2O2-induced DNA damage.

Results

Encapsulation of quercetin inside the supramolecule's cavity enhanced its solubility and retained its oxidation profile. Although the protective ability of the quercetin-2HP-β-CD complex against H2O2 was diminished, iron serves as a chemical stimulus to dissociate the complex and release quercetin.

Conclusions

We found that in a quercetin-2HP-β-CD inclusion complex quercetin retains its oxidation profile similarly to its native state, while iron can operate as a chemical stimulus to release quercetin from its host cavity.

General significance

The oxidation profile of a natural product once it is encapsulated in a supramolecular carrier was unveiled as also it was discovered that decomplexation can be triggered by a chemical stimilus.  相似文献   
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目的:探讨银杏叶提取物(EGb)及其单体槲皮素(Que)对心肌细胞肥大的防治作用及其机制。方法:采用血管紧张素Ⅱ(AngⅡ)诱导新生大鼠心肌细胞肥大模型;分别在培养液中加入EGb(40/μg/ml)或Que(4/μg/m1),观察Lowry法测定心肌细胞蛋白质含量的变化;测定SOD活性和MDA含量观察心肌细胞氧自由基代谢的变化;Western blot方法检测心肌细胞p-ERK1/2、p-JNK和p-P38蛋白表达;应用RT-PCR法检测心肌细胞c-fos mRNA表达。结果:①EGb和Que能明显抑制AngⅡ引起的心肌细胞总蛋白质含量的增加;②EGb和Que可显著提高SOD活性,降低MDA含量;③AngⅡ诱导的心肌细胞p-ERK1/2、p-JNK和p-P38表达均明显增强,Que能明显抑制AngⅡ诱导的p-JNK表达;④EGb、Que、可降低AngⅡ诱导心肌细胞c-fos mRNA表达的上调水平。结论:EGb和Que对AngⅡ诱导的心肌细胞肥大有明显的防治作用,Que的作用机制可能与ROS/JNK/c-fos信号通路有关。氧化应激参与了心肌肥大的发生发展过程。  相似文献   
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Band-gap irradiation of CdS dispersions in alkaline aqueous media (pH 14) containing 0.1 M Na2S produces hydrogen and sulfur. The reaction is photo-decomposition of hydrogen sulfide by two quanta of visible light (λ > 400 nm). Various batches of commercially available cadmium sulfide, as well as CdS precipitated from nitrate, sulfate, and chloride solutions at neutral pH, produce different amounts of hydrogen. Electronically pure CdS (puratronic grade) generates almost no hydrogen. By contrast, CdS precipitates prepared in the presence of excess cadmium yield forty times more hydrogen than CdS prepared in the presence of excess sodium sulfide. Differences are rationalized in terms of possible surface modification and/or changes in the active sites by anions present as ‘impurities’ which could affect separation and recombination of the charge carries, eCB and hVB+, in CdS.  相似文献   
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