高效液相色谱法测定桑寄生中槲皮素的含量

目的建立测定桑寄生中有效成分槲皮素含量的方法。方法采用高效液相色谱法测定。以甲醇-0．4％磷酸溶液（45：55）为流动相,检测波长为360nm。柱温为室温。结果槲皮素在0．003208—0．03208μg范围内呈良好线性关系,回归方程为Y=1764．1846X-11．322（r=0．9994）。槲皮素的平均回收率为97．24%（RSD=1．12％,n=6）。结论方法简便,分离效果好,结果准确可靠．可以用于桑寄生的质量控制。     

HPLC法测定青钱柳中槲皮素和山柰素的含量

目的:建立高效液相色谱法测定青钱柳中槲皮素和山柰素的含量测定方法.方法: Kromasil C18(250 mm×4.6 mm,5 μm);流动相:甲醇-0.4%磷酸溶液(60∶40);检测波长:360 nm;柱温:30℃.结果: 槲皮素和山柰素的回收率分别为100.4%、99.5%;线性范围分别为0.0258～0.645 μg、0.0632～1.58 μg.结论:该法 结果准确,重复性好,可用于该产品的质量控制.     

Synergistic neurotoxicity induced by methylmercury and quercetin in mice

Methylmercury (MeHg) is a highly neurotoxic pollutant, whose mechanisms of toxicity are related to its pro-oxidative properties. A previous report showed under in vivo conditions the neuroprotective effects of plants of the genus Polygala against MeHg-induced neurotoxicity. Moreover, the flavonoid quercetin, isolated from Polygala sabulosa, displayed beneficial effects against MeHg-induced oxidative damage under in vitro conditions. In this study, we sought for potential beneficial effects of quercetin against the neurotoxicity induced by MeHg in Swiss female mice. Animals were divided into six experimental groups: control, quercetin low dose (5 mg/kg), quercetin high dose (50 mg/kg), MeHg (40 mg/L, in tap water), MeHg + quercetin low dose, and MeHg + quercetin high dose. After the treatment (21 days), a significant motor deficit was observed in MeHg + quercetin groups. Biochemical parameters related to oxidative stress showed that the simultaneous treatment with quercetin and MeHg caused a higher cerebellar oxidative damage when compared to the individual exposures. MeHg plus quercetin elicited a higher cerebellar lipid peroxidation than MeHg or quercetin alone. The present results indicate that under in vivo conditions quercetin and MeHg cause additive pro-oxidative effects toward the mice cerebellum and that such phenomenon is associated with the observed motor deficit.     

Formulation and characterization of polyphenol-loaded lipid nanocapsules

The purpose of this study was to design and characterize two flavonoid-loaded lipid nanocapsules (LNC) by applying the phase inversion process, and to enhance their apparent solubility and/or the stability. The flavonoid-loaded LNC were characterized by particle size, encapsulation efficiency, drug leakage rates, stability and spectroscopic studies. It was observed that quercetin-loaded LNC30 (3%) and LNC60 (2%) carried a particle size of 30.3 and 55.1 nm, respectively and significant higher entrapment efficiency. Encapsulation of quercetin (QC) in LNC enabled us to increase its apparent aqueous solubility by a factor of 100. And in view of calculations and results, it seems most probable that QC is arranged at this LNC interface between the oil phase and the hydrophilic polyethylene glycol moieties of the surfactant. In addition, colloidal suspensions proved to be stable in term of encapsulation for at least 10 weeks and QC was not oxidised. With simple chemical modification of (−)-epigallocatechin-3-gallate or (−)-EGCG, it was possible to reach very high encapsulation rates (95%). Thus we obtained stable colloidal suspensions of (−)-EGCG in water over 4 weeks while free (−)-EGCG solubilised in water exhibited 100% degradation within 4 h. The initial problems (solubility and stability) of these flavonoids were resolved thanks to drug-loaded LNC.     

槲皮素对过氧化氢诱导A375细胞氧化损伤的保护机制研究

目的探讨槲皮素对人A375黑素瘤细胞的氧化损伤是否具有保护作用。方法体外培养人A375黑素瘤细胞,随机分为空白对照组、H2O2损伤组、不同浓度槲皮素预处理组(槲皮素终浓度为5、10、25、50μmol/L)。四甲基偶氮唑蓝(MTT)显色法测定细胞增殖,NaOH法测定黑素含量,流式细胞仪(Annexin V/PI法)测定细胞早期凋亡百分率。结果与H2O2损伤组相比,25μmol/L槲皮素组对细胞增殖有促进作用,其余槲皮素各组与H2O2损伤组相比差异无统计学意义(P0.05);与H2O2损伤组相比,各浓度的槲皮素均对细胞的黑素合成有促进作用(P0.05)。各槲皮素预处理组细胞早期凋亡百分率均低于H2O2损伤组(P0.05)。结论槲皮素可以减轻H2O2对人黑素瘤细胞造成的氧化损伤和早期凋亡。     

Quercetin protects neuroblastoma SH-SY5Y cells against oxidative stress by inhibiting expression of Krüppel-like factor 4

Quercetin is one of flavonoids with cyto-protective activities. It has been demonstrated that quercetin inhibits oxidative stress in some animal models and specific cells, but the particular mechanism is known a little. In the present study, we found that quercetin could decrease the expression of Krüppel-like factor 4 (KLF4) induced by hydrogen peroxide (H₂O₂) in human neuroblastoma SH-SY5Y cells, further increase the expression ratio of bcl-2 to bax, which were apoptotic-related target genes of KLF4, thus alleviate the apoptotic rate and caspase-3 enzyme activity of SH-5YSY cells; the overexpression or inhibition of KLF4 demonstrated the mediated role of KLF4 for the protective effect of quercetin on cell damage induced by H₂O₂. All results suggest a potential molecular mechanism of quercetin protecting against the oxidative damage, which may be applied in the treatment of oxidative related diseases, such as neurodegeneration diseases.     

壮药依肝达颗粒质量标准研究

目的 建立壮药依肝达颗粒的质量标准.方法 采用薄层色谱法进行定性鉴别,以高效液相色谱法测定槲皮素的含量.结果 薄层色谱分离度好,专属性强.槲皮素的线性范围为0.058～0.58 μg(r=0.999 8,n=6),平均回收率为103.82％,RSD =0.84％ (n=6).结论 所建立的方法简便、准确、专属性强、重复性好,可有效控制壮药依肝达颗粒的质量.     

桑树寄主的4种桑寄生科药用植物槲皮素含量测定

目的 对同以桑树为寄主4种桑寄生科药用植物槲皮素含量进行测定,为扩大桑寄生药材来源的可能性提供科学的理论依据.方法 采用RP - HPLC法对4种桑寄生科药用植物槲皮素含量进行测定,并与桑寄生药材对照品槲皮素含量比较,槲皮素采用甲醇-盐酸(4:1)回流提取,用Agilent Eclipse XDB - C18柱,甲醇-0.05％磷酸溶液(47:53)为流动相,流速1.0ml/min,检测波长254 nm.结果 槲皮素的线性范围0.41 ～6.56 mg(r=0.999 9),平均回收率为99.25％,4种桑寄生科药用植物槲皮素含量分别为:三色鞘花0 mg/g,小红花寄生8.01 mg/g,红花寄生7.82 mg/g,广寄生5.27 mg/g.结论 4种药用植物除三色鞘花检测不到槲皮素,不能作为桑寄生药用外,小红花寄生和红花寄生的槲皮素含量较高,提示小红花寄生和红花寄生亦可作桑寄生药材使用.     

Ins and outs of dietary phytochemicals in cancer chemoprevention

A voluminous number of evidence suggests that an increased consumption of fruit and vegetables is a relatively easy and practical strategy to reduce significantly the incidence of chronic diseases, such as cancer, cardiovascular diseases and other aging-related pathologies. This review will critically discuss the applications of chemical and dietary chemoprevention, intending the protecting effects against cancer of chemically synthesized molecules, or phytochemicals present in the regular diet. The length of chemopreventive treatments requires the administration of low doses of chemopreventive agents, to avoid toxic side effects. This poses the question, here discussed, of the bioavailability of these compounds, usually very modest. Another key issue is whether purified phytochemicals have the same protective effects, as do the whole food or mixture of foods in which these compounds are present. These aspects will be analysed at the light of the "antioxidant hypothesis" in cancer prevention and the "combination chemoprevention", both referring to the pleiotropic and synergistic effects of compounds present in the diet. Single molecules may evolve in perfect chemopreventive agents, as in the case of tamoxifen, or generate ambiguity. Resveratrol and quercetin represent two paradoxes, discussed here.     

Differential protein expression of peroxiredoxin I and II by benzo(a)pyrene and quercetin treatment in 22Rv1 and PrEC prostate cell lines

Mechanisms of benzo(a)pyrene (BaP)-mediated toxicity and chemopreventative potential of quercetin in prostate cancer are poorly understood. Two-dimensional gel electrophoresis was used to map the differences in protein expression in BaP (1 microM)- and quercetin (5 microM)-treated 22Rv1 human prostate cancer cells. As compared to DMSO, 26 proteins in BaP and 41 proteins in quercetin were found to be differentially expressed (+/-2-fold). Western blots confirmed that BaP increased peroxiredoxin (Prx) Prx I and decreased Prx II in 22Rv1 cells. Similar results were found in PrEC normal prostate epithelial cells. Quercetin (up to 10 microM) upregulated Prx II without altering Prx I levels in 22Rv1 cells whereas in PrEC cells, it did not alter the constitutive protein expression of Prx I or II. The lack of quercetin-mediated changes in Prx expression suggests that quercetin does not interfere with H(2)O(2) levels, and thus may have no deleterious effect in normal prostate cells. Quercetin inhibited both BaP-mediated effects on Prx I and II in 22Rv1 cells. In PrEC cells, quercetin inhibited BaP-mediated upregulation of Prx I and had tendency to neutralize BaP-mediated downregulation of Prx II. Quercetin also inhibited BaP-induced concentrations of reactive oxygen species in both 22Rv1 and PrEC cells. These results suggest that Prx I and II may be involved in BaP-mediated toxicity and the potential chemopreventative mechanisms of quercetin.