高效液相色谱法测定复方矮地茶止咳合剂中的槲皮素和山奈酚含量

目的建立高效液相色谱法测定复方矮地茶止咳合剂中槲皮素和山奈酚的含量。方法采用SUPELCO Discovery C18（4．6mm×250nm,5μm）色谱柱,流动相：甲醇-0．4％磷酸溶液（50：50）,流速：1．0mL·min^-1,检测波长：370nm,柱温：40℃,进样量：10μL。结果槲皮素和山奈酚分别在6．484-155．6μg·mL^-1、5．708～137．0μg·mL^-1与峰面积线性关系良好,低、中、高3个剂量组的平均回收率分别为93．6％、97．2％、98．2％与95．2％、94．9％、100．2％。结论所建立的方法准确可靠、灵敏度高、专属性强,可有效控制复方矮地茶止咳合剂的质量。     

Antinociceptive activity of Syzygium cumini leaves ethanol extract on orofacial nociception protocols in rodents

Context: Syzygium cumini (L.) Skeels (Myrtaceae) is a tree with dark purple fruits, popularly known as “jambolão” or “jambolan”. In folk medicine, this plant is used for the treatment of diabetes and inflammatory conditions.

Objective: We investigated the antinociceptive effect of ethanol extract (EE) from S. cumini leaves on orofacial nociception.

Material and methods: The antinociceptive effects of the EE obtained from the leaves of S. cumini were evaluated in mice using formalin- and glutamate-induced orofacial nociception.

Results: ESI-MS/MS analyses demonstrated that major constituents in the analyzed samples coincided with the mass of the phenolic acids and flavonoids. In pharmacological approach, pre-treatment with EE (100, 200, or 400?mg/kg, p.o.) significantly reduced (p?p?G-nitro-l-arginine (l-NOARG). The extract, all doses, also caused a marked inhibition (p?p?Conclusions: We can suggest that the antinociceptive effect of the EE is mediated by peripheral mechanisms, possibly involving K_ATP channels and the nitric oxide pathways. These effects appear to be related to the presence of flavonoids compounds, such as quercetin.     

Effects of quercetin and fish n‐3 fatty acids on testicular injury induced by ethanol in rats

The aim of this study was to investigate the effects of quercetin and fish n‐3 fatty acids on the changes in testis induced by ethanol. Forty‐five rats divided into five groups, control, ethanol, ethanol+quercetin, ethanol+fish n‐3 fatty acids and ethanol+quercetin+fish n‐3 fatty acids. At the end of 8 weeks, all the rats were sacrificed. Degenerative changes in histopathological analyses, the decreased body weight gain and seminiferous tubule diameters in ethanol group have been observed. TUNEL assay also showed an increase in apoptotic cell number. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH‐Px), xanthine oxidase (XO) and testosterone levels were decreased as well as the levels of malondialdehyde (MDA) and nitric oxide (NO) were increased in ethanol group. Histopathological changes caused by ethanol have been improved by quercetin and fish n‐3 fatty acids. It was also found that protection was provided by increasing SOD, CAT and GSH‐Px activities in groups administered quercetin, fish n‐3 fatty acids and quercetin+fish n‐3 fatty acids, and by decreasing the levels of MDA and NO in groups administered both quercetin and fish n‐3 fatty acids together. These results suggest that quercetin and fish n‐3 fatty acids are beneficial agents to reduce testicular injury induced by ethanol except for testosterone levels.     

Bioavailability of plant pigment phytochemicals in Angelica keiskei in older adults: A pilot absorption kinetic study

BACKGROUND/OBJECTIVES

Angelica keiskei is a green leafy vegetable rich in plant pigment phytochemicals such as flavonoids and carotenoids. This study examined bioavailability of flavonoids and carotenoids in Angelica keiskei and the alteration of the antioxidant performance in vivo.

SUBJECTS AND MATERIALS

Absorption kinetics of phytochemicals in Angelica keiskei were determined in healthy older adults (> 60 y, n = 5) and subjects with metabolic syndrome (n = 5). Subjects consumed 5 g dry Angelica keiskei powder encapsulated in gelatin capsules with a low flavonoid and carotenoid liquid meal. Plasma samples were collected at baseline, 0.5, 1, 2, 3, 4, 5, 6, 7, and 8 h. Samples were analyzed for flavonoids and carotenoids using HPLC systems with electrochemical and UV detection, respectively, and for total antioxidant performance by fluorometry.

RESULTS

After ingestion of Angelica keiskei increases in plasma quercetin concentrations were observed at 1-3 and 6-8 hr in the healthy group and at all time points in the metabolic syndrome group compared to baseline (P < 0.05). Plasma lutein concentrations were significantly elevated in both the healthy and metabolic syndrome groups at 8 hr (P < 0.05). Significant increases in total antioxidant performance were also observed in both the healthy and the metabolic syndrome groups compared to baseline (P < 0.05).

CONCLUSIONS

Findings of this study clearly demonstrate the bioavailability of phytonutrients of Angelica keiskei and their ability to increase antioxidant status in humans.     

黄酮类成分黄芩素、槲皮素、丹参素钠对吸烟致细胞毒性和DNA损伤的保护作用

目的评价吸烟致细胞毒性和DNA损伤以及黄酮类成分黄芩素、槲皮素、丹参素钠的保护作用。方法以自动吸烟机按照FTC协议吸烟产生的主流烟雾在线染毒B-16细胞和人颊黏膜细胞两种真核细胞,通过MTT比色法和单细胞凝胶电泳法检测吸烟所致的细胞毒性和DNA损伤,并考察黄芩素、槲皮素、丹参素钠的保护作用。结果吸烟可致体外培养的B-16细胞活力明显下降,两种细胞的DNA明显损伤。随着烟气作用时间的延长,表征细胞内DNA损伤程度的彗星尾矩、Olive尾矩都有增加;1 mmol/L槲皮素、黄芩素和丹参素均可明显缓解吸烟引起的细胞毒性和DNA损伤,对B-16细胞的活力提升50%左右,对人颊黏膜细胞的DNA保护效果超过60%。结论吸烟可致细胞毒性和细胞DNA损伤,但是黄酮类成分黄芩素、槲皮素、丹参素钠均对细胞和DNA具有保护作用。     

Codelivery of Adriamycin and P-gp Inhibitor Quercetin Using PEGylated Liposomes to Overcome Cancer Drug Resistance

Transmembrane protein P-gp's overexpression at the drug-resistant cell membrane is the most important characteristic of multidrug resistance (MDR). Quercetin (QUE) can effectively suppress the function of P-gp to reverse MDR. This study uses QUE as the P-gp inhibitor andfilm-ultrasound technique with ammonium sulfate transmembrane gradient method to prepare long-circulating liposomes simultaneously encapsulating QUE and Adriamycin (doxorubicin) (AMD/DOX). The optimal conditions for the preparation of AMD_QUE_long-circulating liposomes (SLs) are as follows: hydrogenated soybean phospholipids (HSPC):cholesterol:DSPE-PEG 2000 = 73.07:24.36:2.57 mol/mol, QUE:HSPC = 1:20 mol/mol, AMD:HSPC = 1:7.9 w/w (NH₄₎₂SO₄ 0.15 mol/L, drug loaded (AMD) at 55°C for 25 min). The average encapsulation efficiency of AMD and QUE was 97.49% and 95.50%, respectively. The average particle size is 85 nm (n = 3), and the average zeta potential is ?14.9 mV. First, the pharmacokinetic study proved that codelivery liposomes enveloping QUE and AMD (AMD_QUE_SL) can obviously increase the blood concentration of AMD (C_max: 140.50 ± 32.37 μg/mL) and extend the half-life period of AMD in plasma (t_1/2:14.02 ± 1.54 h). Second, AMD_QUE_SL can obviously enhance the cell toxicity to AMD-resistant cell strains (HL-6/ADR and MCF-7/ADR), and the reverse effects on the resistance of HL-6/ADR and MCF-7/ADR is increased to 4.81-fold and 3.21-fold, respectively. Third, according to the in vivo pharmacodynamic study, the relative tumor volume and relative tumor growth of the AMD_QUE_SL group were the lowest. The inhibition rate of tumor growth of this group was the highest. It can be concluded that AMD_QUE_SL can effectively reverse MDR, lower cardiac toxicity of AMD in clinical treatment, and improve the clinical treatment effect of AMD.     

Neuro-protective potential of quercetin during chlorpyrifos induced neurotoxicity in rats

Chlorpyrifos (CPF) has been considered as one of the most potent organophosphates and is linked to several neurological disorders. On the other hand, Quercetin is a vital plant flavanoid and has been reported to regulate a number of physiological processes in the central nervous system. The present study was conducted to investigate the protective potential of quercetin during chlorpyrifos induced neurotoxicity. Female Wistar rats weighing 150–200?g were divided into four different groups viz: Normal control, CPF treated (13.5?mg/kg.b.wt. every alternate day), Quercetin treated (50?mg/kg.b.wt./day) and combined CPF and quercetin-treated. All the treatments were carried out for a total duration of eight weeks. Chlorpyrifos treatment showed significant alterations in the cognitive behavior and motor activities of rats, which were appreciably improved upon simultaneous supplementation with quercetin. Further, CPF treatment caused a significant inhibition in the enzyme activities of acetylcholinesterase and choline acetyltransferase, but caused an increase in the levels of acetylcholine in the brain. Further, chlorpyrifos exposure significantly elevated the levels of lipid peroxidation and protein carbonyl contents as well as the activities of catalase, superoxide dismutase, which were interestingly found to be decreased following co-treatment with quercetin. In contrast, CPF treatment decreased the activities of glutathione reductase, transferase, as well as levels of reduced and total glutathione in both the cerebrum and cerebellum but co-administration of quercetin, increased these levels. Chlorpyrifos treatment altered the neuro-histoarchitecture, which showed improvement upon quercetin supplementation. Hence, this study suggests that quercetin can be used as a prophylactic intervention to prevent CPF induced neurotoxicity.     

Activation of Nrf2 signaling by sitagliptin and quercetin combination against β-amyloid induced Alzheimer's disease in rats

The objective of this study was to evaluate the neuroprotective effect of sitagliptin (Sita), quercetin (QCR) and its combination in β-amyloid (Aβ) induced Alzheimer's disease (AD). Male Sprague–Dawley rats, weighing between 220 and 280 g were used for experiment. Rats were divided into 5 groups (n = 10) and the groups were as follows: (a) Sham control; (b) Aβ injected; (c) Aβ injected + Sita 100; (d) Aβ injected + QCR 100; and (e) Aβ injected + Sita 100 + QCR 100. Cognitive performance was observed by the Morris water maze (MWM), biochemical markers, for example, MDA, SOD, CAT, GSH, Aβ1-42 level, Nrf2/HO-1 expression and histopathological study of rat brain were estimated. Pretreatment with Sita, QCR and their combination showed a significant increase in escape latency in particular MWM cognitive model. Further co-administration of sita and QCR significantly reduced Aβ1-42 level when compared with individual treatment. Biochemical markers, for example, increased SOD, CAT and GSH, decreased MDA were seen, and histopathological studies revealed the reversal of neuronal damage in the treatment group. Additionally, Nrf2/HO-1 pathway in rat's brain was significantly increased by Sita, QCR and their combination. Pretreatment with QCR potentiates the action of Sita in Aβ induced AD in rats. The improved cognitive memory could be because of the synergistic effect of the drugs by decreasing Aβ1-42 level, antioxidant activity and increased expression of Nrf2/HO-1 in rat brain.     

Inhibitory effects of quercetin on guinea-pig ileum contractions

The inhibitory effect of quercetin on the guinea-pig ileum contractile responses was examined to further clarify its mechanism of action. Quercetin inhibited, from doses of 5 μM , the spontaneous phasic contractions of the guinea-pig ileum, as well as the phasic and tonic components of either acetylcholine- or KCl-elicited contractions, in a dose-dependent way. The former effect was reversible and was unaffected by nicotinic blockade. The tonic component of the contractions was more responsive to quercetin than the phasic component. The inhibition of the tonic contraction was, at least partially, due to the blockade of calcium channels by quercetin, since increasing calcium concentration in the tissue bath reversed the inhibition when the organ was contracted by KCl. Quercetin may also interfere with calcium release from intracellular stores, since it inhibited acetylcholine-elicited phasic contraction even in a calcium-free solution. Finally, quercetin shifted the concentration-response curves to carbachol downwards, without modifying the ED₅₀ of the agonist, whereas the concentration-response curves to CaCl₂ were shifted downwards and to the right. In conclusion, quercetin inhibits the contractile responses of guinea-pig ileum, decreasing the calcium concentration available for contractile machinery.     

Dietary Supplementation for Attenuating Exercise-Induced Muscle Damage and Delayed-Onset Muscle Soreness in Humans

Dietary supplements are widely used as a nutritional strategy to improve and maintain performance and achieve faster recovery in sports and exercise. Exercise-induced muscle damage (EIMD) is caused by mechanical stress and subsequent inflammatory responses including reactive oxygen species and cytokine production. Therefore, dietary supplements with anti-inflammatory and antioxidant properties have the potential to prevent and reduce muscle damage and symptoms characterized by loss of muscle strength and delayed-onset muscle soreness (DOMS). However, only a few supplements are considered to be effective at present. This review focuses on the effects of dietary supplements derived from phytochemicals and listed in the International Olympic Committee consensus statement on muscle damage evaluated by blood myofiber damage markers, muscle soreness, performance, and inflammatory and oxidative stress markers. In this review, the effects of dietary supplements are also discussed in terms of study design (i.e., parallel and crossover studies), exercise model, and such subject characteristics as physical fitness level. Future perspectives and considerations for the use of dietary supplements to alleviate EIMD and DOMS are also discussed.