| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
| 5g | 电议 |
Animal experiment: | Mice are inoculated subcutaneously with 5×105 PC-3 cells suspended in 100μL PBS and 2×108 LNCaP cells suspended in 100μL of matrigel and PBS mixture (1:1) on the right back. When xenograft tumors reach a volume of approximately 100 mm3, mice are randomLy assigned to four groups (n=8 each group) and treated intraperitoneally. Therapeutic schedule based on our in vitro results, preliminary experiments and many other researchers' studies is as follows: (1) Vehicle control group: vehicle of quercetin on day 1, vehicle of 2-ME on day 2, (2) Quercetin treated group: quercetin 75 mg/kg on day 1, vehicle of 2-ME on day 2, (3) 2-ME treated group: vehicle of quercetin on day 1, 2-ME 150 mg/kg on day 2, (4) Combination treatment group: quercetin 75 mg/kg on day 1, 2-ME 150 mg/kg on day 2. Two days is a treatment cycle and the whole treatment process lasted for 4 weeks. Tumor sizes are monitored every 2 days using caliper and tumor volume are calculated according to the formula: L×S2×0.5, in which L represents the longest diameter and S represents the shortest diameter of tumor. Mice are weighed as well. At the end of treatment procedure, on day 29, mice are anesthetized with chloral hydrate and sacrificed by cervical dislocation. Xenograft tumors are taken out quickly and weighed. One part of it is put into liquid nitrogen immediately for future biomarker analysis and the other part is fixed in 10% neutral buffered formalin for immunohistochemical analysis. Serum biochemical parameters such as ALT, AST, creatinine and urea nitrogen that reflected drug toxicity are also detected. |
| 文献引用 | |
| 产品描述 | Quercetin is an important dietary flavonoid, present in vegetables, fruits, seeds, nuts, tea and red wine. It has various biological functions in terms of tumor prevention. Quercetin is a strong inhibitor of PI3K, NF-κB, and other kinases involved in intracellular signaling. It can also mildly inhibit Akt1/2, and slightly affect PKC, p38 and ERK1/2 [1]. A number of reports have demonstrated that Quercetin possessed anti-inflammatory, anti-oxidant and pro-apoptotic functions in cancer cells and inhibited tumor progress with different mechanisms. Quercetin increased cytosolic Ca2+ levels and disrupted the mitochondrial membrane potential (MMP), which in turn promoted the release of cytochrome c in the cytoplasm, thus activating multiple caspases such as caspase-3, -8 and -9 and subsequently inducing apoptosis via mitochondrial pathway [2]. Quercetin induced cell-cycle arrest and apoptosis, which was associated with the function of p53. Quercetin could promote p53 phosphorylation and therefore stabilize p53 both at the mRNA and protein level [3]. However, several studies investigated that cells with impaired p53 became more sensitive to Quercetin mediated cytotoxicity and apoptosis [4]. In vivo studies showed that administration of Quercetin before the initiation stage of carcinogenesis dramatically reduced various chemical agents induced tumor burden in mice models, including benzo(a)pyrene-induced lung tumor burden, azoxymethane-induced preneoplastic lesions in rat colon and N-nitrosodiethylamine-induced hepatocarcinoma etc. [5]. References: |
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