Natural flavonoid in green tea; COX-1/cyclooxygenase-1

在 70 μg/mL 和 IC50 为 1.4 μM 时，(+)-儿茶素对环加氧酶-1 (COX-1) 具有 >95% 的抑制作用 [1]。使用 (+)-儿茶素处理 24 小时后，观察到颜色呈剂量依赖性下降。在测试的 (+)-儿茶素最高浓度 (160 μg/mL) 下，54.76% 的细胞死亡，(+)-儿茶素的 IC50 为 127.62 μg/mL。用 (+)-儿茶素处理 MCF-7 细胞导致细胞凋亡的诱导增加，且呈剂量和时间依赖性。 24小时后，与对照细胞相比，用150 μg/mL和300 μg/mL (+)-儿茶素处理的细胞有40.7%和41.16%经历细胞凋亡。用 150 μg/mL (+)-儿茶素处理 24 小时后，MCF-7 细胞的 Caspase-3、-8 和 -9 表达水平分别增加了 5.81、1.42、3.29 和 2.68 倍。与未处理的对照细胞水平进行比较[2]。

尽管差异不具有统计显着性，但以最低测试剂量（即 50 mg/kg，口服）（+）-儿茶素治疗的动物在选择试验中探索不熟悉的靶标的频率明显更高。 (+)-儿茶素以剂量依赖性方式预防时间引起的情景记忆丧失；口服200 mg/kg是最有效的剂量。与单独使用 DOX 治疗组相比，(+)-儿茶素治疗可防止 MPO 水平升高（海马中为 21.98±9.44%，额叶皮层为 36.76±4.39%）[3]。

体外研究[2]
IMR-32细胞系是高加索人种的雄性神经母细胞瘤细胞系。它购自NCCS，在含有10%胎牛血清的DMEM培养基中传代培养。这些细胞用于细胞活力和细胞保护研究。神经保护研究中儿茶素和DOX的治疗是同时进行的（不改变培养基），其中Catechin在DOX添加前1小时添加。

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未分化IMR-32细胞的MTT法[2]
将每孔5000个细胞接种在由50µl培养基组成的微孔板中，孵育24小时。24小时后，在孔中加入50µl浓度在31.23至250µg/ml范围内的儿茶素，持续一小时。随后，加入50µl DOX（1或2µg/ml）并孵育24小时。接着，加入50μl MTT（2mg/ml）并在37°C下孵育3小时，然后取出培养基并加入100µl DMSO，在轨道振荡器上振荡约5分钟。使形成的Formazan晶体溶解在DMSO中。DMSO溶解的甲赞的吸光度在540nm处读取（Shi等人，2015）。通过使用GraphPad Prism将数据拟合到非线性回归中，计算出儿茶素的IC50。

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细胞周期分析[2]
流式细胞术用于评估儿茶素对DOX诱导的细胞周期改变的影响。将100万个分化的细胞接种在培养瓶中过夜，在37°C下用儿茶素（40µg/ml）孵育2小时，然后用1.5µg/ml的DOX孵育24小时。通过胰蛋白酶消化将细胞从培养瓶中分离出来，用PBS离心洗涤。收集细胞颗粒，用70%冰冷的甲醇固定，并在-20°C下储存24小时。然后用PBS洗涤细胞沉淀，并加入等渗PI溶液（25µM碘化丙啶、0.03%NP-40和40µg/ml RNase A）进行染色。在激发波长488nm和发射波长575/40nm下，用Accuri C6流式细胞仪分析染色细胞进行细胞周期研究（Reddy等人，2015；Simon等人，2016）。

In vivo studies[2]
Selection of doses In the preliminary experiments for assessing the procognitive effect of Catechin, the selected doses were 50, 100 and 200 mg/kg for dose–response analysis. In later studies for chemobrain i.e., DOX-induced memory deficit model, the dose of Catechin selected was 100 mg/kg as it showed a promising effect in preliminary studies and moreover, the treatment was on a chronic basis. The dose of DOX selected was 2.5 mg/kg according to the previous studies and standardized laboratory procedures (Steiniger et al. 2004; Swamy et al. 2011; Grandhi et al. 2016).[2]
Preparation and administration of drugs In the preliminary study for assessing the nootropic effect of Catechin using time induced memory deficit model, the doses were prepared at 50, 100, 200 mg/kg in 0.25% w/v sodium carboxy methylcellulose (CMC) and administered orally for 7 days prior to and during the experimental trials. Four experimental groups were used (n = 9 each) for one vehicle (CMC) and three groups of Catechin (three doses).[2]
For inducing neurotoxicity and systemic toxicity, DOX (Adriamycin at 2.5 mg/kg) was administered intraperitoneally in 10 cycles on every 5 days. Three experimental groups (n = 12 each) were used viz., vehicle control (0.25% w/v CMC), DOX alone and Catechin (100 mg/kg in 0.25% CMC p.o.). Catechin was administered orally for 57 days including one-week treatment prior to the first cycle of DOX. Following the last cycle of DOX on day 57, i.e., on day 58, the behavioral study was conducted. All treatments, as well as the behavioral analysis, were carried out between 9 a.m. to 4 p.m. Body weight of the animals was taken once in 3 days throughout the study. During the experimental trials, the oral treatment was given 1 h before the familiarization trial.

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Time-induced natural memory deficits model[2]
Episodic memory deficits can be induced in rats naturally by increasing the time delay between familiarization and choice trials. Hence the initial experiment was conducted to assess the effect of Catechin on time -induced memory deficits by using an ITI of 24 h. In this test, rats were habituated to the arenas on day 1 and were subjected to familiarization trial on day 2. Then after an ITI of 24 h, i.e., on day 3, animals were subjected to recognition trial with one novel object replacing the familiar object. Four experimental groups were used. Rats were treated with either Catechin (50, 100 and 200 mg/kg, p.o.) or CMC (10 ml/kg, p.o.) for 7 days before the trial initiation. During the experimental trials, treatment was given 1 h before the actual trial in familiarization and choice trials

[1]. Potential cancer-chemopreventive activities of wine stilbenoids and flavans extracted from grape (Vitis vinifera) cell cultures. Nutr Cancer. 2001;40(2):173-9.

[2]. Catechin ameliorates doxorubicin-induced neuronal cytotoxicity in in vitro and episodic memory deficit in in vivo in Wistar rats. Cytotechnology. 2018 Feb;70(1):245-259.

[3]. Alshatwi AA. Catechin hydrate suppresses MCF-7 proliferation through TP53/Caspase-mediated apoptosis. J Exp Clin Cancer Res. 2010 Dec 17;29:167.

(+)-catechin monohydrate is the monohydrate of (+)-catechin. It has a role as a geroprotector. It contains a (+)-catechin.

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(+)-catechin is the (+)-enantiomer of catechin and a polyphenolic antioxidant plant metabolite. It has a role as an antioxidant and a plant metabolite. It is an enantiomer of a (-)-catechin.
An antioxidant flavonoid, occurring especially in woody plants as both (+)-catechin and (-)-epicatechin (cis) forms.
Cianidanol has been reported in Camellia sinensis, Paeonia obovata, and other organisms with data available.
Catechin is a metabolite found in or produced by Saccharomyces cerevisiae.
An antioxidant flavonoid, occurring especially in woody plants as both (+)-catechin and (-)-epicatechin (cis) forms.
See also: Gallocatechin (has subclass); Crofelemer (monomer of); Bilberry (part of) ...

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Moderate consumption of wine is associated with a reduced risk of cancer. Grape plant cell cultures were used to purify 12 phenols: the stilbenoids trans-astringin, trans-piceid (2), trans-resveratroloside, trans-resveratrol, trans-piceatannol, cis-resveratroloside, cis-piceid, and cis-resveratrol; the flavans (+)-catechin, (-)-epicatechin, and epicatechin 3-O-gallate; and the flavan dimer procyanidin B2 3'-O-gallate. These compounds were evaluated for potential to inhibit cyclooxygenases and preneoplastic lesion formation in carcinogen-treated mouse mammary glands in organ culture. At 10 micrograms/ml, trans-astringin and trans-piceatannol inhibited development of 7,12-dimethylbenz[a]anthracene-induced preneoplastic lesions in mouse mammary glands with 68.8% and 76.9% inhibition, respectively, compared with untreated glands. The latter compound was the most potent of the 12 compounds tested in this assay, with the exception of trans-resveratrol (87.5% inhibition). In the cyclooxygenase (COX)-1 assay, trans isomers of the stilbenoids appear to be more active than cis isomers: trans-resveratrol [50% inhibitory concentration (IC50) = 14.9 microM, 96%] vs. cis-resveratrol (IC50 = 55.4 microM). In the COX-2 assay, among the compounds tested, only trans- and cis-resveratrol exhibited significant inhibitory activity (IC50 = 32.2 and 50.2 microM, respectively). This is the first report showing the potential cancer-chemopreventive activity of trans-astringin, a plant stilbenoid recently found in wine. trans-Astringin and its aglycone trans-piceatannol were active in the mouse mammary gland organ culture assay but did not exhibit activity in COX-1 and COX-2 assays. trans-Resveratrol was active in all three of the bioassays used in this investigation. These findings suggest that trans-astringin and trans-piceatannol may function as potential cancer-chemopreventive agents by a mechanism different from that of trans-resveratrol.[1]

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Cognitive dysfunction by chemotherapy compromises the quality of life in cancer patients. Tea polyphenols are known chemopreventive agents. The present study was designed to evaluate the neuroprotective potential of (+) catechin hydrate (catechin), a tea polyphenol, in IMR-32 neuroblastoma cells in vitro and alleviation of episodic memory deficit in Wistar rats in vivo against a widely used chemotherapeutic agent, Doxorubicin (DOX). In vitro, neuroprotective studies were assessed in undifferentiated IMR-32 cells using percentage viability and in differentiated cells by neurite length. These studies showed catechin increased percentage viability of undifferentiated IMR-32 cells. Catechin pretreatment also showed an increase in neurite length of differentiated cells. In vivo neuroprotection of catechin was evaluated using novel object recognition task in time-induced memory deficit model at 50, 100 and 200 mg/kg dose and DOX-induced memory deficit models at 100 mg/kg dose. The latter model was developed by injection of DOX (2.5 mg/kg, i.p.) in 10 cycles over 50 days in Wistar rats. Catechin showed a significant reversal of time-induced memory deficit in a dose-dependent manner and prevention of DOX-induced memory deficit at 100 mg/kg. In addition, catechin treatment showed a significant decrease in oxidative stress, acetylcholine esterase and neuroinflammation in the hippocampus and cerebral cortex in DOX-induced toxicity model. Hence, catechin may be a potential adjuvant therapy for the amelioration of DOX-induced cognitive impairment which may improve the quality of life of cancer survivors. This improvement might be due to the elevation of antioxidant defense, prevention of neuroinflammation and inhibition of acetylcholine esterase enzyme.[2]

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Catechin hydrate (CH), a strong antioxidant that scavenges radicals, is a phenolic compound that is extracted from plants and is present in natural food and drinks, such as green tea and red wine. CH possesses anticancer potential. The mechanism of action of many anticancer drugs is based on their ability to induce apoptosis. In this study, I sought to characterize the downstream apoptotic genes targeted by CH in MCF-7 human breast cancer cells. CH effectively kills MCF-7 cells through induction of apoptosis. Apoptosis was confirmed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and real-time PCR assays. Cells were exposed to 150 μg/ml CH and 300 μg/mL CH for 24 hours, which resulted in 40.7% and 41.16% apoptotic cells, respectively. Moreover, a 48-hour exposure to 150 μg/ml CH and 300 μg/ml CH resulted in 43.73% and 52.95% apoptotic cells, respectively. Interestingly, after 72 hours of exposure to both concentrations of CH, almost 100% of cells lost their integrity. These results were further confirmed by the increased expression of caspase-3,-8, and -9 and TP53 in a time-dependent and dose-dependent manner, as determined by real-time quantitative PCR. In summary, the induction of apoptosis by CH is affected by its ability to increase the expression of pro-apoptotic genes such as caspase-3, -8, and -9 and TP53.[3]

C15H14O6

290.2681

308.089

C, 58.44; H, 5.23; O, 36.33

225937-10-0

(±)-Catechin;7295-85-4;Catechin;154-23-4

107957

Off-white to yellow solid powder

630.4ºC at760mmHg

175-177ºC

335ºC

9.29E-17mmHg at 25°C

1.481

119.61

6

7

1

22

364

2

C1[C@@H]([C@H](OC2=CC(=CC(=C21)O)O)C3=CC(=C(C=C3)O)O)O.O

OFUMQWOJBVNKLR-NQQJLSKUSA-N

InChI=1S/C15H14O6.H2O/c16-8-4-11(18)9-6-13(20)15(21-14(9)5-8)7-1-2-10(17)12(19)3-7;/h1-5,13,15-20H,6H2;1H2/t13-,15+;/m0./s1

(2R,3S)-2-(3,4-dihydroxyphenyl)-3,4-dihydro-2H-chromene-3,5,7-triol;hydrate

(+)-Catechin Hydrate; 225937-10-0; Catechin hydrate; 88191-48-4; (+)-catechin monohydrate; (2R,3S)-2-(3,4-Dihydroxyphenyl)chroman-3,5,7-triol hydrate; MFCD00149354; (+)-Cyanidol-3;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL

配方 1 中的溶解度: ≥ 2.5 mg/mL (Infinity mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (Infinity mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (Infinity mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
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7、 以上所有助溶剂都可在 Invivochem.cn网站购买。