表没食子儿茶素没食子酸酯对心血管疾病防治作用的研究进展

中国在公元前3 000年以前就有饮用绿茶的记载。现代技术发现绿茶含有大量的茶多酚,儿茶素是茶多酚的主要成分,包括4种单体物质,即表没食子儿茶素没食子酸酯[(-)-epigallocatechin gallate, EGCG]、表儿茶素没食子酸酯(epicatechin gallate,ECG)、表没食子儿茶素(epigallocatechin,EGC)和表儿茶素(epicatechin,EC),其中最主要的活性成分EGCG被认为具有抗癌、减肥、抗糖尿病、抗菌、抗病毒、预防龋齿等作用^[1]。大量研究发现饮茶也会减少心血管疾病的发生风险,对心脏具有明确的保护作用,本文就EGCG对心血管疾病的预防作用研究进展进行综述。     

五倍子抗口腔致病菌活性物质筛选及其体外抑菌效果评价

目的:研究3种五倍子提取物对6种常见口腔致病菌生长、代谢的影响.方法:通过一系列提取分离纯化,从五倍子中筛选出3种活性单体,即没食子酸、没食子酸甲酯、没食子乙酯.采用液体稀释法研究这3种五倍子活性单体对变形链球菌、粘性放线菌、牙龈卟啉单胞菌、粪肠球菌、具核梭杆菌及白色念珠菌生长、代谢的影响.结果:没食子酸对6种细菌的MIC值(mg/ml)为2.5～5、没食子酸甲酯为2.0～4.0,没食子酸乙酯为1.25～2.5,浓度为1 mg/ml时,3种提取物均能抑制这6种口腔致病菌生长、产酸及产胞外多糖.且没食子酸乙酯作用最强.结论:没食子酸、没食子酸甲酯、没食子酸乙酯在较低浓度下对口腔主要致病菌的生长、酸代谢和糖代谢都有一定的抑制作用.     

表没食子儿茶素没食子酸酯对131I辐射损伤所致甲减大鼠模型抗氧化体系的保护作用

目的：探讨不同剂量表没食子儿茶素没食子酸酯（EGCG）对131I辐射损伤所致甲状腺功能减退症（甲减）大鼠抗氧化体系的保护作用。方法3月龄健康SD大鼠52只,随机分成6组,即空白组、模型组、甲状腺片组、EGCG低剂量组（25 mg·kg-1·d-1）、EGCG中剂量组（50 mg·kg-1·d-1）、EGCG高剂量组（100 mg·kg-1·d-1）。除空白组外,其余5组给予131I灌胃2周以造甲减大鼠模型,造模成功后,空白组、模型组给予生理盐水,其他组给予相应的药物。4周后,利用生物化学方法测定大鼠血清中游离三碘甲状腺原氨酸（FT3）、游离甲状腺素（FT4）、TSH水平,同时测定超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）的含量。结果与模型组相比,甲状腺片组、EGCG组大鼠血清FT3、FT4水平均有升高,甲状腺片组、EGCG高剂量组TSH水平明显降低,EGCG低剂量组、EGCG中剂量组差异无统计学意义;与模型组相比,甲状腺片组、EGCG组的SOD水平明显降低,GSH-Px水平明显升高;EGCG中、高剂量组CAT水平显著升高。结论 EGCG能减轻131I辐射对大鼠甲状腺组织的氧化损伤,可保护大鼠抗氧化体系。     

表没食子儿茶素没食子酸酯对人胃癌细胞株MKN45诱导凋亡作用的研究

目的了解表没食子儿茶素没食子酸酯（EGCG）是否诱导人胃癌细胞株MKN45凋亡及其凋亡信号传导途径，为其临床应用提供进一步的理论依据。方法用四甲基偶氮唑蓝（MTT）比色法检测EGCG对MKN45细胞生长的抑制作用；膜连蛋白V-异硫氰基荧光素（Annexin V-FITE）＋碘化丙啶（PI）方法测定EGCG作用后MKN45细胞的凋亡率；酶联免疫吸附测定（ELISA）检测EGCG对MKN45细胞内castmse-3活性的影响；Rhodamine123染色检测EGCG作用后MKN45细胞内线粒体膜电位的改变情况。结果EGCG作用后MKN45细胞发生凋亡，随着EGCG作用时间的延长及浓度的增加．凋亡率增加。在EGCG作用8h后MKN45细胞内的caspase-3的活性开始升高，并于作用12h后活性明显升高。线粒体的膜电位于EGCG作用4h后就开始明显下降，并与时间和浓度正相关。结论EGCG可以诱导人胃癌细胞株MKN45细胞凋亡，且与作用时间及浓度正相关。EGCG对MKN45细胞凋亡的诱导是通过线粒体途径发生的．     

The Preventive Effect of Oral EGCG in a Fetal Alcohol Spectrum Disorder Mouse Model

Background: Fetal alcohol spectrum disorder (FASD) is a challenging public health problem. Previous studies have found an association between FASD and oxidative stress. In the present study, we assessed the role of oxidative stress in ethanol‐induced embryonic damage and the effect of (‐)‐epigallocatechin‐3‐gallate (EGCG), a powerful antioxidant extracted from green tea, on the development of FASD in a murine model. Methods: Pregnant female mice were given intraperitoneal ethanol (25%, 0.005 to 0.02 ml/g) on gestational day 8 (G8) to establish the FASD model. On G10.25, mice were sacrificed and embryos were collected and photographed to determine head length (HL), head width (HW), and crown rump length (CRL). For mice given EGCG, administration was through a feeding tube on G7 and G8 (dose: 200, 300, or 400 mg/kg/d, the total amount for a day was divided into 2 equal portions). G10.25 embryos were evaluated morphologically. Brain tissues of G9.25 embryos were used for RT‐PCR and western blotting of neural marker genes and proteins and detection of oxidative stress indicators. Results: Administration of ethanol to pregnant mice on G8 led to the retardation of embryonic growth and down‐regulation of neural marker genes. In addition, administration of ethanol (0.02 ml/g) led to the elevation of oxidative stress indicators [hydrogen peroxide (H₂O₂) and malondialdehyde (MDA)]. Administration of EGCG on G7 and G8 along with ethanol on G8 ameliorated the ethanol‐induced growth retardation. Mice given EGCG (400 mg/kg/d) along with ethanol had embryo sizes and neural marker genes expression similar to the normal controls. Furthermore, EGCG (400 mg/kg on G7 and G8) inhibited the increase in H₂O₂ and MDA. Conclusions: In a murine model, oxidative stress appears to play an important role in ethanol‐induced embryonic growth retardation. EGCG can prevent some of the embryonic injuries caused by ethanol.     

表没食子儿茶素没食子酸酯对结肠肿瘤生长与转移的作用

目的 观察不同浓度表没食子儿茶素没食子酸酯(epigallocatechin gallate,EGCG)对结肠肿瘤原位生长与转移的作用.方法 将40只BALB/C裸鼠均分为对照组和低、中、高剂量组.除对照组外,其他3组分别给了低、中或高浓度EGCG(分别为5、10和20 mg·kg~(-1)·d~(-1)),观察对结肠原位种植肿瘤的生长和转移的影响.HE染色观察肝、肺组织病理学改变;免疫组化检测结肠肿瘤组织中核因子E2p45相关因子2(NF-E2-related factor 2,Nrf2)基因的蛋白表达水平;RT-PCR检测Nrf2、尿苷二磷酸葡萄糖醛酸基转移酶(UGT)1A、UGT1A8和UGT1A10基因的mRNA表达水平.结果 低、中、高剂量EGCG组裸鼠肿瘤的平均重量为(152±63)、(76±42)和(18±10)mg,与对照组L(564±130)mg]比较差异有统计学意义(P值均<0.05).3组的肿瘤抑制率分别是73.0%、86.5%和96.8%.EGCG对肿瘤生长的抑制率与EGCG的剂量呈正相关(P值均<0.05).不同剂量EGCG组Nrf2基因的蛋白表达水平明显高于对照组(P<0.05),且有核转录现象.不同剂量EGCG组Nrf2、UGT1A、UGT1A8和UGT1A10基因的mRNA表达水平明显高于对照组(P<0.05).结论 不同浓度的EGCG能预防裸鼠HT-29结肠原位肿瘤的局部生长和远处转移,且有剂最依赖效应.这种作用可能通过诱导Nrf2,UGT1A、UGT1A8和UGT1A10基因的表达起作用.     

Emerging role of bioflavonoids in gastroenterology: Especially their effects on intestinal neoplasia

Flavonoids,secondary plant products which could be essential for normal physiology in humans and animals,may be the vitamins of the next century.Flavonoids belong to the polyphenols and possess antioxidative,anti-inflammatory,antimutagenic and anticarcinogenic properties.Among the various flavonoid species,tea flavonoids such as apigenin (from camomile) and epigallocatechin gallate (EGCG from green tea) can be used for the prevention of intestinal neoplasia,especially for adenoma and cancer prevention in the gastrointestinal tract.Numerous experimental studies with molecular and biological end points support the therapeutic efficacy of bioflavonoids.Clinical studies with cohorts and case-control trials suggest that flavonoids are effective in tertiary bioprevention but,as yet,there are no controlled randomized clinical trials.Flavonoids can inhibit inflammatory pathways and could be useful for chronic inflammatory bowel diseases.Flavonoid deficiency syndromes could be therapeutic targets in the future.     

Protection of brain and pancreas from high-fat diet: effects of catechin and caffeine

To investigate the effect of a high-fat diet on brain and pancreas functions, we used SAMP10 mice that have characteristics of brain atrophy and cognitive dysfunction with aging. Simultaneously, we investigated the effect of green tea catechin consumption on high-fat diet feeding, because green tea catechin has been reported to improve brain atrophy, brain dysfunction and obesity. The body weight of mice fed a high-fat diet from 2 to 12 months was higher than that of the control, although the calorie intake was not. The high-fat diet also increased insulin secretion; however, the hypersecretion of insulin and obesity were suppressed when mice were fed a high-fat diet with green tea catechin and caffeine. Furthermore, brain atrophy was suppressed and the working memory, tested using Y-maze, improved in mice fed a high-fat diet containing green tea catechin and caffeine. The secretion of insulin might affect both obesity and brain function. A strong correlation was found between working memory and insulin release in mice fed a high-fat diet with green tea catechin and/or caffeine. The results indicate the protective effect of green tea catechin and caffeine on the functions of brain and pancreas in mice fed a high-fat diet.