(-)-儿茶素没食子酸酯和(+)-表儿茶素对心肌细胞保护作用研究

目的:观察(-)-儿茶素没食子酸酯[(-)-CG]和( )-表儿茶素[( )-EC]对心肌细胞黄嘌呤/黄嘌呤氧化酶体系损伤的保护作用.方法:建立心肌细胞黄嘌呤/黄嘌呤氧化酶体系损伤模型,倒置显微镜观察加入(-)-CG、( )-EC后细胞形态学变化;噻唑盐比色法测定细胞活性;测定细胞培养液中乳酸脱氢酶(LDH)、丙二醛(MDA)、超氧化物歧化酶(SOD)含量.结果:(-)-CG、( )-EC能够增加心肌细胞存活率,降低心肌细胞LDH的漏出量,增加SOD活性,降低培养液中MDA的含量.结论:(-)-CG、( )-EC具有抗体外培养大鼠乳鼠心肌细胞黄嘌呤/黄嘌呤氧化酶体系损伤的作用.     

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。     

Protective Effect of Propyl Gallate Against Oxidized Low-Density Lipoprotein-Induced Injury of Endothelial Cells

Objective:To evaluate the protective effect of propyl gallate(PG),an alkyl ester of gallic acid which is an active ingredient of Radix Paeoniae,against oxidized low-density lipoprotein(ox-LDL)-induced apoptosis and death in endothelial cells(ECs) and to find out its preliminary mechanism.Methods:The cultured endothelial cells were divided into normal,model(ox-LDL),control(fetal bovine serum),PG high dose(20 μg/mL),PG middle dose(10 μg/mL),and PG low dose(5 μg/mL) groups,each derived from three different pools of umbilical cords.The model of injured human umbilical vein endothelial cells(HUVECs)was induced by ox-LDL.The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide(MTT) assay,Hoechst 33258 staining,flow cytometry and measurement of nitrogen monoxidum(NO) release were used to evaluate the protective effect of PG against ox-LDL-induced apoptosis and death in HUVECs.To find out the mechanism of this protective effect,the expression of endothelial nitric oxide synthase(eNOS) mRNA,eNOS protein expression,immunofluorescence of intracellular reactive oxygen species(ROS) and activities of malondialdehyde(MDA),superoxidedismutase(SOD) and glutathione peroxidase(GPx) were observed.Results:PG significantly reduced ox-LDL-induced apoptosis and cell death.The percentage of cells death and apoptosis was significantly higher in the ox-LDL group than that in the control group(P0.05).Compared with the control group,the cells death and apoptosis of PG group was no different(P0.05).As compared with the ox-LDL group,results of the PG high dose group showed that cell viability was significantly increased(P0.05),the level of NO release,expression of eNOS mRNA,densitometric value of eNOS protein expression,as well as the activities of SOD and GPx were all significantly higher(all P0.05).Conclusion:PG could potentially serve as a novel endothelial protective agent against ox-LDL-induced injury of endothelial cell.     

The protective effect of green tea catechins on ketamine-induced cystitis in a rat model

ObjectiveTo investigate the protective effect of green tea epigallocatechin gallate (EGCG) on long-term ketamine-induced ulcerative cystitis (KIC) using a ketamine addiction rat model.Materials and methodsThirty Sprague-Dawley rats were divided into three groups which received saline, ketamine (25 mg/kg/d), or ketamine combined with EGCG (10 μM/kg) for a period of 28 days. In each group, cystometry and a metabolic cage micturition pattern study were performed weekly. Masson's trichrome study was done to evaluate the morphologic changes. Western blot analyses were carried out to examine the expressions of inflammatory protein [transforming growth factor-β (TGF-β)] and fibrosis proteins (fibronectin and type I collagen) in bladder tissues.ResultsChronic ketamine treatment resulted in bladder hyperactivity with a significant increase in micturition frequency and a decrease in bladder compliance. These alterations in micturition pattern were accompanied by increases in the expressions of inflammatory and fibrosis markers, TGF-β, fibronectin, and type I collagen after long-term ketamine treatment. Masson's trichrome stain showed that ketamine treatment decreased urothelium thickness while increasing the collagen to smooth muscle ratio and exacerbating interstitial fibrosis. By contrast, simultaneous EGCG and ketamine treatment reversed ketamine-induced damage to almost control levels, showing the protective effect of EGCG.ConclusionThis protective effect of EGCG may come from its antiinflammatory and antifibrotic properties.     

基于Wnt信号通路研究表没食子酸儿茶素没食子酸酯对肝星状细胞活化的作用及机制

目的 基于Wnt信号通路探究表没食子酸儿茶素没食子酸酯(epigallocatechin gallate,EGCG)对人肝星状细胞LX-2活化的影响及其作用机制.方法 体外培养LX-2细胞,CCK-8法筛选EGCG的实验浓度;取对数生长期的LX-2细胞,设置对照组(正常培养)、模型组[10ng/mL转化生长因子-β1(...     

表没食子儿茶素没食子酸酯对高尿酸血症大鼠血管内皮炎症因子的作用

目的探讨表没食子儿茶素没食子酸酯(EGCG)对高尿酸血症大鼠血管内皮炎症因子的作用。方法将36只雄性SD大鼠分为正常对照组、模型对照组、EGCG低剂量组、EGCG中剂量组、EGCG高剂量组、别嘌呤醇组,5周后,运用RT-PCR检测大鼠主动脉MCP-1、TNF-α、ICAM-1、ET-1及e NOS表达量,以及大鼠血清尿酸、肌酐、尿素氮和黄嘌呤氧化酶(XO)水平。结果模型对照组大鼠的血尿酸和XO水平显著高于正常对照组(P0.01),EGCG各浓度组及别嘌呤醇组大鼠的血尿酸和XO水平与模型对照组相比较则有不同程度下降(P0.01)。模型对照组大鼠主动脉MCP-1、TNF-α、ICAM-1的mRNA表达量较正常对照组显著升高(P0.01),EGCG各浓度组和别嘌呤组大鼠主动脉TNF-α、ICAM-1的mRNA表达量与模型对照组相比显著下降(P0.01),EGCG高剂量组和别嘌呤组MCP-1 mRNA表达量与模型对照组相比显著下降(P0.05)。EGCG中剂量组和别嘌呤组ET-1 mRNA表达量与模型对照组相比显著下降(P0.05)。结论 EGCG干预可以降低高尿酸血症大鼠的血尿酸水平,同时减少血管内皮炎症因子的表达。     

表没食子儿茶素没食子酸酯抗感染特性研究进展

表没食子儿茶素没食子酸酯[(⁃)⁃epigallocatechin⁃3⁃O⁃gallate, EGCG]是绿茶中含量最丰富的多酚类化合物,具有抗氧化、抗炎、抗血栓、抗辐射、抗突变、抗肿瘤、抗纤维化等广泛生物学功能,对糖尿病、肥胖、哮喘、癌症、心血管系统和神经系统疾病等有一定改善和治疗作用,亦可提高机体免疫力。近年来研究发现,EGCG在细菌、真菌、病毒、寄生虫等病原微生物引起的感染性疾病中发挥重要作用。本文就EGCG抗感染特性研究进展进行综述,以揭示其在预防和治疗感染性疾病中的潜在作用。     

羟氯喹及没食子酸酯对HaCaT细胞光照射的影响

目的 探讨羟氯喹和绿茶活性成分表没食子儿茶素没食子酸酯(EGCG)对中波紫外线(UVB)损伤永生化角质形成细胞株(HaCaT细胞)的保护作用及其机制。方法 采用UVB定时及定量照射培养的HaCaT细胞,分别加入羟氯喹和EGCG干预处理,以RT-PCR法检测各受试组p53、p21、c-fos基因表达水平。结果 UVB照射后可明显增加HaCaT细胞中p53,p21,c-fos mRNA表达,羟氯喹和EGCG可不同程度地下调上述基因表达水平。结论 羟氯喹和EGCG的光保护作用在HaCaT细胞可能与其抑制p53,p21,c-fos基因表达有关。     

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。