Protective effects of epigallocatechin gallate after UV irradiation of cultured human lens epithelial cells

PURPOSE: To evaluate the protective effects of epigallocatechin gallate (EGCG) against UV irradiation of cultured human lens epithelial cells. METHODS: We irradiated cultured human lens epithelial cells with a 30-second pulse from a UV lamp with an irradiance of 0.6 mW/cm(2). Five minutes and 1 hour after UV irradiation, we administered 0, 5, 10, 15, 25, 50, or 100 uM EGCG. The cell number was measured with a microscopic counting chamber and cell viability was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. RESULTS: Compared to untreated cells, the total number of cultured human lens epithelial cells was markedly higher after UV irradiation. In a dose-dependent manner, viability was also higher in EGCG-treated cells. CONCLUSIONS: EGCG increased the cell count and cell viability after UV irradiation of cultured human lens epithelial cells, indicating that EGCG can protect lens epithelium against UV damage.     

Diet does not ensure normal development in galactosemia.

This review deals with the treatment of inherited classical galactosemia by a lactose-free diet. Although, with dietary treatment, there is a remarkable improvement in the acute phase of the disease, the long-term outcome has been disappointing for most patients, especially regarding the central nervous system and ovarian dysfunction in females. There is a need for new approaches to treatment, in combination with diet therapy, that could improve the outcome of patients with galactosemia.     

Green tea supplementation increases glutathione and plasma antioxidant capacity in adults with the metabolic syndrome

Green tea, a popular polyphenol-containing beverage, has been shown to alleviate clinical features of the metabolic syndrome. However, its effects in endogenous antioxidant biomarkers are not clearly understood. Thus, we tested the hypothesis that green tea supplementation will upregulate antioxidant parameters (enzymatic and nonenzymatic) in adults with the metabolic syndrome. Thirty-five obese participants with the metabolic syndrome were randomly assigned to receive one of the following for 8 weeks: green tea (4 cups per day), control (4 cups water per day), or green tea extract (2 capsules and 4 cups water per day). Blood samples and dietary information were collected at baseline (0 week) and 8 weeks of the study. Circulating carotenoids (α-carotene, β-carotene, lycopene) and tocopherols (α-tocopherol, γ-tocopherol) and trace elements were measured using high-performance liquid chromatography and inductively coupled plasma mass spectroscopy, respectively. Serum antioxidant enzymes (glutathione peroxidase, glutathione, catalase) and plasma antioxidant capacity were measured spectrophotometrically. Green tea beverage and green tea extract significantly increased plasma antioxidant capacity (1.5 to 2.3 μmol/L and 1.2 to 2.5 μmol/L, respectively; P < .05) and whole blood glutathione (1783 to 2395 μg/g hemoglobin and 1905 to 2751 μg/g hemoglobin, respectively; P < .05) vs controls at 8 weeks. No effects were noted in serum levels of carotenoids and tocopherols and glutathione peroxidase and catalase activities. Green tea extract significantly reduced plasma iron vs baseline (128 to 92μg/dL, P < .02), whereas copper, zinc, and selenium were not affected. These results support the hypothesis that green tea may provide antioxidant protection in the metabolic syndrome.     

表儿茶素及其衍生物表儿茶素没食子酸酯通过MAPK-ERK44/42通路抑制前列腺间质细胞增殖

[目的]探究锁阳中表儿茶素(EC)及其衍生物表儿茶素没食子酸酯(ECG)对前列腺间质细胞WPMY-1增殖的影响及其机制。[方法]体外培养WPMY-1细胞,加入不同剂量的ECG和EC,用噻唑蓝(MTT)法检测对细胞增殖的影响,用聚合酶链反应(PCR)和蛋白免疫印迹(Western blotting)法检测对增殖相关抗原PCNA mRNA和蛋白水平表达的影响;用Western blotting法分别检测ECG和EC对MAPK通路ERK44/42、P38、SAPK/JNK激活的抑制作用;加入ERK44/42激动剂C6-Ceramide(C6)及P38、SAPK/JNK联合激动剂Anisomycin(ANI)后,用MTT法检测对ECG和EC抑制细胞增殖的影响。[结果]1 nmol/L至10μmol/L的ECG和EC均可以明显抑制WPMY-1细胞的增殖(P0.01)。10 nmol/L的ECG和EC可以明显抑制WPMY-1细胞中PCNA mRNA和蛋白水平的表达(P0.05)。ECG和EC均能抑制ERK44/42和SAPK/JNK的磷酸化,但对P38的磷酸化作用不明显;加入C6后,ECG和EC抑制WPMY-1增殖的能力明显降低(P0.05或P0.01),加入ANI后,则细胞增殖能力改变不明显。[结论]ECG和EC通过ERK44/42抑制前列腺间质细胞增殖,这可能是其抗良性前列腺增生的重要机制之一。     

EGCG 对Ro52 介导的THP-1 细胞凋亡 及炎症因子的影响

目的 探讨表没食子儿茶素没食子酸酯（EGCG）对SSA/Ro52（Ro52）介导的人单核- 巨噬 细胞株THP-1 凋亡及炎症因子分泌的影响。方法 构建稳定Ro52 过表达质粒（pCMV-Ro52）,pCMVRo52 转染THP-1 细胞48 h,检测Ro52 mRNA 和蛋白表达水平的变化,采用膜联蛋白- 荧光素异硫氰酸酯 和碘化丙锭双染检测THP-1 细胞凋亡率,酶联免疫吸附法检测肿瘤坏死因子-α（TNF-α）、白介素-1β （IL-1β）、IL-13 水平。pCMV-Ro52 质粒转染48 h 后, 分别使用0、5、10、20 和50 mg/L EGCG 处理细 胞24 h,检测Ro52 表达的变化、THP-1 细胞的凋亡,以及TNF-α、IL-1β、IL-13 水平。结果 pCMVRo52 促进Ro52 表达（P <0.05）,上调THP-1 细胞凋亡率及TNF-α、IL-1β、IL-13 水平（P <0.05）; 在Ro52 过表达的THP-1 细胞中,与0 mg/L EGCG 组相比,10、20 和50 mg/L EGCG 组Ro52 蛋白表达水 平、凋亡率及TNF-α、IL-1β、IL-13 水平降低（P <0.05）。结论 Ro52 过表达可促进人单核- 巨噬细胞 THP-1 凋亡及炎症因子TNF-α、IL-1β、IL-13 分泌;EGCG 可减弱Ro52 介导的THP-1 细胞凋亡,减 少炎症因子TNF-α、IL-1β、IL-13 的分泌。     

表没食子儿茶素没食子酸酯全乙酰化衍生物的合成及急性毒性试验

目的 合成表没食子儿茶素没食子酸酯(EGCG)的全乙酰化衍生物(AcEGCG),并研究EGCG和AcEGCG对小鼠的急性毒性作用.方法 EGCG为反应底物,乙酸酐为酰化剂,吡啶为催化剂,在乙酸乙酯中反应过夜,反应液经酸洗、碱洗及水洗后干燥得到AcEGCG,高效液相色谱法(HPLC)检测其纯度,1H-NMR和13C-NMR鉴定其结构.取昆明种小白鼠,灌胃给药,连续14 d观察其急性毒性症状.采用改进寇氏法计算半数致死量(LD50).结果 合成的EGCG乙酰化衍生物经1H-NMR和13C-NMR鉴定为AcEGCG,HPLC测定纯度为99%.EGCG组小鼠给药后第1～5天出现死亡,中毒表现开始为多动,不安定,随后缩成一团,嗜睡,呼吸急促,最后痉挛,死亡.LD50=761.5 mg/kg.AcEGCG组小鼠无死亡,病理检查与正常对照组无差异.最大耐受量为8 300 mg/kg.结论 EGCG有一定的毒性,而AcEGCG无明显毒性反应.