BACKGROUND： The neuroprotective effects of （-）-epigallocatechin-3-gallate （EGCG）, the main polyphenolic constituent of green tea, have been widely reported. However, the action mechanisms, in particular in D-gala...BACKGROUND： The neuroprotective effects of （-）-epigallocatechin-3-gallate （EGCG）, the main polyphenolic constituent of green tea, have been widely reported. However, the action mechanisms, in particular in D-galactose-induced aging mice, remain poorly understood. OBJECTIVE： The present study investigated the protective effects of EGCG on D-galactose-induced hippocampus neuronal apoptosis in aging mice, as well as the relationship with expression of p751CD, JNK2, and p53 proteins. DESIGN, TIME AND SETTING： A randomized, controlled, molecular biological, animal experiment was performed at the Laboratory of Pharmacology, Pharmaceutical College of China Medical University, China, from September 2006 to July 2008. MATERIALS： D-galactose and EGCG （Sigma, USA）, as well as terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling （TUNEL） In Situ Cell Apoptosis Detection Kit （Promega, USA）, were used in this study. METHODS： A total of 64 mice were equally and randomly divided into D-galactose model, low-dose EGCG, high-dose EGCG, and control groups. Mice in the D-galactose model, low-dose EGCG, and high-dose EGCG groups were subcutaneously injected with 3% D-galactose （150 mg/kg）, daily for 6 weeks, to establish a mouse model of aging. Mice in the control group were treated with saline （5 mL/kg）. At 3 weeks following injection, mice in the low-dose EGCG and high-dose EGCG groups were orally administered EGCG at a dose of 2 mg/kg and 6 mg/kg, respectively, once a day, for 4 consecutive days. Mice in the control and D-galactose model groups received distilled water （5 mL/kg）. MAIN OUTCOME MEASURES： Memory function was evaluated using a step-through passive avoidance test. Neuronal apoptosis in the mouse hippocampus was detected using TUNEL staining. Expression levels of the intracellular domain of the p75 neurotrophin receptor （p75NTR）-p751CD, JNK2, and p53 proteins in the hippocampus were determined using Western blot analysis. RESULTS： The aging mouse model was induced by subcutaneous injection of D-galactose, which resulted in obvious memory impairment, increased apoptotic index, and increased protein expression levels of p751CD, JNK2, and p53 in the hippocampus, compared with control mice （P 〈 0.01）. Oral EGCG administration （2 or 6 mg/kg） for 4 weeks significantly improved levels of memory deficit in the aging mice and reduced apoptotic indices and protein expression levels of p751CD, JNK2, and p53 in the mouse hippocampus （P 〈 0.01）. CONCLUSION： Results from this study demonstrated increased protein expression levels of p751CD, JNK2, and p53, as well as increased hippocampal neuronal apoptosis in a D-galactose-induced mouse model of aging. EGCG provided protective effects against D-galactose-induced neuronal apoptosis in the hippocampus by reducing protein expression levels of p751CD, JNK2, and p53 proteins in the hippocampus of aging mice.展开更多
目的探讨冠心宁片对气滞血瘀证冠心病伴轻度高血压病患者血清C1q/肿瘤坏死因子相关蛋白3(CTRP3)、脂蛋白相关磷脂酶A2(Lp-PLA2)、半乳糖凝聚素-3(Gal-3)水平的影响。方法收集气滞血瘀证冠心病伴轻度高血压病患者84例,按照随机数字表法...目的探讨冠心宁片对气滞血瘀证冠心病伴轻度高血压病患者血清C1q/肿瘤坏死因子相关蛋白3(CTRP3)、脂蛋白相关磷脂酶A2(Lp-PLA2)、半乳糖凝聚素-3(Gal-3)水平的影响。方法收集气滞血瘀证冠心病伴轻度高血压病患者84例,按照随机数字表法分为治疗组和对照组,每组42例。对照组给予曲美他嗪治疗,治疗组患者在对照组的基础上联合冠心宁治疗,两组连续观察3个月。比较两组心功能指标、24 h动态血压、气滞血瘀证评分以及血清CTRP3、Lp-PLA2、Gal-3水平。结果治疗后,治疗组的左心室舒张末期内径(LVEDD)、左心室收缩末期内径(LVESD)均低于对照组,左室射血分数(LVEF)以及舒张早期/舒张晚期最大血流速度(E/A)均高于对照组,差异均有统计学意义(t分别=3.96、4.99、-5.04、-5.38,P均<0.05);治疗组的24 h收缩压(24 h SBP)与24 h舒张压(24 h DBP)均低于对照组(t分别=3.34、1.74,P均<0.05);治疗组的气滞血瘀证评分低于对照组(t=7.50,P<0.05);治疗组的CTRP3水平高于对照组,Lp-PLA2、Gal-3水平低于对照组,差异均有统计学意义(t分别=-6.00、2.84、8.80,P均<0.05)。结论冠心宁片对气滞血瘀证冠心病伴轻度高血压病患者的疗效显著,可调节血清CTRP3、Lp-PLA2、Gal-3水平,改善其疗效。展开更多
文摘BACKGROUND： The neuroprotective effects of （-）-epigallocatechin-3-gallate （EGCG）, the main polyphenolic constituent of green tea, have been widely reported. However, the action mechanisms, in particular in D-galactose-induced aging mice, remain poorly understood. OBJECTIVE： The present study investigated the protective effects of EGCG on D-galactose-induced hippocampus neuronal apoptosis in aging mice, as well as the relationship with expression of p751CD, JNK2, and p53 proteins. DESIGN, TIME AND SETTING： A randomized, controlled, molecular biological, animal experiment was performed at the Laboratory of Pharmacology, Pharmaceutical College of China Medical University, China, from September 2006 to July 2008. MATERIALS： D-galactose and EGCG （Sigma, USA）, as well as terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling （TUNEL） In Situ Cell Apoptosis Detection Kit （Promega, USA）, were used in this study. METHODS： A total of 64 mice were equally and randomly divided into D-galactose model, low-dose EGCG, high-dose EGCG, and control groups. Mice in the D-galactose model, low-dose EGCG, and high-dose EGCG groups were subcutaneously injected with 3% D-galactose （150 mg/kg）, daily for 6 weeks, to establish a mouse model of aging. Mice in the control group were treated with saline （5 mL/kg）. At 3 weeks following injection, mice in the low-dose EGCG and high-dose EGCG groups were orally administered EGCG at a dose of 2 mg/kg and 6 mg/kg, respectively, once a day, for 4 consecutive days. Mice in the control and D-galactose model groups received distilled water （5 mL/kg）. MAIN OUTCOME MEASURES： Memory function was evaluated using a step-through passive avoidance test. Neuronal apoptosis in the mouse hippocampus was detected using TUNEL staining. Expression levels of the intracellular domain of the p75 neurotrophin receptor （p75NTR）-p751CD, JNK2, and p53 proteins in the hippocampus were determined using Western blot analysis. RESULTS： The aging mouse model was induced by subcutaneous injection of D-galactose, which resulted in obvious memory impairment, increased apoptotic index, and increased protein expression levels of p751CD, JNK2, and p53 in the hippocampus, compared with control mice （P 〈 0.01）. Oral EGCG administration （2 or 6 mg/kg） for 4 weeks significantly improved levels of memory deficit in the aging mice and reduced apoptotic indices and protein expression levels of p751CD, JNK2, and p53 in the mouse hippocampus （P 〈 0.01）. CONCLUSION： Results from this study demonstrated increased protein expression levels of p751CD, JNK2, and p53, as well as increased hippocampal neuronal apoptosis in a D-galactose-induced mouse model of aging. EGCG provided protective effects against D-galactose-induced neuronal apoptosis in the hippocampus by reducing protein expression levels of p751CD, JNK2, and p53 proteins in the hippocampus of aging mice.
文摘目的探讨冠心宁片对气滞血瘀证冠心病伴轻度高血压病患者血清C1q/肿瘤坏死因子相关蛋白3(CTRP3)、脂蛋白相关磷脂酶A2(Lp-PLA2)、半乳糖凝聚素-3(Gal-3)水平的影响。方法收集气滞血瘀证冠心病伴轻度高血压病患者84例,按照随机数字表法分为治疗组和对照组,每组42例。对照组给予曲美他嗪治疗,治疗组患者在对照组的基础上联合冠心宁治疗,两组连续观察3个月。比较两组心功能指标、24 h动态血压、气滞血瘀证评分以及血清CTRP3、Lp-PLA2、Gal-3水平。结果治疗后,治疗组的左心室舒张末期内径(LVEDD)、左心室收缩末期内径(LVESD)均低于对照组,左室射血分数(LVEF)以及舒张早期/舒张晚期最大血流速度(E/A)均高于对照组,差异均有统计学意义(t分别=3.96、4.99、-5.04、-5.38,P均<0.05);治疗组的24 h收缩压(24 h SBP)与24 h舒张压(24 h DBP)均低于对照组(t分别=3.34、1.74,P均<0.05);治疗组的气滞血瘀证评分低于对照组(t=7.50,P<0.05);治疗组的CTRP3水平高于对照组,Lp-PLA2、Gal-3水平低于对照组,差异均有统计学意义(t分别=-6.00、2.84、8.80,P均<0.05)。结论冠心宁片对气滞血瘀证冠心病伴轻度高血压病患者的疗效显著,可调节血清CTRP3、Lp-PLA2、Gal-3水平,改善其疗效。
