Aim:To investigate the effects of epigallocatechin gallate ( EGCG) combined with vitamin E ( VitE) on learning and memory ability and antioxidative damage in hippocampus of progestational lead -exposed newborn mice .Meth-ods:A total of 20 healthy mice were exposed to 2 g/L lead acetate aqueous solution , and 4 mice were given lead-free dei-onized water for 21 days.After that, the female and male mice were fed in one cage with 2:1 ratio.At the 21th day after delivery, the offspring of lead-exposed female mice were divided into 7 groups randomly: physiological saline group , corn oil group, EGCG group(3.0 mg/kg), VitE group(30 IU/kg ), combination group Ⅰ(EGCG 3.0 mg/kg+VitE 30 IU/kg), combination group Ⅱ(EGCG 1.5 mg/kg+VitE 60 IU/kg), combination group Ⅲ(EGCG 6.0 mg/kg+VitE 15 IU/kg), and received corresponding intervention for 28 days,10 in each group;the offspring(n=10) of lead-free female mice were the normal control , and received lead-free deionized water for 28 days.After the intervention , the learning and memo-ry ability of mice was measured by Morris water maze ,the blood lead level was measured by voltammetry , and the activities of SOD and the concentration of MDA in hippocampus were measured by Oxidase Kit .Results:Compared with the normal control group, the escape latency of the physiological saline group and the corn oil group increased , the times across the platform decreased, the blood lead level and MDA concentration increased , and SOD activity decreased(P<0.05).Com-pared with the physiological saline group and the corn oil group , the escape latency of the 5 intervention groups dcreased , the times across the platform increased, the blood lead level reduced in different degree (P <0.05); the SOD activity of combination group Ⅰand Ⅲ increased, and MDA concentration decreased (P <0.05).Conclusion: EGCG and VitE might improve the learning and memory ability of lead-exposed offspring mice through increasing the SOD activity in hippo-campus, which could protect the lead-exposed offspring mice from nerve damage .

OBJECT:To investigate the effects of sulforaphane (SFN) and vitamin E (VE) on spatial learning and memory ability and oxidative damage of hippocampus in lead-exposed mice at lactation.METHODS:A total of 18 adult Kunming mice, all 12 female mice were divided into two groups by body weight randomly, 10 mice drank water containing 0.2% lead acetate at lactation, the other 2 mice drank lead free deionized water named as the normal group. Then, they were mated at a 1:2 ratio of male to female. After weaning, the pups were divided into 5 groups by weight randomly (10 each group): normal saline (NS) group, corn oil (CO) group, SFN group, VE group and SFN+VE group. They were subject to gavage daily for four weeks. Gavage doses of SFN and VE were 25mg/kg and 30 IU/kg respectively. Meanwhile, 10 pups of the normal group were selected randomly as the control (C) group. The C group was normally raised for 4 weeks. The spatial learning and memory ability of them were evaluated by the Morris water maze test, and the lead level in the blood was determined by polarography. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) level in hippocampus were measured by the kits.RESULTS:Compared with the NS and CO groups, the lead level in the blood of SFN and SFN+VE group had a significant decrease. In water maze test, the mice treated with SFN or/and VE performed better than mice of the NS and CO groups. In addition, a remarkable decrease in MDA level was found in mice treated with SFN or/and VE than those in NS and CO groups. What's more, there was no statistical distinction of SOD activity in SFN group than that of NS group. SOD activity significantly increased was observed in VE and SFN+VE groups than that of CO group.CONCLUSION:Sulforaphane and vitamin E could ameliorate cognitive decline and oxidative damage in pups with lead exposure at lactation from maternal milk.

Objective To explore the association between esophageal cancer and serum vitamin E level and to provide evidences for researches and prevention of esophageal cancer.Methods Case-control studies on esophageal cancer and serum vitamin E level published from January 1980 to December 2015 were searched through China National Knowledge Infrastructure,Wanfang Database,PubMed,and Web of Science.Meta-analysis was performed with Stata 12.0.Results A total of 9 literatures (7 in Chinese and 2 in English),involving in 358 esophageal cancer cases and 538 controis,were included in the meta-analysis.The meta-analysis showed that the serum vitamin E level of esophageal cancer cases was lower than that of the controls (standardized mean difference [SMD] =-0.50,95 ％ confidence interval [95 ％ CI] =-0.65-0.36,P ＜ 0.001).Subgroup analysis found that the serum vitamin E levels of the esophageal cancer cases were lower than those of the controls for the studies conducted in China (SMD =-0.50,95％ CI =-0.67-0.33) and in United States (SMD =-0.51,95％ CI =-0.77-0.25),with the controls selected from communities (SMD =-0.54,95％ CI=-0.69-0.39),with the sample size of larger than 50 (SMD =-0.56,95％ CI=-0.71-0.41),with age-matched controls (SMD =-0.57,95％ CI =-0.72-0.42),and with serum vitamin E level detection using high performance liquid chromatography (HPLC) (SMD =-0.41,95％ CI =-0.59-0.24) and using method other than HPLC (SMD =-0.67,95％ CI =-0.91-0.43) (all P ＜ 0.001).Sensitivity analysis and publication bias test showed that the results of the study were stable and there was no publication bias for the literatures included in the study.Conclusion Serum vitamin E level is low in esophageal cancer patients.

Aim:To explore the effects of epigallocatechin gallate( EGCG) on spatial learning memory performance and antioxidative damage ability in lead exposed offspring mice during lactation.Methods: A total of ten healthy preg-nant C5 BL/6 mice were randomly allocated into control group and lead exposed group, which were treated with drinking double evaporated water and Pb containing water, respectively from the beginning of offspring birth and lasted until wea-ning.There were 2 pregnant mice in control group and 8 pregnant mice in lead exposed group.The offspring mice were exposed to lead by maternal milk.Forty lead exposed offspring mice and ten control offspring mice were employed as the research objects.According to the body weight, the mice were stochastically allocated into five groups: lead exposed group( normal saline) ,low,middle,high dose EGCG interfering groups and control group( ten control offspring mice) and each group was administered for by lavage 21 d.The spatial learning and memory ability was evaluated by Morris water maze,SOD and GSH-Px activity levels and MDA level in hippocampus tissue were measured by corresponding kits.Re-sults: The escape latency in each group measured at different days had significant differences and there were also differ-ences between different groups( P<0.001);the activity levels of SOD and GSH-Px were higher in middle,high interfer-ing groups than those in lead exposed group, while the content of MDA was lower(P<0.05).Conclusion:EGCG may protect offspring mice from lead-induced peroxidation and enhance the spatial learning and memory ability through impro-ving antioxidant enzymes activity.

Objective To explore the effects of different doses of epigallocatechin 3 gallate,table gallic catechin gallic acid ester (EGCG)on the learning and memory ability,amyloid beta and neprilysin enzymes in lactation mice which were exposed to lead.Methods SPF pregnant C57BL/6 mice were divided into control group (drank distilled water, n=4)and lead exposure group (drank 0.5% Pb-contaminated acetic acid solution,n=14).Another 40 male lead-ex-posed mice were divided into 4 groups,low EGCG group (1.5 mg/kg),which are moderate EGCG group (3.0 mg/kg),&nbsp;high EGCG group (4.5 mg/kg)and lead exposure group,with 10 mice in each group.Another 10 male mice served as the control group (normal saline).After 21 days of treatment,all rats’learning and memory ability was tested with Morris water maze experiment;the lead content in blood and hippocampus was determined with graphite furnace atomic absorption spectrometer;the protein contents of Aβ1-40 ,Aβ1-42 ,AβPP mRNA,AβPP and the neprilysin enzyme were also detected.Results The lead exposure group,and low,moderate and high EGCG groups had significantly higher content of blood lead than the control group (P<0.05).There was no difference among EGCG groups and lead expo-sure group (P=0.174,0.086,0.071).Lead exposure group had longer escaping latency than the control group (P<0.001),while the EGCG group had shorter escaping latency than the control group (P<0.001).Compared with the control group,the lead exposure group had increased content of Aβ1-40 and Aβ1-42(P<0.001),and decreased Nep con-tent (P<0.001);the moderate and high EGCG groups had decreased Aβ1-40 and Aβ1-42 content and increased Nep con-tent (P<0.001),and the high EGCG group had better interventional effect.Conclusion EGCG intervention can sig-nificantly improve the learning and memory ability of mice.EGCG can reduce Aβ1-40 and Aβ1-42 contents in the hippo-campus,inhibit the expression of related gene AβPP,and upregulate the Nep protein expression.

Mesenchymal-cell proliferation is the main process in shelf outgrowth. Both all-trans-retinoic acid (atRA) and transforming growth factor-β3 (TGF-β3) play an important role in mouse embryonic palate mesenchymal (MEPM) cell proliferation. In the present study, we investigated the crosstalk between RA and TGF-β signaling in MEPM-cell proliferation. We found that atRA inhibited MEPM-cell proliferation by downregulating TGF-β/Smad signaling and that TGF-β3 treatment was able to antagonize RA signaling. Transforming growth-interacting factor (TGIF) is a transcriptional repressor that suppresses both TGF-β- and retinoid-driven gene transcription. Furthermore, we investigated the role of TGIF in the interaction between both TGF-β and RA signaling in MEPM-cell proliferation. The results showed that both atRA and TGF-β3 significantly increased the expression level of TGIF, and TGIF mediated the negative interaction between TGF-β and RA signaling pathways, which depended on TGIF binding to Smad2 or RARβ (RA receptor beta). Moreover, after deletion of TGIF, both the effects of atRA on TGF-β-dependent protein expression and the effects of TGF-β on RA-dependent protein expression were lost. So we conclude that there is a negative functional interplay of RA and TGF-β signaling mediated by TGIF to modulate MEPM-cell proliferation.

目的 探讨铅暴露对小鼠学习记忆能力及海马组织中β-淀粉样前体蛋白(β-Amyloid Precursor Protein,β-APP)表达的影响.方法 采用自由饮水模式建立铅暴露动物模型,将40只21日龄小鼠随机分为低、中、高剂量染毒组和对照组,分别饲以2g/L,4g/L,6g/L的乙酸铅水溶液和去离子水.3个月后,Morris水迷宫试验测定小鼠学习记忆能力,石墨炉原子吸收光谱仪测定血液和海马中铅含量,wstem blot技术检测各组小鼠海马组织中APP蛋白的表达情况.结果 与对照组相比,各剂量铅暴露组小鼠逃避潜伏期差异有统计学意义(P＜0.05),随暴露剂量的增大而延长.与对照组相比,中、高剂量组穿越平台的次数明显减少(P＜0.05),差异有统计学意义;各剂量铅暴露组血铅及海马铅含量与对照组相比,差异均有统计学意义(P＜0.05),其中高剂量暴露组血铅和海马铅含量均高于其他各剂量暴露组,差异具有统计学意义(P＜0.05);各剂量铅暴露组APP蛋白的表达量明显高于对照组,差异具有统计学意义(P＜0.05),并随染毒剂量增加,表达量增高.结论 铅可能诱导APP蛋白的过度表达造成神经系统损伤,从而影响小鼠学习记忆能力,这可能是铅致小鼠认知功能障碍的机制之一.