锌与锗对小鼠抗氧化作用影响的实验研究

对２４０只小鼠的血清、肝脏、肌肉进行了锌和锗含量，抗化指标ＳＯＤ活性、ＭＤＡ含量测定。观察结果表明，微量元素锌与锗在小鼠血清中有一定的竞争作用。血清锌锗与肌肉、肝脏锌、锗及ＳＯＤ有一定的相关性。由于锌和锗含量的变化，小鼠抗氧化作用受到了影响。当两者联合应用时，ＳＯＤ活性有不同程度增加，ＭＤＡ含量随之下降，提示了锌与锗在小鼠抗氧化方面有一定的协同作用。     

稀土对锌铝合金镀层作用机理的研究

研究了镧、铈混合稀土对锌铝合金镀层结构及性能的影响。性能检测证实,添加稀土的锌铝合金镀层具有优异的附着力、塑性和加工成型性。经化学分析和微观测试,确定了稀土在镀层中的数量、存在形式及分布,从而初步探讨了稀土对改善镀层外观及性能的作用机理。     

锌对你同样也有神奇的作用

英国戴安娜王妃美艳动人，仪态万千，据说是微量元素锌之赐。戴妃原本是一个既瘦削又腼腆的女学生，是锌令她变为曲线玲珑、女人味十足的王妃。专家指出，锌同样对你也有这样的神奇作用。     

离子对高效液相色谱—TPPS4光度法测定痕量锰锌铜的研究

本实验用磺化四苯基卟啉作柱前衍生试剂，研究了在Ｈｇ（ＩＩ）催化下，于ＰＨ５．５时，ＴＰＰＳ４与Ｍｎ（ＩＩ），Ｚｎ（ＩＩ），Ｃｕ（ＩＩ）的配位反应，提出了以苄基三乙基氯化铵作离子对试剂，反相离子对高效液相色谱－光度法分离和测定痕量Ｍｎ（ＩＩ），Ｚｎ（ＩＩ），Ｃｕ（ＩＩ）的新方法，检测下限（×１０＾－９ｇ／ｍＬ）：Ｍｎ＾２＋０．１５，Ｚｎ＾２＋０．２０，Ｃｕ＾２＋０．１１。所确立的方法用于茶汤中锰，锌     

离子对高效液相色谱—磺化四苯基卟啉光度法同时测定痕量锌和铜的研究

用ＴＰＰＳ４作柱前衍生试剂，寻找到试剂与锌（Ⅱ）和铜（Ⅱ）的最佳反应条件，然后在ＯＤＳ柱上，以乙腈－水体系（２４：７６，Ｖ／Ｖ）作流动相，四乙基磺化锭作离子对试剂，在４１５ｎｍ处检测，确立了离子对高效液相色谱－光度法快速分离测定痕量锌和铜的新方法，检测下限（×１０＾－９ｇ／ｍＬ）：Ｚｎ０．１０，Ｃｕ０．０９．所建立的方法用于花生样品中锌和铜的测定，结果令人满意。     

在儿童生长发育中铅的危害与锌的作用

综述了在儿童生长发育中铅的危害与锌的作用。认为铅中毒和锌缺乏将严重影响儿童的生长发育。铅对儿童是以中枢神经系统损坏为主,中构神经毒性最普遍的表现形式是智力和行为的异常。锌被誉为“生命之花”,在人的机体内具有极其重要的生理和生化功能,缺锌儿童发育迟缓、智力差、免疫力低下、食欲不振等。而且,锌能够减少组织中铅的蓄积和铅毒性作用的影响,补锌能有效降低人体铅的含量。葡萄糖酸是唯一被列入非处方药（OTC）目录的理想的有机锌补充剂。     

锌对环磷酰胺引起的小鼠胸腺和脾脏重量变化的影响

应用硫酸锌，复合蛋白锌对环磷酰胺引起的小鼠脾脏及胸腺重量变化的影响进行了观察。结果表明，胸腺微量元素锌含量高于脾脏，复合蛋白锌组胸腺重量及其指数高于环磷酰胺组，与 酸锌组无差异。     

锌金属硫蛋白预防甲基汞对细胞膜损伤作用的实验研究

不同剂量的Ｚｎ可以诱导小鼠肝脏产生ＺｎＭＴ,随着实验组Ｚｎ剂量的增加,肝脏内ＺｎＭＴ的含量也相应增加,呈剂量效应增加（ｒ＝０．９９６）。ＺｎＭＴ具有保护膜构象、膜ＳＨ基、拮抗ＭｅＨｇ对膜流动性及膜通透性的损伤作用。本实验结果为ＺｎＭＴ预防甲基汞中毒提供了科学依据,同时显示了诱导ＺｎＭＴ的锌剂量要适当,过高则有毒性作用。     

锌在硫酸溶液中腐蚀速度及其缓蚀作用的研究

锌在硫酸溶液中腐蚀速度及其缓蚀作用的研究杨春芬，沈报春（云南大学化学系，昆明６５０Ｏ９１）金属的腐蚀及其缓蚀作用的研究具有重要的实际意义。近年来，有关锌腐蚀动力学及寻找高效缓蚀剂的研究有一些报道￣［１－３］，但多在中性介质及用电化学方法研究，本文是在...     

Multiple Roles of Black Raspberry Anthocyanins Protecting against Alcoholic Liver Disease

This study aimed to investigate the protective effect of black raspberry anthocyanins (BRAs) against acute and subacute alcoholic liver disease (ALD). Network analysis and docking study were carried out to understand the potential mechanism. Thereafter, the serum biochemical parameters and liver indexes were measured, the histopathological changes of the liver were analyzed in vivo. The results showed that all tested parameters were ameliorated after the administration of BRAs with alcohol. Meanwhile, there was increased protein expression of NF-κB and TGF-β in extracted livers, which was associated with hepatitis and hepatic fibrosis. Furthermore, BRAs and cyanidin-3-O-rutinoside exhibited cytotoxic effects on t-HSC/Cl-6, HepG2, and Hep3B and induced the apoptosis of HepG2 cells; downregulated the protein expression level of Bcl-2; upregulated the level of Bax; and promoted the release of cytochrome C, cleaved caspase-9, cleaved caspase-3, and cleaved PARP in HepG2 cells. In addition, the antioxidant activity of BRAs was tested, and the chemical components were analyzed by FT-ICR MS. The results proved that BRAs exert preventive effect on ALD through the antioxidant and apoptosis pathways.     

Red Quinoa Bran Extract Prevented Alcoholic Fatty Liver Disease via Increasing Antioxidative System and Repressing Fatty Acid Synthesis Factors in Mice Fed Alcohol Liquid Diet

Alcohol is metabolized in liver. Chronic alcohol abuse results in alcohol-induced fatty liver and liver injury. Red quinoa (Chenopodium formosanum) was a traditional staple food for Taiwanese aborigines. Red quinoa bran (RQB) included strong anti-oxidative and anti-inflammatory polyphenolic compounds, but it was usually regarded as the agricultural waste. Therefore, this study is to investigate the effect of water and ethanol extraction products of RQB on the prevention of liquid alcoholic diet-induced acute liver injury in mice. The mice were given whole grain powder of red quinoa (RQ-P), RQB ethanol extract (RQB-E), RQB water extract (RQB-W), and rutin orally for 6 weeks, respectively. The results indicated that RQB-E, RQB-W, and rutin decreased alcoholic diet-induced activities of aspartate aminotransferase and alanine aminotransferase, and the levels of serum triglyceride, total cholesterol, and hepatic triglyceride. Hematoxylin and eosin staining of liver tissues showed that RQB-E and RQB-W reduced lipid droplet accumulation and liver injury. However, ethanol extraction process can gain high rutin and antioxidative agents contents from red quinoa, that showed strong effects in preventing alcoholic fatty liver disease and liver injury via increasing superoxide dismutase/catalase antioxidative system and repressing the expressions of fatty acid synthesis enzyme acetyl-CoA carboxylase.     

Monascin and Ankaflavin of Monascus purpureus Prevent Alcoholic Liver Disease through Regulating AMPK-Mediated Lipid Metabolism and Enhancing Both Anti-Inflammatory and Anti-Oxidative Systems

Alcohol metabolism causes an excessive accumulation of liver lipids and inflammation, resulting in liver damage. The yellow pigments monascin (MS) and ankaflavin (AK) of Monascus purpureus-fermented rice were proven to regulate ethanol-induced damage in HepG2 cells, but the complete anti-inflammatory and anti-fatty liver mechanisms in the animal model are still unclear. This study explored the roles of MS and AK in improving alcoholic liver injury. MS and AK were simultaneously fed to evaluate their effects and mechanisms in C57BL/6J mice fed the Lieber–DeCarli liquid alcohol diet for 6 weeks. The results indicated that MS and AK significantly reduced the serum aspartate aminotransferase and alanine aminotransferase activity, as well as the total liver cholesterol and triglyceride levels. The histopathological results indicated that MS and AK prevented lipid accumulation in the liver. MS and AK effectively enhanced the activity of antioxidant enzymes and reduced the degree of lipid peroxidation; AK was particularly effective and exhibited a superior preventive effect against alcoholic liver injury and fatty liver. In addition to inhibiting the phosphorylation of the MAPK family, MS and AK directly reduced TNF-α, IL-6, and IL-1β levels, thereby reducing NF-κB and its downstream iNOS and COX-2 expressions, as well as increasing PPAR-γ, Nrf-2, and HO-1 expressions to prevent liver damage. MS and AK also directly reduced TNF-α, IL-6, and IL-1β expression, thereby reducing the production of NF-κB and its downstream iNOS and COX-2, and increasing PPAR-γ, Nrf-2, and HO-1 expressions, preventing alcohol damage to the liver.     

锌与疾病关系的探讨

综述了锌与健康的关系，包括：锌的代谢，锌的主要功能，锌与疾病治疗等方面，参考文献16篇。     

两亲性酞菁锌对人体肝癌细胞的光灭活作用

采用四甲基偶氮唑蓝比色法(MTT法),考察了两亲性α-四(对-羧基苯氧基)酞菁锌(Ⅱ)光敏剂对Bel-7402人体肝癌细胞的离体光动力学行为,研究了浓度和光照时间对光灭活作用的影响.结果发现:在适宜的浓度下,酞菁锌光敏剂表现出了良好的抑制作用,且此抑制过程遵循一级反应的动力学规律.另外,酞菁在光催化下产生的单重态氧能损坏癌变的细胞膜,导致靶对细胞的死亡.     

A Peptide HEPFYGNEGALR from Apostichopus japonicus Alleviates Acute Alcoholic Liver Injury by Enhancing Antioxidant Response in Male C57BL/6J Mice

Liver-related disease caused by alcohol is a frequent disorder of the hepatic tract. Heavy consumption of alcohol in a short period causes oxidative damage to the liver. Sea cucumber is abundant in nutrients and its various extracts have been studied for antioxidant properties. One peptide was isolated and identified from Apostichopus japonicus in our recent study. We investigated the benefits of the peptide in a model of acute ethanol-induced male C57BL/6J mice. Dietary intake of the peptide could attenuate hepatomegaly, hepatitis and the accumulation of lipid droplets, and increase antioxidant enzyme activities in mice with acute alcoholic liver injury. The results indicated that a 20 mg/kg peptide supplement could activate the Nrf2/HO-1 pathway and block the nuclear translocation of NF-κB to alleviate oxidative stress and inflammation. In addition, the preventive effects of peptide supplementation may be related to autophagy. This study suggests that dietary supplementation with a sea cucumber-derived peptide is one of the potential candidates to alleviate acute alcoholic liver injury.     

Hepatoprotective Effects of Ixeris chinensis on Nonalcoholic Fatty Liver Disease Induced by High-Fat Diet in Mice: An Integrated Gut Microbiota and Metabolomic Analysis

Ixeris chinensis (Thunb.) Nakai (IC) is a folk medicinal herb used in Mongolian medical clinics for the treatment of hepatitis and fatty liver diseases even though its pharmacological mechanism has not been well characterized. This study investigated the hepatoprotective mechanism of IC on mice with nonalcoholic fatty liver disease (NAFLD) by integrating gut microbiota and metabolomic analysis. A high-fat diet (HFD) was used to develop nonalcoholic fatty liver disease, after which the mice were treated with oral IC (0.5, 1.5 and 3.0 g/kg) for 10 weeks. HFD induced NAFLD and the therapeutic effects were characterized by pathological and histological evaluations, and the serum indicators were analyzed by ELISA. The gut microbial and metabolite profiles were studied by 16S rRNA sequencing and untargeted metabolomic analysis, respectively. The results showed that the administration of IC resulted in significant decreases in body weight; liver index; serum biomarkers such as ALT, TG, and LDL-C; and the liver inflammatory factors IL-1β, IL-6, and TNF-α. The 16S rRNA sequencing results showed that administration of IC extract altered both the composition and abundance of the gut microbiota. Untargeted metabolomic analysis of liver samples detected a total of 212 metabolites, of which 128 were differentially expressed between the HFD and IC group. IC was found to significantly alter the levels of metabolites such as L-glutamic acid, pyridoxal, ornithine, L-aspartic acid, D-proline, and N4-acetylaminobutanal, which are involved in the regulation of glutamine and glutamate, Vitamin B6 metabolism, and arginine and proline metabolic pathways. Correlation analysis indicated that the effects of the IC extract on metabolites were associated with alterations in the abundance of Akkermansiaceae, Lachnospiraceae, and Muribaculaceae. Our study revealed that IC has a potential hepatoprotective effect in NAFLD and that its function might be linked to improvements in the composition of gut microbiota and their metabolites.     

Preparation of Active Peptides from Camellia vietnamensis and Their Metabolic Effects in Alcohol-Induced Liver Injury Cells

Liver damage seriously affects human health. Over 35% of cases of acute liver damage are caused by alcohol damage. Thus, finding drugs that can inhibit and effectively treat this disease is necessary. This article mainly focuses on the effect of the metabolome physical activity of active peptides in Camellia vietnamensis active peptide (CMAP) and improving liver protection. DEAE Sepharose FF ion-exchange column chromatography was used in separating and purifying crude peptides from Camellia vietnamensis Two components, A1 and A2, were obtained, and the most active A1 was selected. Sephadex G-100 gel column chromatography was used in A1 separation and purification. Three components, Al-1, Al-2, and Al-3, were obtained. Through antioxidant activity in vitro as an index of inspection, the relatively active component A1-2 was removed. Reverse-phase high-performance liquid chromatography showed that the purity of component A1-2 was 93.45%. The extracted CMAPs acted on alcoholic liver injury cells. Metabolomics studies revealed that the up-regulated metabolites were ribothymidine and xanthine; the down-regulated metabolites were hydroxyphenyllactic acid, creatinine, stearoylcarnitine, and inosine. This study provides an effective theoretical support for subsequent research.     

The Ameliorative Effects of Fucoidan in Thioacetaide-Induced Liver Injury in Mice

Liver disorders have been recognized as one major health concern. Fucoidan, a sulfated polysaccharide extracted from the brown seaweed Fucus serratus, has previously been reported as an anti-inflammatory and antioxidant. However, the discovery and validation of its hepatoprotective properties and elucidation of its mechanisms of action are still unknown. The objective of the current study was to investigate the effect and possible modes of action of a treatment of fucoidan against thioacetamide (TAA)-induced liver injury in male C57BL/6 mice by serum biochemical and histological analyses. The mouse model for liver damage was developed by the administration of TAA thrice a week for six weeks. The mice with TAA-induced liver injury were orally administered fucoidan once a day for 42 days. The treated mice showed significantly higher body weights; food intakes; hepatic antioxidative enzymes (catalase, glutathione peroxidase (GPx), and superoxide dismutase (SOD)); and a lower serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and C-reactive protein (CRP) levels. Additionally, a reduced hepatic IL-6 level and a decreased expression of inflammatory-related genes, such as cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) mRNA was observed. These results demonstrated that fucoidan had a hepatoprotective effect on liver injury through the suppression of the inflammatory responses and acting as an antioxidant. In addition, here, we validated the use of fucoidan against liver disorders with supporting molecular data.