AIM To investigate the effects of hydrogen-rich water(HRW) treatment on prevention of ethanol(Et OH)-induced early fatty liver in mice.METHODS In vitro reduction of hydrogen peroxide by HRW was determined with a chemi...AIM To investigate the effects of hydrogen-rich water(HRW) treatment on prevention of ethanol(Et OH)-induced early fatty liver in mice.METHODS In vitro reduction of hydrogen peroxide by HRW was determined with a chemiluminescence system. Female mice were randomly divided into five groups: control,Et OH,Et OH + silymarin,Et OH + HRW and Et OH + silymarin + HRW. Each group was fed a Lieber-De Carli liquid diet containing Et OH or isocaloric maltose dextrin(control diet). Silymarin was used as a positive control to compare HRW efficacy against chronic Et OH-induced hepatotoxicity. HRW was freshly prepared and given at a dosage of 1.2 m L/mouse trice daily. Blood and liver tissue were collected after chronic-binge liquid-diet feeding for 12 wk.RESULTS The in vitro study showed that HRW directly scavenged hydrogen peroxide. The in vivo study showed that HRW increased expression of acyl ghrelin,which was correlated with food intake. HRW treatment significantly reduced Et OH-induced increases in serum alanine aminotransferase,aspartate aminotransferase,triglycerol and total cholesterol levels,hepatic lipid accumulation and inflammatory cytokines,including tumor necrosis factor-alpha(TNF-α) and interleukin(IL)-6. HRW attenuated malondialdehyde level,restored glutathione depletion and increased superoxide dismutase,glutathione peroxidase and catalase activities in the liver. Moreover,HRW reduced TNF-α and IL-6 levels but increased IL-10 and IL-22 levels.CONCLUSION HRW protects against chronic Et OH-induced liver injury,possibly by inducing acyl ghrelin to suppress the pro-inflammatory cytokines TNF-α and IL-6 and induce IL-10 and IL-22,thus activating antioxidant enzymes against oxidative stress.展开更多
旨在探究β-catenin在lα,25-(OH)2D3调控小鼠体外破骨细胞(osteoclast,OC)形成中的作用。体外诱导小鼠OC形成,添加1α,25-(OH)2D3观察其对OC形成及β-连环蛋白(β-catenin)表达的影响;敲低β-catenin进一步观察1α,25-(OH)2D3对OC形成...旨在探究β-catenin在lα,25-(OH)2D3调控小鼠体外破骨细胞(osteoclast,OC)形成中的作用。体外诱导小鼠OC形成,添加1α,25-(OH)2D3观察其对OC形成及β-连环蛋白(β-catenin)表达的影响;敲低β-catenin进一步观察1α,25-(OH)2D3对OC形成的影响。结果显示,1α,25-(OH)2D3极显著(P<0.01)抑制体外培养小鼠OC形成和骨吸收活性。敲低β-catenin,OC数量及OC形成标志物基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)蛋白和激活T-细胞核因子1(nuclear factor of activated T cells,cytoplasmic 1,Nfatc1)mRNA表达显著(P<0.05)升高。1α,25-(OH)2D3可促进OC形成过程中β-catenin基因Ctnnb1 mRNA的表达,但敲低β-catenin基因,1α,25-(OH)2D3仍可抑制OC形成。试验表明,β-catenin可抑制体外培养OC形成,但对1α,25-(OH)2D3抑制OC形成无影响。展开更多
自发现一些免疫细胞上存在维生素D受体（vitamin D receptor，VDR），维生素D（VD）对免疫调节的研究成为热点。巨噬细胞是一类重要的免疫细胞，受刺激后可产生炎性细胞因子，如肿瘤坏死因子（tumor necrosis factor-alpha，TNF-α）、...自发现一些免疫细胞上存在维生素D受体（vitamin D receptor，VDR），维生素D（VD）对免疫调节的研究成为热点。巨噬细胞是一类重要的免疫细胞，受刺激后可产生炎性细胞因子，如肿瘤坏死因子（tumor necrosis factor-alpha，TNF-α）、一氧化氮（nitricoxide，NO）等。脂多糖（1ipopolysaccharide，LPS）是革兰阴性细菌细胞壁外膜上的主要结构成分，是其主要的致病因子，可刺激内皮细胞、巨噬细胞、成纤维细胞产生大量的炎性细胞因子（TNF-α、NO、IL-6等）。展开更多
基金Supported by a grant from the Chung Shan Medical University,No.CSMU0150011
文摘AIM To investigate the effects of hydrogen-rich water(HRW) treatment on prevention of ethanol(Et OH)-induced early fatty liver in mice.METHODS In vitro reduction of hydrogen peroxide by HRW was determined with a chemiluminescence system. Female mice were randomly divided into five groups: control,Et OH,Et OH + silymarin,Et OH + HRW and Et OH + silymarin + HRW. Each group was fed a Lieber-De Carli liquid diet containing Et OH or isocaloric maltose dextrin(control diet). Silymarin was used as a positive control to compare HRW efficacy against chronic Et OH-induced hepatotoxicity. HRW was freshly prepared and given at a dosage of 1.2 m L/mouse trice daily. Blood and liver tissue were collected after chronic-binge liquid-diet feeding for 12 wk.RESULTS The in vitro study showed that HRW directly scavenged hydrogen peroxide. The in vivo study showed that HRW increased expression of acyl ghrelin,which was correlated with food intake. HRW treatment significantly reduced Et OH-induced increases in serum alanine aminotransferase,aspartate aminotransferase,triglycerol and total cholesterol levels,hepatic lipid accumulation and inflammatory cytokines,including tumor necrosis factor-alpha(TNF-α) and interleukin(IL)-6. HRW attenuated malondialdehyde level,restored glutathione depletion and increased superoxide dismutase,glutathione peroxidase and catalase activities in the liver. Moreover,HRW reduced TNF-α and IL-6 levels but increased IL-10 and IL-22 levels.CONCLUSION HRW protects against chronic Et OH-induced liver injury,possibly by inducing acyl ghrelin to suppress the pro-inflammatory cytokines TNF-α and IL-6 and induce IL-10 and IL-22,thus activating antioxidant enzymes against oxidative stress.
文摘旨在探究β-catenin在lα,25-(OH)2D3调控小鼠体外破骨细胞(osteoclast,OC)形成中的作用。体外诱导小鼠OC形成,添加1α,25-(OH)2D3观察其对OC形成及β-连环蛋白(β-catenin)表达的影响;敲低β-catenin进一步观察1α,25-(OH)2D3对OC形成的影响。结果显示,1α,25-(OH)2D3极显著(P<0.01)抑制体外培养小鼠OC形成和骨吸收活性。敲低β-catenin,OC数量及OC形成标志物基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)蛋白和激活T-细胞核因子1(nuclear factor of activated T cells,cytoplasmic 1,Nfatc1)mRNA表达显著(P<0.05)升高。1α,25-(OH)2D3可促进OC形成过程中β-catenin基因Ctnnb1 mRNA的表达,但敲低β-catenin基因,1α,25-(OH)2D3仍可抑制OC形成。试验表明,β-catenin可抑制体外培养OC形成,但对1α,25-(OH)2D3抑制OC形成无影响。
文摘自发现一些免疫细胞上存在维生素D受体（vitamin D receptor，VDR），维生素D（VD）对免疫调节的研究成为热点。巨噬细胞是一类重要的免疫细胞，受刺激后可产生炎性细胞因子，如肿瘤坏死因子（tumor necrosis factor-alpha，TNF-α）、一氧化氮（nitricoxide，NO）等。脂多糖（1ipopolysaccharide，LPS）是革兰阴性细菌细胞壁外膜上的主要结构成分，是其主要的致病因子，可刺激内皮细胞、巨噬细胞、成纤维细胞产生大量的炎性细胞因子（TNF-α、NO、IL-6等）。
