Predator stress-induced depression is associated with inhibition of hippocampal neurogenesis in adult male mice

Stress has been suggested to disturb the 5-hydroxytryptamine system and decrease neurogenesis, which contribute to the development of depression. Few studies have investigated the effect of predator stress, a type of psychological stress, on depression and hippocampal neurogenesis in adult mice; we therefore investigated this in the present study. A total of 35 adult male Kunming mice were allocated to a cat stress group, cat odor stress group, cat stress + fluoxetine group, cat odor stress + fluoxetine group, or a control group(no stress/treatment). After 12 days of cat stress or cat odor stress, behavioral correlates of depression were measured using the open field test, elevated plus maze test, and dark-avoidance test. The concentrations of hippocampal 5-hydroxytryptamine and 5-hydroxyindoleacetic acid were measured using high-performance liquid chromatography-electrochemical detection. Neurogenesis was also analyzed using a bromodeoxyuridine and doublecortin double-immunostaining method. Cat stress and cat odor stress induced depression-like behaviors; this effect was stronger in the cat stress model. Furthermore, compared with the control group, cat stress mice exhibited lower 5-hydroxytryptamine concentrations, higher 5-hydroxyindoleacetic acid concentrations, and significantly fewer bromodeoxyuridine+/doublecortin+-labeled cells in the dentate gyrus, which was indicative of less neurogenesis. The changes observed in the cat stress group were not seen in the cat stress + fluoxetine group, which suggests that the effects of predator stress on depression and neurogenesis were reversed by fluoxetine. Taken together, our results indicate that depression-like behaviors induced by predator stress are associated with the inhibition of hippocampal neurogenesis.

Mangiferin ameliorates hyperglycemia by inhibiting oxidation and α-glucosidase activity

目的：芒果苷（MF）是从知母根提取出来的-种多元酚.本研究旨在探讨芒果苷对胰岛素抵抗和链脲霉素（STZ）引起的糖尿病动物模型的高血糖的影响.方法：通过多次皮下注射氢化可的松琥珀酸钠（HCSS）（70mg/kg）或单次静脉内注射STZ（130mg/kg）建立糖尿病模型.同时连续口服10天不同剂量（50,100和200mg/kg）的MF.腹腔注射胰岛素（0.5U/kg）后,收集不同时间的血糖数值来检测胰岛素抵抗.同时测定肾脏氧自由基吸收能力（ORAC）和超氧化物歧化酶（SOD）活性.建立体外实验,研究MF对α-葡萄糖苷酶的抑制能力.结果：口服芒果苷能够显著抑制由注射HCSS引起的胰岛素抵抗.STZ诱导的糖尿病症状也有所改善,包括空腹血糖,糖化血红蛋白,血浆甘油三酯,肝糖原,肾脏SOD和ORAC水平.体外实验证明芒果苷具有较强的α-葡萄糖苷酶抑制活性.结论：结果表明芒果苷能改善胰岛素抵抗和STZ诱导的糖代谢紊乱.芒果苷通过提高抗氧化能力,促进肝糖原合成,抑制α-葡萄糖苷酶活性发挥保护作用.

Antioxidative and antiapoptotic effects of （＋）-clausenamide on acetaminophen-induced nephrotoxicity in mice

目的：（＋）-黄皮酰胺（（＋）-CLA）是从黄皮叶中分离得到的-种黄皮活性成分,我们旨在评价（＋）-黄皮酰胺在对乙酰氨基酚（APAP）诱导小鼠肾损伤中的保护作用.方法：小鼠分成正常组、APAP组以及高低剂量（＋）-CLA组,连续5天给予（＋）-CLA（50和100mg/kg）进行预处理,末次给药后,小鼠腹腔注射单剂量APAP（600mg/kg）.通过苏木素-伊红染色观察肾组织病理学特征,用相应试剂盒检测丙二醛（MDA）和谷胱甘肽（GSH）的水平以及过氧化氢酶（CAT）和超氧化物歧化酶（SOD）的活性,免疫印迹法分析肾组织中凋亡相关蛋白的表达.结果：与正常组相比,APAP组的血清肌酐和尿素氮水平上升.MDA水平的增加,GSH的耗竭以及CAT和SOD活性的降低表明APAP诱导的肾损伤由氧化应激调控.Bax,caspase-3,cleavagecaspase-3以及细胞浆细胞色素c表达上调,而Bcl-2和线粒体细胞色素c表达下调,这些说明APAP诱导的肾损伤明显增加肾细胞的凋亡.（＋）-CLA能逆转上述大多数参数并恢复肾的正常结构.结论：氧化应激与凋亡被认为是APAP肾毒性的潜在机制.（＋）-CLA的抗氧化和抗凋亡作用可能是对APAP急性肾损伤的-个有前景的解毒剂.