Brain-derived neurotrophic factor prevents beta-amyloid-induced apoptosis of pheochromocytoma cells by regulating Bax/Bcl-2 expression

Brain-derived neurotrophic factor was utilized in the present study to treat cell injury models induced by aggregated β-amyloid（25 35）. Methylthiazolyldiphenyl-tetrazolium bromide assay and western blot analysis showed that brain-derived neurotrophic factor provided neuroprotection against cellular apoptosis by suppressing the decline in β-amyloid（25 35）-induced cell activity and the increasing ratio of Bax/Bcl-2. After treating pheochromocytoma cells with tyrosine kinase receptor B receptor inhibitor K252a, brain-derived neurotrophic factor reverses the above- mentioned changes. The experimental findings suggested that brain-derived neurotrophic factor prevented β-amyloid peptide-induced cellular apoptosis by modulating Bax/Bcl-2 expression, and this effect was associated with binding to the specific tyrosine kinase receptor B receptor.

Brain-derived neurotrophic factor protects PC12 cells from beta-amyloid-induced neurotoxicity through the tropomyosin-related kinase B receptor pathway

The present study utilized beta amyloid （Aβ）-induced cell apoptosis in PC12 cells as a cell model of Alzheimer＇s disease to investigate the interaction between brain-derived neurotrophic factor （BDNF） and the tropomyosin-related kinase B receptor. Results showed that Aβ（25-35） can reduce survival of PC12 cells and increase cleaved caspase-3 expression in PC12 cells. However, BDNF inhibited Aβ（25-35）-induced cytotoxicity and cleaved casapase-3 expression. Interestingly, pretreatment with the tropomyosin-related kinase receptor inhibitor K252a for 20 minutes prior to BDNF blocked the neuroprotective effect of BDNF on PC12 cells.

肠道菌群的功能及其在自身免疫病和过敏性疾病中的作用

自身免疫病和过敏性疾病是临床上较为常见的困扰全球患者和医护人员的疾病,二者主要由于机体免疫反应过度引起。目前,临床主要采用糖皮质激素治疗,但糖皮质激素长期使用可能会有严重的副作用。因此,迫切需要寻找一种有效的干预策略来治疗自身免疫病和过敏性疾病。近年来的研究显示:机体肠道菌群失调及其相关代谢产物与自身免疫病和过敏性疾病的发生发展具有一定的相关性。在介绍肠道菌群与健康、疾病,和药物之间关系的基础上,通过整理和分析近几年发表的相关文章,对肠道菌群在自身免疫病和过敏性疾病中的作用进行综述。