With age and ATP decrease in the body, the transcription factors hypophosphorylation weakens the transcription of and hinders the expression of the iron discharger ferroportin. This may lead to iron accumulation in the brain and the catalysis of free radicals that damage cerebral neurons and eventually lead to Alzheimer's disease (AD). To prevent AD caused by brain iron excretion disorders and reveal the mechanism of J bs-5YP peptide restoring ferroportin. We prepared J bs-YP peptide and administered it to the senile mice with dementia. Then, the intelligence of the mice was tested using a Morris Water Maze. The ATP content in the body was detected using the ATP hydrophysis and Phosphate precipitation method. The activation of Slc40a1 transcription was assayed with ATAC seq and the ferroportin, as well as the phosphorylation levels of Ets1 in brain were detected by Western Blot. The phosphorylation level of Ets1in brain was enhanced, and subsequently, the transcription of was activated and ferroportin was increased in the brain, the levels of iron and free radicals were reduced, with the neurons protection, and the dementia was ultimately alleviated in the senile mice. J bs-5YP can recover the expression of ferroportin to excrete excessive iron in the brain of senile mice with dementia by enhancing the transcription of via phosphorylating Ets1, revealing the potential of J bs-5YP as a drug to alleviate senile dementia.

中文翻译：

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J bs-5YP肽可通过恢复Slc40a1的转录以分泌脑中过量的铁来减轻老年小鼠的痴呆症

随着年龄的增长和体内 ATP 的减少，转录因子低磷酸化会削弱铁转运蛋白的转录并阻碍铁转运蛋白的表达。这可能导致铁在大脑中积聚，并催化自由基，损害大脑神经元，最终导致阿尔茨海默病（AD）。预防脑铁排泄障碍引起的AD，揭示J bs-5YP肽恢复铁转运蛋白的机制。我们制备了J bs-YP肽并将其给予患有痴呆的老年小鼠。然后，使用莫里斯水迷宫测试小鼠的智力。采用ATP水理法和磷酸盐沉淀法检测体内ATP含量。采用ATAC seq检测Slc40a1转录激活情况，Western Blot检测脑内Ets1磷酸化水平。脑内Ets1磷酸化水平增强，随后脑内Ets1转录被激活，铁转运蛋白增加，铁和自由基水平降低，对神经元起到保护作用，最终使老年小鼠的痴呆症得到缓解。 J bs-5YP可以通过磷酸化Ets1增强转录，恢复痴呆老年小鼠脑内铁转运蛋白的表达，从而排出过量的铁，揭示了J bs-5YP作为缓解老年痴呆药物的潜力。