Abstract：
BACKGROUND: Aluminum has definite neurotoxicity and can lead to apoptosis of nerve cells, but the specific mechanism remains to be further explored. The aim of this study was to investigate the role of Nrf2/HO-1 signaling pathway in neural cell apoptosis induced by aluminum exposure.
METHODS: In this study, PC12 cells were used as the research object, aluminum maltol [Al(mal)3] was used as the exposure agent, and tert-butyl hydroquinone (TBHQ), an agonist of Nrf2, was used as the intervention agent to construct an in vitro cell model. Cell viability was detected by CCK-8 method, cell morphology was observed by light microscope, cell apoptosis was measured by flow cytometry, and expression of Bax and Bcl-2 proteins and Nrf2/HO-1 signaling pathway proteins were investigated by western blotting.
RESULTS: With the increase of Al(mal)3 concentration, PC12 cell viability decreased, the early apoptosis rate and total apoptosis rate increased, the ratio of Bcl-2 and Bax protein expression decreased, and Nrf2/HO-1 pathway protein expression decreased. The use of TBHQ could activate the Nrf2/HO-1 pathway and reverse the apoptosis of PC12 cells induced by aluminum exposure.
CONCLUSIONS: Nrf2/HO-1 signaling pathway plays a neuroprotective role in the apoptosis of PC12 cells caused by Al(mal)3, which provides a possible target for the intervention of aluminum induced neurotoxicity.
METHODS: In this study, PC12 cells were used as the research object, aluminum maltol [Al(mal)3] was used as the exposure agent, and tert-butyl hydroquinone (TBHQ), an agonist of Nrf2, was used as the intervention agent to construct an in vitro cell model. Cell viability was detected by CCK-8 method, cell morphology was observed by light microscope, cell apoptosis was measured by flow cytometry, and expression of Bax and Bcl-2 proteins and Nrf2/HO-1 signaling pathway proteins were investigated by western blotting.
RESULTS: With the increase of Al(mal)3 concentration, PC12 cell viability decreased, the early apoptosis rate and total apoptosis rate increased, the ratio of Bcl-2 and Bax protein expression decreased, and Nrf2/HO-1 pathway protein expression decreased. The use of TBHQ could activate the Nrf2/HO-1 pathway and reverse the apoptosis of PC12 cells induced by aluminum exposure.
CONCLUSIONS: Nrf2/HO-1 signaling pathway plays a neuroprotective role in the apoptosis of PC12 cells caused by Al(mal)3, which provides a possible target for the intervention of aluminum induced neurotoxicity.
摘要：
背景：铝具有明确的神经毒性，可导致神经细胞凋亡，但具体机制有待进一步探讨。本研究旨在探讨Nrf2/HO-1信号通路在铝暴露诱导神经细胞凋亡中的作用。
方法：在本研究中，以PC12细胞为研究对象,铝麦芽酚[Al(mal)3]用作暴露剂，和叔丁基对苯二酚(TBHQ)，Nrf2的激动剂被用作构建体外细胞模型的干预剂。CCK-8法检测细胞活力,用光学显微镜观察细胞形态,通过流式细胞术测量细胞凋亡，免疫印迹法检测Bax和Bcl-2蛋白及Nrf2/HO-1信号通路蛋白的表达。
结果：随着Al（mal）3浓度的增加，PC12细胞活力下降，早期凋亡率和总凋亡率增加，Bcl-2和Bax蛋白表达的比率降低，Nrf2/HO-1通路蛋白表达降低。使用TBHQ可以激活Nrf2/HO-1通路,逆转铝暴露诱导的PC12细胞凋亡。
结论：Nrf2/HO-1信号通路对Al(mal)3引起的PC12细胞凋亡具有神经保护作用，为铝诱导的神经毒性干预提供了可能的作用靶点。
方法：在本研究中，以PC12细胞为研究对象,铝麦芽酚[Al(mal)3]用作暴露剂，和叔丁基对苯二酚(TBHQ)，Nrf2的激动剂被用作构建体外细胞模型的干预剂。CCK-8法检测细胞活力,用光学显微镜观察细胞形态,通过流式细胞术测量细胞凋亡，免疫印迹法检测Bax和Bcl-2蛋白及Nrf2/HO-1信号通路蛋白的表达。
结果：随着Al（mal）3浓度的增加，PC12细胞活力下降，早期凋亡率和总凋亡率增加，Bcl-2和Bax蛋白表达的比率降低，Nrf2/HO-1通路蛋白表达降低。使用TBHQ可以激活Nrf2/HO-1通路,逆转铝暴露诱导的PC12细胞凋亡。
结论：Nrf2/HO-1信号通路对Al(mal)3引起的PC12细胞凋亡具有神经保护作用，为铝诱导的神经毒性干预提供了可能的作用靶点。
