中国组织工程研究

中国组织工程研究 ›› 2026, Vol. 30 ›› Issue (7): 1800-1807.doi: 10.12307/2026.537

• 干细胞培养与分化 stem cell culture and differentiation • 上一篇    下一篇

血小板裂解物调控腺苷酸活化蛋白激酶抑制镉诱导的神经细胞凋亡

刘安婷，陆江涛，张文杰，贺  玲，唐宗生，陈晓玲   

  1. 皖南医学院弋矶山医院输血科，安徽省芜湖市  241001
  • 收稿日期:2024-12-06 修回日期:2025-04-16 接受日期:2025-05-13 出版日期:2026-03-08 发布日期:2025-08-20
  • 通讯作者: 陈晓玲，博士，助理研究员，皖南医学院弋矶山医院输血科，安徽省芜湖市 241001 唐宗生，博士，副教授，皖南医学院弋矶山医院输血科，安徽省芜湖市 241001
  • 作者简介:刘安婷，女，2000年生，皖南医学院在读硕士，主要从事神经细胞凋亡调控方面的研究。
  • 基金资助:
    安徽省教育厅高等学校科学研究重点项目(2022AH051214)，项目负责人：陈晓玲；2022年度医院引进人才专项科研启动基金项目(YR202202)，项目负责人：陈晓玲；安徽省省属公立医疗卫生机构引进高层次人才奖补项目(GCCRC2022003)，项目负责人：陈晓玲

Regulation of AMP-activated protein kinase by platelet lysate inhibits cadmium-induced neuronal apoptosis 

Liu Anting, Lu Jiangtao, Zhang Wenjie, He Ling, Tang Zongsheng, Chen Xiaoling   

  1. Department of Blood Transfusion, The First Affiliated Hospital of Wannan Medical College, Wuhu 241001, Anhui Province, China 
  • Received:2024-12-06 Revised:2025-04-16 Accepted:2025-05-13 Online:2026-03-08 Published:2025-08-20
  • Contact: Chen Xiaoling, PhD, Assistant researcher, Department of Blood Transfusion, The First Affiliated Hospital of Wannan Medical College, Wuhu 241001, Anhui Province, China Tang Zongsheng, PhD, Associate professor, Department of Blood Transfusion, The First Affiliated Hospital of Wannan Medical College, Wuhu 241001, Anhui Province, China
  • About author:Liu Anting, Master candidate, Department of Blood Transfusion, The First Affiliated Hospital of Wannan Medical College, Wuhu 241001, Anhui Province, China
  • Supported by:
     Natural Science Research Project of Anhui Educational Committee, No. 2022AH051214 (to CXL); 2022 Scientific Research Foundation for Advanced Talents of Hospital, No. YR202202 (to CXL); Project for Introduction of Advanced Talents Reward Compensation of Anhui Provincial Public Medical and Health Institutions, No. GCCRC2022003 (to CXL)

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摘要：

文题释义：

血小板裂解物：是一种从富血小板血浆中提取的生物制剂，富含多种生长因子、细胞因子和蛋白质，可作为一种替代胎牛血清的培养基添加剂，具有促进细胞增殖、分化和神经元修复的作用，应用在细胞培养、组织工程、神经再生医学等领域。
镉：是人类生活中较为常见的有毒重金属元素之一，流行病学研究表明长期接触镉会导致机体各种病变及损伤，如神经退行性疾病等，主要病因之一是镉能诱导过量活性氧产生从而扰乱机体氧化还原体系平衡，进而导致非正常细胞凋亡损伤。

摘要
背景：人源血小板裂解物已被证明在伤口愈合、神经修复和组织再生等疾病治疗中具有潜在作用。但血小板裂解物在重金属镉诱导神经细胞凋亡过程中的作用尚不清楚。
目的：探讨人源血小板裂解物对镉诱导神经细胞凋亡的影响及作用途径。
方法：将SH-SY5Y细胞分为空白对照组、血小板裂解物(体积分数5%)组、10 μmol/L镉处理组、血小板裂解物+10 μmol/L镉处理组、20 μmol/L镉处理组、血小板裂解物+20 μmol/L镉处理组，先用血小板裂解物预处理24 h，再用镉处理24 h。采用CCK-8法检测细胞活性，流式细胞术检测细胞凋亡情况，JC-1染色检测细胞线粒体膜电位、DCFH-DA荧光探针染色检测细胞内活性氧水平，免疫印迹法检测p-AMPKα (Thr172)、Cleaved-Caspase-3、Cleaved-PARP、Bax和Bcl-2蛋白表达水平。

结果与结论：①与镉处理组相比，血小板裂解物能够显著提升神经细胞活性(P < 0.05)；②与空白对照组相比，镉处理组细胞内线粒体膜电位显著降低(P < 0.05)，而经血小板裂解物预处理后线粒体膜电位显著升高(P < 0.05)；③与空白对照组相比，镉处理组细胞内活性氧水平显著升高(P < 0.05)，而经血小板裂解物预处理后活性氧水平显著降低(P < 0.05)；④与空白对照组相比，镉处理组细胞凋亡率显著升高(P < 0.05)，而经血小板裂解物预处理后细胞凋亡率显著降低(P < 0.05)；⑤与镉处理组相比，血小板裂解物预处理后SH-SY5Y细胞中凋亡相关蛋白Bax、Cleaved-Caspase-3、Cleaved-PARP表达显著降低(P < 0.05)，抗凋亡蛋白Bcl-2表达显著升高(P < 0.05)，p-AMPKα(Thr172)表达显著升高(P < 0.05)。以上结果表明，人源血小板裂解物通过激活腺苷酸活化蛋白激酶通路，减轻线粒体损伤和减少细胞氧化应激，在镉诱导神经细胞损伤中发挥抗凋亡保护作用。 

https://orcid.org/0000-0002-2031-2867(陈晓玲)


中国组织工程研究杂志出版内容重点：干细胞；骨髓干细胞；造血干细胞；脂肪干细胞；肿瘤干细胞；胚胎干细胞；脐带脐血干细胞；干细胞诱导；干细胞分化；组织工程


关键词: 血小板裂解物, 镉, SH-SY5Y细胞, 腺苷酸活化蛋白激酶(AMPK)信号通路, 神经退行性疾病, 凋亡, 氧化应激, 线粒体功能障碍

Abstract: BACKGROUND: Human platelet lysate has been shown to have potential effects in the treatment of diseases such as wound healing, nerve repair, and tissue regeneration. However, the role of platelet lysate in the process of neuronal apoptosis induced by the heavy metal cadmium remains unclear. 
OBJECTIVE: To investigate the effect of human platelet lysate on cadmium-induced apoptosis in neuronal cells and its underlying mechanisms.
METHODS: SH-SY5Y neural cells were divided into blank control group, human platelet lysate (5% volume fraction) group, cadmium 10 μmol/L group, human platelet lysate + cadmium 10 μmol/L group, cadmium 20 μmol/L group, and human platelet lysate + cadmium 20 μmol/L group. Platelet lysate was used for pretreatment for 24 hours, followed by cadmium treatment for 24 hours. CCK-8 assay was utilized to detect cell viability. Flow cytometry was employed to detect apoptosis. JC-1 staining was used to measure the mitochondrial membrane potential of SH-SY5Y cells. DCFH-DA fluorescent probe staining was utilized to detect intracellular reactive oxygen species levels. The expression levels of p-AMPKα (Thr172), cleaved-caspase-3, cleaved-PARP, Bax, and Bcl-2 proteins were analyzed using western blotting.
RESULTS AND CONCLUSION: (1) Human platelet lysate significantly enhanced the viability of neurocytes compared with the cadmium treatment group (P < 0.05). (2) Intracellular mitochondrial membrane potential in the cadmium treatment group was significantly reduced compared with the blank control group (P < 0.05). However, the mitochondrial membrane potential was significantly increased after platelet lysate pretreatment (P < 0.05). (3) Compared with the blank control group, the intracellular reactive oxygen level in the cadmium treatment group was significantly increased (P < 0.05), while the reactive oxygen level was significantly decreased after platelet lysate pretreatment (P < 0.05). (4) Compared with the blank control group, the apoptosis rate of the cells in the cadmium treatment group was significantly increased (P < 0.05), while the apoptosis rate of the cells after platelet lysate pretreatment was significantly decreased (P < 0.05). (5) Compared with the cadmium treatment group, the expression levels of apoptosis-related proteins Bax, cleaved-caspase-3, and cleaved-PARP in SH-SY5Y cells were significantly decreased after platelet lysate pretreatment (P < 0.05), the expression of anti-apoptotic protein Bcl-2 was significantly increased (P < 0.05), and the expression of p-AMPKα (Thr172) was significantly increased (P < 0.05). The above results indicate that human platelet lysate plays an anti-apoptotic protective role in cadmium-induced neuronal injury by activating the AMP-activated protein kinase pathway, alleviating mitochondrial damage and reducing cellular oxidative stress.

Key words: platelet lysate, cadmium, SH-SY5Y cell, AMP-activated protein kinase (AMPK) signaling pathway, neurodegenerative disease, apoptosis, oxidative stress, mitochondrial dysfunction 

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