中国组织工程研究

中国组织工程研究 ›› 2026, Vol. 30 ›› Issue (19): 4934-4941.doi: 10.12307/2026.249

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

大黄素减缓高糖诱导HT-22细胞衰老发生的作用及机制

饶彬阐1，2，许永劼2，徐梦玲1，2，陈  迪1，2，朱丽英1，3，杨思远4，李  兴5，王正蓉1，2，潘  卫1，2   

  1. 1贵州医科大学医学检验学院，贵州省贵阳市   550004；贵州医科大学附属医院，2贵州省产前诊断中心，3临床检验中心，4心外科，贵州省贵阳市   550004；5贵州中医药大学基础医学院，贵州省贵阳市   550025
  • 收稿日期:2025-09-03 接受日期:2025-11-29 出版日期:2026-07-08 发布日期:2026-02-14
  • 通讯作者: 潘卫，博士，教授，贵州医科大学医学检验学院，贵州省贵阳市 550004；贵州医科大学附属医院贵州省产前诊断中心，贵州省贵阳市 550004； 共同通讯作者：王正蓉，博士，贵州医科大学医学检验学院，贵州省贵阳市 550004；贵州医科大学附属医院贵州省产前诊断中心，贵州省贵阳市 550004
  • 作者简介:饶彬阐，女，2000年生，贵州医科大学在读硕士，主要从事胚胎发育的遗传学研究及糖尿病并发症发病机制研究。
  • 基金资助:
    国家自然科学基金地区科学基金项目(82260165)，项目负责人：潘卫；国家自然科学基金青年科学基金项目(82300920)，项目负责人：许永劼；贵州省科技计划项目(黔科合基础-ZK[2024]一般199)，项目负责人：许永劼；贵州省卫生健康委科学技术基金项目(gzwkj2024-081)，项目负责人：许永劼；国家自然科学基金地区科学基金项目(8226020146)，项目负责：杨思远；国家自然科学基金地区科学基金项目(82560169)，项目负责人：朱丽英

Role and mechanism of emodin in slowing down the senescence of HT-22 cells induced by high glucose

Rao Binchan1, 2, Xu Yongjie2, Xu Mengling1, 2, Chen Di1, 2, Zhu Liying1, 3, Yang Siyuan4, Li Xing5, Wang Zhengrong1, 2, Pan Wei1, 2   

  1. 1School of Clinical Laboratory Science, Guizhou Medical University, Guiyang 550004, Guizhou Province, China; 2Guizhou Provincial Prenatal Diagnosis Center, 3Clinical Laboratory Center, 4Cardiac Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, Guizhou Province, China; 5School of Basic Medical Sciences, Guizhou University of Traditional Chinese Medicine, Guiyang 550025, Guizhou Province, China
  • Received:2025-09-03 Accepted:2025-11-29 Online:2026-07-08 Published:2026-02-14
  • Contact: Pan Wei, PhD, Professor, School of Clinical Laboratory Science, Guizhou Medical University, Guiyang 550004, Guizhou Province, China; Guizhou Provincial Prenatal Diagnosis Center, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, Guizhou Province, China; Co-corresponding author: Wang Zhengrong, PhD, School of Clinical Laboratory Science, Guizhou Medical University, Guiyang 550004, Guizhou Province, China; Guizhou Provincial Prenatal Diagnosis Center, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, Guizhou Province, China
  • About author:Rao Binchan, Master candidate, School of Clinical Laboratory Science, Guizhou Medical University, Guiyang 550004, Guizhou Province, China; Guizhou Provincial Prenatal Diagnosis Center, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, Guizhou Province, China
  • Supported by:
    National Natural Science Foundation of China (Regional Science Foundation), No. 82260165 (to PW); National Natural Science Foundation of China (Youth Science Foundation), No. 82300920 (to XYJ); Guizhou Provincial Science and Technology Plan Project, No. ZK[2024]199 (to XYJ); Guizhou Provincial Health Commission Science and Technology Foundation, No. gzwkj2024-081 (to XYJ); National Natural Science Foundation of China (Regional Science Foundation), No. 8226020146 (to YSY); National Natural Science Foundation of China (Regional Science Foundation), No. 82560169 (to ZLY)

PDF

114

摘要：

文题释义：

大黄素：是一种天然蒽醌类化合物，广泛存在于何首乌、大黄、虎杖等中草药中，具有多种生物活性，如抗炎、抗氧化、抗衰老、抗肿瘤及调节代谢等作用。
Lamin A/C：是由LMNA基因编码的核纤层蛋白，属于中间纤维蛋白家族，在维持细胞核结构、染色质组织、基因表达调控及信号转导中发挥关键作用，是衰老机制研究的重要靶点。

摘要
背景：糖尿病脑病的发生可能与神经元衰老密切相关，然而潜在的分子机制尚未完全明确。因此，探讨神经元衰老在糖尿病脑病中的作用，对于进一步揭示糖尿病脑病的发病机制具有重要的研究意义。
目的：探讨大黄素在高糖环境下对HT-22细胞衰老发生的作用及机制。
方法：将HT-22细胞分为对照组(葡萄糖浓度25 mmol/L)、高糖组(葡萄糖浓度55 mmol/L)、高糖+大黄素组(葡萄糖浓度55 mmol/L，大黄素浓度100 µmol/L)培养48 h。镜下观察各组细胞的生长状态；CCK-8检测各组细胞活力变化；ELISA检测各组细胞端粒酶反转录酶活性；RT-qPCR以及Western blot检测各组细胞中衰老相关蛋白P53、P21、P16的表达；免疫荧光、RT-qPCR以及Western blot检测各组细胞中核纤层蛋白Lamin A/C的表达。
结果与结论：①与对照组相比，高糖组细胞在镜下呈现明显的生长抑制状态，具体表现为细胞数量减少、体积增大、形态趋于扁平；与高糖组相比，高糖+大黄素组细胞数量显著增加，形态趋于规则；②与对照组相比，高糖组细胞活力显著降低(P < 0.000 1)；与高糖组相比，高糖+大黄素组细胞活力明显升高(P < 0.000 1)；③与对照组相比，高糖组端粒酶反转录酶活性显著降低(P < 0.001)；④与对照组相比，高糖组P53、P21、P16表达水平显著升高(P < 0.05)；与高糖组相比，高糖+大黄素组P53、P21、P16表达水平显著降低(P < 0.05)；⑤与对照组相比，高糖组核纤层蛋白Lamin A/C表达水平显著降低(P < 0.000 1)；与高糖组相比，高糖+大黄素组核纤层蛋白Lamin A/C表达水平显著升高(P < 0.05)。研究结果表明大黄素可能通过上调核纤层蛋白Lamin A/C的表达，减缓高糖环境诱导的HT-22细胞衰老发生。

关键词: 糖尿病脑病, 高糖环境, 海马神经元衰老, 核纤层蛋白(Lamin A/C), 大黄素

Abstract: BACKGROUND: The occurrence of diabetic encephalopathy may be closely related to neuronal aging, but its underlying molecular mechanism is not fully understood. Therefore, exploring the role of neuronal aging in diabetic encephalopathy is of great significance for further revealing the pathogenesis of diabetic encephalopathy. 
OBJECTIVE: To explore role and mechanism of emodin in slowing down the senescence of HT-22 cells induced by high glucose.
METHODS: HT-22 cells were divided into a control group (glucose concentration of 25 mmol/L), a high glucose group (glucose concentration of 55 mmol/L), and a high glucose + emodin group (glucose concentration of 55 mmol/L, emodin concentration of 100 µmol/L) and cultured for 48 hours. Cell growth in each group was observed microscopically. Cell viability was assessed by CCK-8 assay. Telomerase reverse transcriptase activity was measured by ELISA in each group. Expression of senescence-related proteins P53, P21, and P16 in each group was determined by RT-qPCR and western blot assay. Expression of lamin A/C in each group was determined by immunofluorescence, RT-qPCR, and western blot assay.
RESULTS AND COUCLUSION: (1) Compared with the control group, the cells in the high-glucose group showed obvious growth inhibition under the microscope, which was manifested as a decrease in the number of cells, an increase in size, and a flattened morphology. Compared with the high-glucose group, the number of cells in the high-glucose emodin group increased significantly, and the morphology tended to be regular. (2) Compared with the control group, the cell viability of the high glucose group was significantly decreased (P < 0.000 1). Compared with the high glucose group, the cell viability in the high glucose + emodin group was significantly increased (P < 0.000 1). (3) Compared with the control group, the telomerase reverse transcriptase activity in the high glucose group was significantly decreased (P < 0.001). (4) Compared with the control group, the expression levels of P53, P21, and P16 in the high glucose group were significantly increased (P < 0.05). Compared with the high glucose group, the expression levels of P53, P21, and P16 in the high glucose + emodin group were significantly decreased (P < 0.05). (5) Compared with the control group, the expression level of lamin A/C in the high glucose group was significantly decreased (P < 0.000 1). Compared with the high glucose group, the expression levels of lamin A/C in the high glucose + emodin group were significantly increased (P < 0.05). These results suggest that emodin may mitigate high glucose-induced senescence in HT-22 cells by upregulating lamin A/C expression. 

Key words: diabetes encephalopathy, high-glucose environment, aging of hippocampal neurons, LaminA/C protein, emodin

中图分类号: