摘要
目的 探讨二氢杨梅素(dihydromyricetin,DMY)对人晶状体上皮细胞SRA01/04增殖、凋亡的影响及其分子机制。方法 将SRA01/04细胞分为正常对照(normal control,NC)组、DMY组、anti-miR-NC组、anti-miR-199b-5p组、miR-NC组、miR-199b-5p组、DMY+miR-NC组和DMY+miR-199b-5p组。通过定量反转录聚合酶链反应检测miR-199b-5p的表达水平。采用MTT法和流式细胞术检测细胞增殖和凋亡情况。结果 DMY可抑制SRA01/04细胞增殖,诱导细胞凋亡(P<0.05),并可促进SRA01/04细胞miR-199b-5p的表达(P<0.05)。过表达miR-199b-5p可抑制SRA01/04细胞增殖,诱导细胞凋亡(P<0.05)。抑制miR-199b-5p表达可促进SRA01/04细胞增殖,抑制细胞凋亡(P<0.05),且能够逆转DMY对SRA01/04细胞的增殖抑制和凋亡促进作用(P<0.05)。结论 DMY可抑制人晶状体上皮细胞SRA01/04增殖,诱导细胞凋亡,其机制与上调miR-199b-5p表达相关。
Objective To investigate the effects of dihydromyricetin (DMY) on the proliferation,apoptosis of human lens epithelial cells SRA01/04 and its possible molecular mechanism.Methods SRA01/04 cells were divided into normal control (NC) group,DMY group,anti-miR-NC group,anti-miR-199b-5p group,miR-NC group,miR-199b-5p group,and DMY+miR-NC group and DMY+miR-199b-5p group.The expression level of miR-199b-5p was detected by quantitative reverse transcriptase-mediated polymerase chain reaction(qRT-PCR).Cell proliferation and apoptosis were detected by MTT assay and flow cytometry.Results DMY could inhibit the proliferation and induce apoptosis of SRA01/04 cells (P<0.05)and promote the expression of miR-199b-5p in SRA01/04 cells (P<0.05).Overexpressing miR-199b-5p could inhibit the proliferation and induce apoptosis of SRA01/04 cells (P<0.05).Inhibiting miR-199b-5p could promote the proliferation and inhibit apoptosis of SRA01/04 cells (P<0.05) and could reverse the proliferation inhibition and apoptosis promotion effects of DMY on SRA01/04 cells (P<0.05).Conclusions DMY can inhibit the proliferation and induce apoptosis of human lens epithelial cells SRA01/04,and the mechanism is related to the up-regulation of miR-199b-5p expression.
作者
付婷婷
栾红
徐衍红
秦贵娟
刘兵
FU Tingting;LUAN Hong;XU Yanhong;QIN Guijuan;LIU Bing(Department of Ophthalmology Rizhao Central Hospital,Rizhao276800,Shandong Province,China;Department of Laboratory,Rizhao Central Hospital,Rizhao 276800,Shandong Province,China)
出处
《世界临床药物》
CAS
2022年第7期844-850,共7页
World Clinical Drug
