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Abstract：
UNASSIGNED: We established a diquat-induced human kidney-2 cells (HK-2 cells) apoptosis model in this study to identify differentially expressed microRNAs (miRNAs) and signaling pathways involved in diquat poisoning via gene sequencing and bioinformatics analysis and explored the related therapeutic benefits.
UNASSIGNED: The effects of diquat on the viability and apoptosis of HK-2 cells were explored using the CCK-8 and Annexin V-FITC/PI double staining methods. Total RNAs were extracted using the TRizol method and detected by Illumina HiSeq 2500. Bioinformatics analysis was performed to explore differentially expressed (DE) miRNAs, their enriched biological processes, pathways, and potential target genes. The RT-qPCR method was used to verify the reliability of the results.
UNASSIGNED: Diquat led to HK-2 cell injury and apoptosis played an important role, hence an HK-2 cell apoptosis model in diquat poisoning was established. Thirty-six DE miRNAs were screened in diquat-treated HK-2 cells. The enriched biological process terms were mainly cell growth, regulation of apoptotic signaling pathway, extrinsic apoptotic signaling pathway, and Ras protein signal transduction. The enriched cellular components were mainly cell-cell junction, cell-substrate junction, ubiquitin ligase complex, and protein kinase complex. The enriched molecular functions were mainly Ras GTPase binding, ubiquitin-like protein transferase activity, DNA-binding transcription factor binding, ubiquitin-protein transferase activity, nucleoside-triphosphatase regulator activity, transcription coactivator activity, and ubiquitin-like protein ligase binding. Signaling pathways such as MAPK, FoxO, Ras, PIK3-Akt, and Wnt were also enriched.
UNASSIGNED: These findings aid in understanding the mechanisms of diquat poisoning and the related pathways, where DE miRNAs serve as targets for gene therapy.
UNASSIGNED: The effects of diquat on the viability and apoptosis of HK-2 cells were explored using the CCK-8 and Annexin V-FITC/PI double staining methods. Total RNAs were extracted using the TRizol method and detected by Illumina HiSeq 2500. Bioinformatics analysis was performed to explore differentially expressed (DE) miRNAs, their enriched biological processes, pathways, and potential target genes. The RT-qPCR method was used to verify the reliability of the results.
UNASSIGNED: Diquat led to HK-2 cell injury and apoptosis played an important role, hence an HK-2 cell apoptosis model in diquat poisoning was established. Thirty-six DE miRNAs were screened in diquat-treated HK-2 cells. The enriched biological process terms were mainly cell growth, regulation of apoptotic signaling pathway, extrinsic apoptotic signaling pathway, and Ras protein signal transduction. The enriched cellular components were mainly cell-cell junction, cell-substrate junction, ubiquitin ligase complex, and protein kinase complex. The enriched molecular functions were mainly Ras GTPase binding, ubiquitin-like protein transferase activity, DNA-binding transcription factor binding, ubiquitin-protein transferase activity, nucleoside-triphosphatase regulator activity, transcription coactivator activity, and ubiquitin-like protein ligase binding. Signaling pathways such as MAPK, FoxO, Ras, PIK3-Akt, and Wnt were also enriched.
UNASSIGNED: These findings aid in understanding the mechanisms of diquat poisoning and the related pathways, where DE miRNAs serve as targets for gene therapy.
摘要：
■本研究通过基因测序和生物信息学分析，建立了敌快诱导的人肾-2细胞（HK-2细胞）凋亡模型，鉴定了与敌快中毒相关的差异表达的microRNAs（miRNAs）和信号通路，并探讨了相关的治疗益处。
■使用CCK-8和膜联蛋白V-FITC/PI双重染色方法研究了敌快草对HK-2细胞活力和凋亡的影响。使用TRizol方法提取总RNA并通过IlluminaHiSeq2500检测。进行生物信息学分析以探索差异表达（DE）miRNA，它们丰富的生物过程，通路,和潜在的目标基因。采用RT-qPCR方法验证结果的可靠性。
■Diquat对HK-2细胞的损伤和凋亡起了重要作用，因此，建立了敌快中毒的HK-2细胞凋亡模型。在diquat处理的HK-2细胞中筛选了36个DEmiRNA。富集的生物过程术语主要是细胞生长，调节凋亡信号通路，外源性凋亡信号通路，和Ras蛋白信号转导。富集的细胞成分主要是细胞-细胞连接，细胞-基底结，泛素连接酶复合物，和蛋白激酶复合物。富集的分子功能主要是RasGTPase结合，泛素样蛋白转移酶活性，DNA结合转录因子结合，泛素-蛋白转移酶活性，核苷三磷酸酶调节剂活性，转录共激活因子活性，和泛素样蛋白连接酶结合。信号通路如MAPK,福克斯,拉斯，PIK3-Akt,Wnt也丰富了。
■这些发现有助于理解敌快中毒的机制和相关途径，其中DEmiRNA用作基因治疗的靶标。
■使用CCK-8和膜联蛋白V-FITC/PI双重染色方法研究了敌快草对HK-2细胞活力和凋亡的影响。使用TRizol方法提取总RNA并通过IlluminaHiSeq2500检测。进行生物信息学分析以探索差异表达（DE）miRNA，它们丰富的生物过程，通路,和潜在的目标基因。采用RT-qPCR方法验证结果的可靠性。
■Diquat对HK-2细胞的损伤和凋亡起了重要作用，因此，建立了敌快中毒的HK-2细胞凋亡模型。在diquat处理的HK-2细胞中筛选了36个DEmiRNA。富集的生物过程术语主要是细胞生长，调节凋亡信号通路，外源性凋亡信号通路，和Ras蛋白信号转导。富集的细胞成分主要是细胞-细胞连接，细胞-基底结，泛素连接酶复合物，和蛋白激酶复合物。富集的分子功能主要是RasGTPase结合，泛素样蛋白转移酶活性，DNA结合转录因子结合，泛素-蛋白转移酶活性，核苷三磷酸酶调节剂活性，转录共激活因子活性，和泛素样蛋白连接酶结合。信号通路如MAPK,福克斯,拉斯，PIK3-Akt,Wnt也丰富了。
■这些发现有助于理解敌快中毒的机制和相关途径，其中DEmiRNA用作基因治疗的靶标。
