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维生素D3促进感染了……的THP-1细胞中的自噬。 (原文中“infected with”后面内容缺失)

Vitamin D3 promotes autophagy in THP-1 cells infected with .

作者信息

Wu Yiming, Lin Xue, Song Fuyang, Xue Di, Wang Yujiong

机构信息

Key Laboratory of The Ministry of Education for Conservation and Utilization of Special Biological Resources in The West, Yinchuan, Ningxia 750021, P.R. China.

College of Life Science, Ningxia University, Yinchuan, Ningxia 750021, P.R. China.

出版信息

Exp Ther Med. 2022 Mar;23(3):240. doi: 10.3892/etm.2022.11165. Epub 2022 Jan 25.

Abstract

Tuberculosis (TB) is a major disease that causes mortality worldwide. The lethality of this disease is a result of the contagious bacteria . Infection can inhibit phagosomal maturation, with mainly attacking macrophages and inhibiting autophagy and apoptosis. Vitamin D has been used to treat tuberculosis, whereby the active metabolite, 1,25-dihydroxyvitamin D, may enhance the immune response to . Moreover, macrophages infected with have a high demand for Ca. However, the mechanisms by which vitamin D3 protects against and treats TB remain unclear. In the present study, MTT assay showed that vitamin D3 decreased the viability of THP-1 cells in a dose- and time-dependent manner. Autophagy-related factors in THP-1 cells infected with were analyzed by western blotting and RT-qPCR and the results demonstrated that vitamin D3 significantly increased the expression level of p62, LC3Ⅱ/LC3Ⅰ, Beclin-1, ATG-5 and AMPK in THP-1 cells following infection. The Ca concentration assay demonstrated that vitamin D3 may promoted cellular autophagy by inhibiting the concentration of Ca. Furthermore, the effect of vitamin D3 on infection was also assessed using Balb/c mice; pulmonary injury was assessed by H&E staining of the lungs tissue. The results demonstrated that vitamin D3 markedly attenuated cellular damage caused by infection. In conclusion, the present study indicated that vitamin D3 may activate cell autophagy signals by inhibiting the concentration of Ca. These data may improve understanding of the effect of vitamin D3 on infection and help determine the underlying mechanism of vitamin D3 to alleviate and treat the inflammatory response caused by TB.

摘要

结核病(TB)是一种在全球范围内导致死亡的主要疾病。这种疾病的致死性是由传染性细菌引起的。感染可抑制吞噬体成熟,主要攻击巨噬细胞并抑制自噬和凋亡。维生素D已被用于治疗结核病,其活性代谢物1,25 - 二羟基维生素D可能增强对[此处原文缺失相关病原体名称]的免疫反应。此外,感染[此处原文缺失相关病原体名称]的巨噬细胞对钙有很高的需求。然而,维生素D3预防和治疗结核病的机制仍不清楚。在本研究中,MTT分析表明维生素D3以剂量和时间依赖性方式降低THP - 1细胞的活力。通过蛋白质免疫印迹法和逆转录定量聚合酶链反应分析感染[此处原文缺失相关病原体名称]的THP - 1细胞中的自噬相关因子,结果表明维生素D3在感染[此处原文缺失相关病原体名称]后显著增加了THP - 1细胞中p62、LC3Ⅱ/LC3Ⅰ、Beclin - 1、ATG - 5和AMPK的表达水平。钙浓度测定表明维生素D3可能通过抑制钙浓度促进细胞自噬。此外,还使用Balb/c小鼠评估了维生素D3对[此处原文缺失相关病原体名称]感染的影响;通过对肺组织进行苏木精 - 伊红染色评估肺损伤。结果表明维生素D3显著减轻了由[此处原文缺失相关病原体名称]感染引起的细胞损伤。总之,本研究表明维生素D3可能通过抑制钙浓度激活细胞自噬信号。这些数据可能有助于增进对维生素D3对[此处原文缺失相关病原体名称]感染影响的理解,并有助于确定维生素D3减轻和治疗结核病引起的炎症反应的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9e1/8815057/114d66d3e7f9/etm-23-03-11165-g00.jpg

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