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川芎嗪通过下调 miR-302b 降低 LPS 刺激的人牙周膜细胞的炎症水平和细胞凋亡。

Tetramethylpyrazine reduces inflammation levels and the apoptosis of LPS‑stimulated human periodontal ligament cells via the downregulation of miR‑302b.

机构信息

Department of Oral Medicine, Shanxi Provincial People's Hospital, Taiyuan, Shanxi 030000, P.R. China.

Department of Oral Surgery, Shanxi Provincial People's Hospital, Taiyuan, Shanxi 030000, P.R. China.

出版信息

Int J Mol Med. 2020 Jun;45(6):1918-1926. doi: 10.3892/ijmm.2020.4554. Epub 2020 Mar 27.

Abstract

Periodontitis is the main cause of tooth or tissue loss. Human periodontal ligament stem cells (hPDLSCs), which have high proliferative, self‑renewal and multi‑differentiation abilities, are vital for the restoration of periodontitis‑induced injuries. The anti‑inflammatory and anti‑apoptotic agent, tetramethylpyrazine (TMP), is a promising agent used for the protection of PDLSCs from apoptosis and inflammation induced by periodontitis. The aim of the present study was to investigate the effects of TMP on lipopolysaccharide (LPS)‑stimulated hPDLSCs. LPS‑stimulated hPDLSCs were established as the cell model. CCK‑8 assay was performed to evaluate cell viability, western blot analysis was performed to measure protein expression and flow cytometry was performed to detect cell apoptosis levels. Detection kits were used to evaluate the levels of tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β and IL‑6. Reverse transcription‑quantitative PCR analysis was performed to detect gene expression. TMP alleviated the effects of LPS on cell viability, inflammation levels and cell apoptosis. TMP downregulated microRNA (miR)‑302b levels in LPS‑stimulated cells. Transfection with miR‑302b mimic reversed the anti‑inflammatory and anti‑apoptotic effects of TMP on LPS‑stimulated cells. TMP reduced inflammation and the apoptosis of LPS‑stimulated human periodontal ligament cells via the downregulation of miR‑302b. The anti‑inflammatory and anti‑apoptotic effects exerted by TMP render it a promising agent for the protection of PDLSCs from injuries induced by periodontitis. The findings of the present study may aid in the development of a novel strategy for the treatment of periodontitis and may pave the way for further research.

摘要

牙周炎是牙齿或组织丧失的主要原因。人牙周韧带干细胞(hPDLSCs)具有高增殖、自我更新和多向分化能力,对于牙周炎损伤的修复至关重要。抗炎和抗凋亡剂川芎嗪(TMP)是一种有前途的药物,可保护牙周膜干细胞免受牙周炎诱导的细胞凋亡和炎症的影响。本研究旨在探讨 TMP 对脂多糖(LPS)刺激的 hPDLSCs 的影响。建立 LPS 刺激的 hPDLSCs 作为细胞模型。通过 CCK-8 测定法评估细胞活力,通过 Western blot 分析测定蛋白表达,通过流式细胞术检测细胞凋亡水平。使用检测试剂盒评估肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β和 IL-6 的水平。通过逆转录-定量 PCR 分析检测基因表达。TMP 减轻了 LPS 对细胞活力、炎症水平和细胞凋亡的影响。TMP 下调了 LPS 刺激细胞中的 microRNA(miR)-302b 水平。转染 miR-302b 模拟物逆转了 TMP 对 LPS 刺激细胞的抗炎和抗凋亡作用。TMP 通过下调 miR-302b 减轻 LPS 刺激的人牙周韧带细胞的炎症和凋亡。TMP 通过下调 miR-302b 减轻 LPS 刺激的人牙周韧带细胞的炎症和凋亡,从而发挥抗炎和抗凋亡作用,使其成为保护牙周膜干细胞免受牙周炎损伤的有前途的药物。本研究的结果可能有助于开发治疗牙周炎的新策略,并为进一步的研究铺平道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d707/7169953/ab2671be6010/IJMM-45-06-1918-g00.jpg

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