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丙泊酚通过 PI3K/AKT-Wnt 信号通路抑制脂肪来源干细胞的进展。

Propofol suppresses adipose-derived stem cell progression via PI3K/AKT-Wnt signaling pathway.

机构信息

Department of Anesthesiology, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing, 210003, China.

Department of Anesthesiology, Danyang People's Hospital of Jiangsu Province & Danyang Hospital affiliated to Nantong University, Danyang, 212300, Jiangsu, China.

出版信息

BMC Anesthesiol. 2022 Mar 9;22(1):65. doi: 10.1186/s12871-022-01603-x.

Abstract

Adipose-derived stem cell (ADSC) transplantation has become a prospective way to treat cardiovascular diseases and skin traumas. Propofol, a short-acting intravenous anesthetic agent, plays an important role in the induction and maintenance of general anesthesia. In this study, we investigated the effects of propofol on ADSCs. The flow cytometry results showed that ADSCs were positive for CD29, CD44, and CD90 and negative for CD31, CD34, and CD45. The results of MTT and BrdU assays demonstrated that propofol impeded the proliferation of ADSCs. The cell scratch test showed that propofol had an inhibitory effect on the migration of ADSCs. Transwell assay showed that invasive ASDC counts decreased significantly after propofol treatment. Propofol also promoted ADSC apoptosis and arrested ADSCs in the G0/G1 phase. All these effects showed in a dose-dependent manner that the higher the concentration, the stronger the effect. Western blot analysis revealed decreased levels of FAK, PI3K, AKT, and GSK3β phosphorylation, while the phosphorylation of β-catenin increased after 48 h of treatment with propofol. The findings above indicated that the PI3K/AKT-Wnt pathways mediated propofol-inhibited ADSC proliferation, providing new insights into the propofol application in ADSCs.

摘要

脂肪干细胞(ADSC)移植已成为治疗心血管疾病和皮肤创伤的一种有前景的方法。丙泊酚是一种短效静脉麻醉剂,在全身麻醉的诱导和维持中起着重要作用。在这项研究中,我们研究了丙泊酚对 ADSC 的影响。流式细胞术结果表明,ADSC 对 CD29、CD44 和 CD90 呈阳性,对 CD31、CD34 和 CD45 呈阴性。MTT 和 BrdU 检测结果表明,丙泊酚抑制 ADSC 的增殖。细胞划痕试验表明丙泊酚对 ADSC 的迁移具有抑制作用。Transwell 检测表明丙泊酚处理后 ADSC 的侵袭数明显减少。丙泊酚还促进 ADSC 凋亡并将 ADSC 阻滞在 G0/G1 期。所有这些作用均呈剂量依赖性,即浓度越高,作用越强。Western blot 分析显示,丙泊酚处理 48 小时后,FAK、PI3K、AKT 和 GSK3β 的磷酸化水平降低,而β-catenin 的磷酸化水平升高。上述结果表明,PI3K/AKT-Wnt 通路介导了丙泊酚抑制 ADSC 增殖,为丙泊酚在 ADSC 中的应用提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7040/8905820/8e3c7f56788b/12871_2022_1603_Fig1_HTML.jpg

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