文献类型：期刊文献

英文题名：Combined treatment with mesenchymal stem cells and ROCK inhibitor Y-27632 ameliorates PM2.5-induced lung injury

作者：Jiang, He[1];Jin, Lifang[2,3];Tan, Shanshan[2];Huang, Huarong[4];Li, Yinping[2];Fu, Guoquan[2,3];Yan, Junyan[2]

机构：[1]Zhejiang Prov Peoples Hosp, Affiliated Peoples Hosp, Hangzhou Med Coll, Ctr Gen Practice Med,Dept Tradit Chinese Med, 158 Shangtang Rd, Hangzhou 310014, Zhejiang, Peoples R China;[2]Shaoxing Univ, Sch Life & Environm Sci, 900 Chengnan Rd, Shaoxing 312000, Zhejiang, Peoples R China;[3]Hangzhou Hongwang Med Lab Co Ltd, 111 Hongxing Rd,Qiaonan Block, Hangzhou 310020, Zhejiang, Peoples R China;[4]Hangzhou Normal Univ, Coll Life & Environm Sci, 16 Xuelin St,Xiasha Higher Educ Pk, Hangzhou 311121, Zhejiang, Peoples R China

年份：2025

卷号：14

期号：4

外文期刊名：TOXICOLOGY RESEARCH

收录：SCI-EXPANDED(收录号：WOS:001525347300001)、、Scopus(收录号：2-s2.0-105010652994)、WOS

基金：This work was supported by the Zhejiang Provincial Natural Science Foundation of China under Grant No. LQ20B070003.

语种：英文

外文关键词：medical podcast; sexual medicine; urology

外文摘要：Particulate matter 2.5 mu m (PM2.5) can directly enter the human respiratory tract and cause damage to lungs. Mesenchymal stem cells (MSCs) transplantation has emerged as a promising therapeutic strategy for ameliorating lung injury. Nonetheless, the lineage fate of recruited MSCs in the lung can be impacted by Rho-associated protein kinase 1 (ROCK) signaling. The current study investigated whether a combined treatment of MSCs with ROCK inhibitor Y-27632 offers enhanced therapeutic efficacy in addressing PM2.5-induced lung injury. The combined therapeutic efficacy was analyzed by wound healing assay, oxidative response and inflammatory factors in PM2.5-treated A549 cells. Besides, the combined MSCs and Y-27632 therapy was also analyzed by lung pathology, EMT response and inflammatory factors in PM2.5-treated mice. Combined MSCs and Y-27632 treatment more effectively restored wound healing ability and attenuated oxidative stress and inflammatory response in PM2.5-injured A549 cells than MSCs monotherapy. Immunohistochemical analysis result demonstrated that PM2.5 exposure altered markers related to epithelial-to-mesenchymal transition (EMT), such as E-cadherin, alpha-SMA and vimentin in lung tissue. Both MSCs monotherapy and combined MSCs and Y-27632 therapy restored lung injury by reducing lung pathology, oxidative stress, inflammatory response, and EMT process by inhibiting beta-catenin pathway. However, the combined treatment proved more efficacious in mitigating PM2.5-induced lung injury. Although MSCs alleviated PM2.5-induced lung injury, the combined therapeutic efficacy of MSCs and Y-27632 offered a better treatment effect. This study offers valuable insights into the mechanisms of lung injury induced by PM2.5 and potential interventional treatments.