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Human Bone Mesenchymal Stem Cell-Derived Exosomes Inhibit IL-1β-Induced Inflammation in Osteoarthritis Chondrocytes

Journal 2021 · IF 2.479 · 发表于 2021 年 8 月 29 日
作者: Liping Zhou,Haiwei Ye,Lizhen Liu,Yunhua Chen
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摘要

Objective Human bone marrow mesenchymal stem cell (hBMSC)-derived exosomes exhibit protective effects againstinflammatory diseases. This study aimed to explore the effects of hBMSC-derived exosomes on osteoarthritis (OA) invitro and its related mechanisms. Materials and Methods In this experimental study, we characterised exosomes derived from hBMSCs by transmissionelectron microscopy, nanoparticle tracking and Western blot analysis. Cellular uptake of exosomes was observed byfluorescent microscopy. Cell viability of chondrocytes exposed to interleukin-1 beta (IL-1β) was determined by theCell Counting Kit-8 (CCK-8). Real-time quantitative polymerase chain reaction (RT-qPCR) was used to determineexpression levels of genes related to apoptosis, inflammation, cartilage collagen metabolism and mitogen-activatedprotein kinases. Results Fluorescence microscopy revealed that hBMSC-derived exosomes could be taken up by chondrocytes.hBMSC-derived exosomes could significantly enhance cell viability of chondrocytes in response to IL-1β treatment.RT-qPCR showed significant up-regulation of Survivin, Versican, IL-1β, IL-6, NF-κB, MMP-13, MAPK p38, JNK, ERK,Aggrecan and SOX9 expression levels by IL-1β treatment, while their mRNA expression levels decreased after co-culture with exosomes. The anti-inflammatory gene TGF-β was markedly suppressed by IL-1β treatment; however, weobserved its expression after co-culture with exosomes. Additionally, the pro-inflammatory genes IL-1β, IL-6, NF-κB,TNF-α and TNF-β displayed significantly elevated expression levels in the IL-1β group and reduced expression levelsafter co-culture with exosomes. Conclusion hBMSC-derived exosomes may play a protective role in chondrocytes through inhibiting cell apoptosisand the inflammatory response. These results will provide a novel therapeutic strategy for OA.