脂肪间充质干细胞外泌体可减轻过氧化氢诱导 PC12 细胞的凋亡.

BACKGROUND: Mesenchymal stem cell-derived exosomes may play a crucial role in tissue damage repair, and miRNA is an important component of exosomes for therapeutic effects. Among them, miR-29b-3p has the effect of reducing cell apoptosis, promoting axonal regeneration, and angiogenesis. OBJECTIVE: To study the protective effect of adipose-derived mesenchymal stem cell-derived exosome via miR-29b-3p on a neural cell injury model simulated by H2O2-treated PC12 cells, and explore the relevant mechanisms. METHODS: (1) First, the collagenase digestion method was used to extract rat adipose-derived mesenchymal stem cells. Adipose-derived mesenchymal stem cells were transfected with miR-29b-3p mimics and inhibitors. Exosomes were extracted from the culture supernatant by ultracentrifugation and identified so as to construct adipose-derived mesenchymal stem cell-derived exosomes with high expression and knockdown miR-29b-3p. (2) By constructing a neural cell injury model simulated by PC12 cells treated with H2O2, the relevant mechanisms of the protective effect of adipose-derived mesenchymal stem cell-derived exosome via miR-29b-3p on the simulated neuronal cell injury model were studied. RESULTS AND CONCLUSION: (1) Adipose-derived mesenchymal stem cell-derived exosome had a typical cup-shaped shape and a diameter distribution in the range of 50-140 nm, expressed membrane proteins Alix, CD63, and TSG101, which were specific markers on the surface of exosomes, and could be successfully ingested by PC12 cells. (2) Adipose-derived mesenchymal stem cell-derived exosome pretreatment could reduce cell apoptosis induced by H2O2 treatment in PC12 cells, and this protective effect was enhanced with the increase of miR-29b-3p expression in the exosomes and weakened with the decrease of miR-29b-3p expression in the exosomes. The mechanism of its effect was related to adipose-derived mesenchymal stem cell-derived exosome via miR-29b-3p promoting the expression of anti-apoptotic protein Bcl-2 and inhibiting the expression of apoptotic protein Bax. [ABSTRACT FROM AUTHOR]