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Fig. 4 | Stem Cell Research & Therapy

Fig. 4

From: Dissecting molecular mechanisms underlying H2O2-induced apoptosis of mouse bone marrow mesenchymal stem cell: role of Mst1 inhibition

Fig. 4

Mst1 inhibition attenuated H2O2-induced oxidative stress in mBM-MSCs. a Flow cytometry of ROS production in mBM-MSCs using the ROS probe DCFH-DA. (n = 3). Quantitative analysis of the intracellular ROS level. **p < 0.01. b Δψm was analyzed using JC-1 assay (n = 3). Decline in the membrane potential was reflected by the shift of fluorescence from red to green indicated by JC-1. Quantitative data of the red/green ratio (n = 3). **p < 0.01, *p < 0.05. c Keap1, Nrf2, GPx, CAT, SOD1, and SOD2 expression levels were evaluated by Western blot analysis. β-actin was used as the loading control. Data are expressed as mean ± SD. G, K. **p < 0.01, *p < 0.05. sh-Mst1 groups. H2O2, mBM-MSCs exposed to H2O2 only; H2O2 + Neg, mBM-MSCs/Neg followed by exposure to H2O2; H2O2 + sh-Mst1, mBM-MSC/sh-Mst1 followed by exposure to H2O2; H2O2 + sh-Mst1 + 3-MA, mBM-MSCs/sh-Mst1 pretreated with 3-MA followed by exposure to H2O2

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