Hemorrhagic Shock Sensitized the Diaphragm to Ventilator-Induced Dysfunction through the Activation of IL-6/JAK/STAT Signaling-Mediated Autophagy in Rats

Figure 4

JAK/STAT signaling activation mediated the exogenous IL-6-induced autophagy in vitro. (a, b) Western blots for JAK/STAT signaling after IL-6 stimulation. (c, d) LC3B-I/II expression after IL-6 treatment. (e, f) Mitochondrial ROS production after IL-6 administration. (g, h) mitochondrial ROS production after mitochondria-targeted antioxidant MitoTEMPO (MitoT) treatment. (i, j) Western blots for LC3B-I/II expression after MitoT treatment. Western blots for (k, l) JAK/STAT signaling and (m, n) LC3B-I/II expression after JAK/STAT inhibitor ruxolitinib (Rux) treatment. (o, p) Mitochondrial ROS production after Rux treatment. Measurements were repeated three times for each sample. vs. the IL-6 group.

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