Fig. 5

Effects of T-cell EVs on tissue damage, oxidative stress, and inflammation in mice with CLP-induced lung injury were attenuated by PKC/NOX4 inhibition. Mice with CLP were stimulated with EVs isolated from CD4⁺ T cells isolated from healthy subjects treated with 10 μg/mL LPS (LTE), in the absence or presence of LXS-196 or GLX351322. A H and E staining indicated that the severe lung injury by LTE treatment in CLP model mice was restored by LXS-196 or GLX351322 (scale bar, 100 μm). B The severity of histological injury and plasma levels of (C) ALT, (D) AST, and (E) LDH by LTE treatment in CLP model mice was restored by LXS-196 or GLX351322. The elevation of (F) ROS levels and (G) MDA content by LTE treatment in CLP model mice was restored by LXS-196 or GLX351322. The reduction of (H) SOD and (I) GPX activities by LTE treatment in CLP model mice was restored by LXS-196 and GLX351322. J The elevation of DAG content by LTE treatment in CLP model mice was not affected by LXS-196 or GLX351322. K The elevation of PKC activity by LTE treatment in CLP model mice was restored by LXS-196, but not GLX351322. L The elevation of NOX4 protein level by LTE treatment in CLP model mice was restored by LXS-196 and GLX351322, as shown by western blot. M The elevation of mRNA expression of TNF-α, IL-1β, and IL-6 by LTE treatment in CLP model mice was restored by LXS-196 or GLX351322. N The elevation of BALF content of TNF-α, IL-1β, and IL-6 by LTE treatment in CLP model mice was restored by LXS-196 or GLX351322. O The shortened survival in CLP model mice treated with LTE was rescued by LXS-196 and GLX351322. Data presented as mean ± SD. ***P < 0.001 versus control. ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 versus CLP. ^ΔΔΔP < 0.001 versus CLP + LTE + vehicle