Fig. 6

DGKK knockdown attenuated tissue damage, oxidative stress, and inflammation in mice with CLP-induced lung injury. Mice with CLP were injected with virus carrying plasmid expressing shRNA control (shNC) and shRNA targeting DGKK (shDgkk). The elevation of Dgkk abundance at the A mRNA and B protein levels in CLP model mice was restored by DGKK RNAi. C H and E staining indicated that the severe lung injury in CLP model mice was restored by Dgkk RNAi (scale bar, 100 μm). D The severity of histological injury and plasma levels of E ALT, F AST, and G LDH in CLP model mice was restored by DGKK RNAi. The elevation of H ROS levels and I MDA content in CLP model mice was restored by DGKK RNAi. The reduction of J SOD and K GPX activities in CLP model mice was restored by Dgkk RNAi. The elevation of L DAG content and M PKC activity in CLP model mice was restored by Dgkk RNAi. N The elevation of BALF content of TNF-α, IL-1β, and IL-6 in CLP model mice was restored by Dgkk RNAi. O The shortened survival in CLP model mice was restored by Dgkk RNAi. Data are presented as mean ± SD. ***P < 0.001 versus control. ^##P < 0.01, ^###P < 0.001 versus CLP + shNC