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 presented as mean ± SD. ***P < 0.001 versus control. ^##P < 0.01, ^###P < 0.001 versus CLP + shNC