No abstract

Aberrant expression of long non-coding RNAs (lncRNAs) is closely related to the progression of sepsis. According to research, the lncRNA MALAT1 plays an important role in the multiple organ damage caused by sepsis. However, the mechanism associated with MALAT1 in septic testicular injury is not clear. We established an animal model of LPS-induced septic testicular injury and a cellular model of LPS-induced GC-1 cell injury in mice. H&E staining was performed to detect testicular injury after LPS treatment. MALAT1, inflammatory factors and related proteins expression levels in testicular tissues were determined using qRT-PCR, western blotting and immunohistochemistry. The ROS levels in tissue were detected by MDA and SOD. MALAT1, miR-103-3p and inflammatory factors expression levels in GC-1 were detected by qRT- PCR and ELISA assay. cell viability was determined by CCK-8. Western blot, immunofluorescence assay detected proteins expression. Correlation of MALAT1, miR-103-3p and TRPV4 was verified through dual luciferase reporter and Ago2-RIP. Within the present study, our findings suggest that MALAT1 expression is elevated in both cellular and animal models. Furthermore, we discovered that MALAT1 inhibits miR-103-3p expression at the post-transcriptional level while promoting TRPV4 expression, which promotes cellular inflammation and pyroptosis. As a result, we investigated the relationship between MALAT1, miR-103-3p, and TRPV4 and discovered that MALAT1 targets miR-103-3p, whereas miR-103-3p targets TRPV4. Our study showed that MALAT1 promotes testicular inflammation and pyroptosis through modulating miR-103-3p and TRPV4 in a septic testicular injury model, suggesting that MALAT1 may be a potential therapeutic target for septic testicular injury.