H2S Exposure Induces Autophagy Injury in The Jejunum of Broilers Through miR-181a-PKC-δ Axis Mediated ER Stress

Abstract

Background:Hydrogen sulfide (H2S), as a toxic atmospheric and industrial pollutant, is one of the main components of haze. Air exposure to H2S can cause multiple organ and tissue damage. However, studies on the animal intestines of H2S toxicity are limited. To clarify the effect of H2S exposure on intestinal proteomics and the role of autophagy in intestinal injury, in the present study, effects of H2S exposure on jejunum damage of broilers were examined by establishing a 42-day H2S exposure broiler model. Results:We observed the morphological changes that arose, screened differentially expressed proteins (DEPS) and enriched related pathways via electron microscopy, proteomics and bioinformatics analyses, qRT-PCR, and western blot. We obtained 86 proteins that were significantly different under H2S exposure, including proteins related to autophagy and ER stress regulation. Meanwhile, protein-transcriptomics combined analysis found that autophagy and ER stress-associated pathways MAPK signaling pathway, FOXO signaling pathway, mTOR signaling pathway and Autophagy were significantly enriched. Besides, the expression of the autophagy-related indicators LC3II/I, Dynein, Beclin1, BNIP3, and ULK1 were remarkably up-regulated under H2S exposure (P < 0.05). In contrast, the activities of p62 and mTOR were significantly decreased (P < 0.05). Conclusions: The above results indicate that H2S induced autophagy in the jejunum via the miR-181a-PKC-δ axis activates ER stress to induce p38/JNK expression. In our study, the combined analysis of proteomics and transcriptomics on broiler intestines was described for the first time and verified the selected pathways related to ER stress and autophagy. These results provide novel insights into the toxicology of H2S and environmental research.