Abstract
miR-495 is aberrantly expressed and affects the progression of inflammation in various diseases. However, the mechanisms of miR-495 in bovine endometritis remain largely unknown. This study investigated the mechanism of miR-495 in lipopolysaccharide (LPS)-induced bovine endometritis and pyroptosis and found that miR-495 inhibits NLRP3 inflammasome activation and inflammatory immune responses in endometritis tissue and cell models. Bovine endometrial epithelial cells (BENDs) were treated with 10 μg/mL LPS to establish a cell inflammatory model. LPS stimulation activated the NLRP3 inflammasome and elevated the expression of proinflammatory factors in BEND cells. In addition, pyroptosis and methylation-dependent inhibition of miR-495 was discovered in LPS-exposed BENDs. Furthermore, overexpression of miR-495 inhibited activation of the NLRP3 inflammasome in vitro and vivo. Collectively, our data demonstrate that miR-495 can attenuate activation of the NLRP3 inflammasome to protect against pyroptosis and bovine endometritis, which provides novel therapeutic targets for bovine endometritis and other inflammatory diseases.
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