Coptisine attenuates sepsis lung injury by suppressing LPS-induced lung epithelial cell inflammation and apoptosis

Objective: This study aimed to investigate the functioning and mechanism of coptisine in acute lung injury (ALI). Methods: Murine Lung Epithelial 12 (MLE-12) cells were stimulated with lipopolysaccharide (LPS) to construct an in vitro pulmonary injury model to study the functioning of coptisine in sepsis-induced ALI. The viability of MLE-12 cells was assessed by the cell counting kit-8 assay. The cytokine release of tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and IL-1 beta was measured by enzyme-linked-immunosorbent serologic assay. The relative expression levels of TNF-alpha, IL-6, and IL-1 beta mRNA were examined by reverse transcription-quantitative polymerase chain reaction. The cell apoptosis of MLE-12 cells was determined by Annexin V/propidium iodide staining and analyzed by flow cytometry. The expressions of apoptosis-related proteins Bax and cleaved Caspase-3 were observed by Western blot analysis. The activation of nuclear factor kappa B (NF-kappa B) signaling pathway was discovered by the determination of phospho-p65, p65, phospho-nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (I kappa B alpha), and I kappa B alpha through Western blot analysis. Results: Coptisine treatment could significantly restore decrease in MLE-12 cell viability caused by LPS stimulation. The release of TNF-alpha, IL-6, and IL-1 beta was significantly inhibited by coptisine treatment. Coptisine treatment inhibited MLE-12 cell apoptosis induced by LPS, and also inhibited the expression levels of Bax and cleaved Caspase-3. Coptisine treatment along with LPS stimulation, significantly reduced the protein level of phospho-I kappa B alpha, increased the level of I kappa B alpha, and reduced phospho-p65-p65 ratio. Conclusion: These results indicated that coptisine attenuated sepsis lung injury by suppressing lung epithelial cell inflammation and apoptosis through NF-kappa B pathway. Therefore, coptisine may have potential to treat sepsis-induced ALI. (c) 2023 Codon Publications. Published by Codon Publications.