An Exploration of the Antioxidative and Anti-Inflammatory Role of <i>Lactiplantibacillus plantarum</i> 106 via Improving Mitochondrial Function

Abstract

In this present study, bioinformatics analysis and the experimental validation method were used to systematically explore the antioxidant activity and anti-inflammatory effect of Lactiplantibacillus plantarum A106, which was isolated from traditional Chinese pickles, on lipopolysaccharide (LPS)-induced RAW264.7 macrophages. L. plantarum A106 had a good scavenging ability for DPPH, ABTS, and hydroxyl radicals. Furthermore, L. plantarum A106 could increase the activity of RAW264.7 macrophages; raise the SOD and GSH levels, with or without LPS sensitization; or decrease the MDA, TNF–α, and IL–6 levels. In order to deeply seek the antioxidant and anti-inflammatory role and mechanism, bioinformatic analysis, including GO, KEGG, and GSEA analysis, was used to conduct an in-depth analysis, and the results showed that the LPS treatment of RAW264.7 macrophages significantly upregulated inflammatory-related genes and revealed an enrichment in the inflammatory signaling pathways. Additionally, a network analysis via the Cytoscape software (version 3.9.1) identified key central genes and found that LPS also disturbed apoptosis and mitochondrial function. Based on the above bioinformatics analysis, the effects of L. plantarum A106 on inflammation-related gene expression, mitochondrial function, apoptosis, etc., were detected. The results indicated that L. plantarum A106 restored the declined expression levels of crucial genes like TNF–α and IL–6; mitochondrial membrane potential; and apoptosis and the expression of apoptosis-related genes, Bcl–2, Caspase–3, and Bax. These results suggest that L. plantarum A106 exerts antioxidant activity and anti-inflammatory effects through regulating inflammatory and apoptosis-related gene expression, restoring the mitochondrial membrane potential.

Keywords

• <i>Lactiplantibacillus plantarum</i>
• antioxidant
• bioinformatics analysis
• mitochondrial function
• apoptosis