Novel modified probiotic gold nanoparticles loaded with ginsenoside CK exerts an anti-inflammation effect via NF-κB/MAPK signaling pathways

Abstract

Background: Gold nanoparticles (AuNPs) exhibit promising potential as medical materials due to their high biocompatibility, tunable size and shape, and excellent drug delivery capabilities, among other unique physicochemical properties. Previous studies have indicated the remarkable anti-inflammatory activity of ginsenoside compound K (CK). However, the relatively low bioavailability of CK restricts its effective delivery and action within the biological system. Hence, exploring novel delivery methods based on gold nanoparticles emerges as a promising strategy to overcome these challenges in application, thereby enhancing the therapeutic effectiveness of CK. Methods: Probiotic-mediated AuNPs were synthesized using gold salt and the lysates of Bifidobacterium animalis subsp. lactis. Then, CK was loaded with AuNPs to form Bifidobacterium CK AuNPs (Bifi-CKAuNPs). The antiinflammatory activity of Bifi-CKAuNPs was evaluated in vitro using RAW 264.7 cells and in vivo using mice. The NF-kappa B/ mitogen-activated protein kinases (MAPK) pathway was investigated as a potential mechanism of action. Results: In vitro experiments showed that Bifi-CKAuNPs inhibited the activation of reactive oxygen species and reduced the expression of iNOS, COX-2, and pro-inflammatory cytokines (IL-1 beta, IL-6, and TNF-alpha) in RAW 264.7 cells. In vivo experiments showed that Bifi-CKAuNPs significantly reduced inflammation in the lung, kidney, and liver tissues of mice without toxicity. The anti-inflammatory activity of Bifi-CKAuNPs was mediated through the inhibition of NF-kappa B/MAPK signal transduction, which is a well-known and critical pathway in the pathogenesis of inflammation. Conclusion: We have successfully synthesized and characterized Bifi-AuNPs, demonstrating its potent antiinflammatory activity both in vitro and in vivo. Our results indicated that the NF-kappa B/MAPK pathway might play a key role in the mechanism of action of Bifi-CKAuNPs. These findings underscored the significant potential of Bifi-CKAuNPs as a promising platform for drug delivery and anti-inflammatory therapy. The observed efficacy in both cellular and animal models, along with insights into the underlying molecular pathways, positions BifiCKAuNPs as a valuable candidate for advancing therapeutic strategies in the realm of inflammation management.