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Mycelial culture filtrate of Trametes suaveolens KMRB 17121435 attenuates oxidative stress-induced apoptosis and NF-κB-mediated inflammation in cellular models

  • Hyehyun Hong,
  • Byeong-Min Choi,
  • Minkyeong Kim,
  • Changmu Kim,
  • Jin-Soo Park,
  • Won-Jae Chi,
  • Seung-Young Kim

摘要

Background

Aging-associated muscle decline is closely associated with oxidative stress-induced apoptosis and chronic inflammatory signaling. Excessive accumulation of reactive oxygen species disrupts cellular redox homeostasis and promotes mitochondrial dysfunction, ultimately leading to myocyte apoptosis and muscle degeneration. In addition, inflammatory mediators and cytokine signaling pathways further amplify oxidative damage and contribute to progressive muscle deterioration.

Objective

This study evaluated the biological effects of the mycelial culture filtrate of Trametes suaveolens KMRB 17121435 (Ts_MY) on oxidative stress-associated cytotoxicity in C2C12 myoblasts and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 macrophages.

Results

Under H2O2 exposure, Ts_MY treatment increased C2C12 cell viability in a concentration-dependent manner and modulated apoptosis-related regulators, including decreased Bax expression, increased Bcl-2 levels, reduced caspase-9 and caspase-3 cleavage, and attenuated PARP cleavage. In RAW 264.7 macrophages, Ts_MY exhibited no cytotoxicity within the tested concentration range and significantly suppressed nitric oxide and prostaglandin E2 production. Ts_MY also reduced the expression of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), accompanied by decreased inducible nitric oxide synthase and cyclooxygenase-2 expression and inhibition of NF-κB signaling. Radical scavenging activity was confirmed using ABTS and DPPH assays. LC–MS/MS profiling tentatively indicated the presence of phenolic and aromatic metabolites, including protocatechuic acid-related signals based on accurate mass and database matching.

Conclusion

These findings demonstrate that Ts_MY modulates oxidative stress- and inflammation-associated cellular responses in vitro through regulation of apoptosis-related signaling and NF-κB-mediated inflammatory pathways. Because all experiments were conducted in cell-based systems, further studies are required to identify active constituents and validate their biological effects in more complex models.