Mangiferin Inhibits Apoptosis and Autophagy Induced by Staphylococcus aureus in RAW264.7 Cells
Jun Xu1, Hua Yao1, Shichen Wang1
1Beijing Key Laboratory of Traditional Chinese Veterinary Medicine, National Demonstration Center for Experimental Animal Education, Department of Veterinary Medicine, Beijing University of Agriculture, Beijing, People's Republic of China.
Purpose:
Staphylococcus aureus (S. aureus) is an important bacterial pathogen, which creates infective inflammation to human being and animals. Mangiferin (MG) is one of the natural flavonoids with anti-inflammatory, anti-bacterial, and anti-oxidative properties. However, the anti-apoptosis and anti-autophagy of MG are unknown. Hence, this study was aimed to research the inhibition of MG on S. aureus-induced apoptosis and autophagy in RAW264.7 cells.
Methods:
The RAW264.7 cells were pretreated with MG, or pretreated with SP600125 or anisomycin synchronously, and then infected with S. aureus (MOI=100:1). The viability and proliferation status of RAW264.7 cells were detected by MTT and EdU assay. The relative expression of TNF-α, IL-6 and IL-10 protein was tested with ELISA. The levels of Bax, Bcl-2, caspase-3, c-Jun N-terminal kinase (JNK), extracellular-regulated protein kinase (ERK), p38, LC3, Beclin-1, p62, phosphorylated JNK, phosphorylated p38 and phosphorylated ERK in cells were detected by Western blotting. The apoptosis rate of RAW264.7 cells was analyzed by flow cytometric assay.
Results:
The study showed that MG significantly attenuated RAW264.7 cells apoptosis and autophagy caused by S. aureus. MG alleviated S. aureus-induced apoptosis by down-regulating the protein level of active caspase-3 and Bax and up-regulating the level of Bcl-2. MG also inhibited S. aureus-induced autophagy via decreasing the protein level of LC3-II/LC3-I and Beclin-1 or increasing the protein expression of p62. This protective role was dependent on the up-regulation of JNK signal pathway, which was confirmed by using JNK agonist and inhibitor.
Conclusion:
Our results demonstrated that MG might protect RAW264.7 cells from S. aureus-induced apoptosis and autophagy via inhibiting JNK/Bax-dependent signal pathway. Therefore, MG may be a potential agent against pathological cell damage induced by S. aureus infection.
Insights
Mangiferin (MG) protects against Staphylococcus aureus (S. aureus) infection by inhibiting cell apoptosis and autophagy. This natural flavonoid down-regulates key cell death proteins and modulates signaling pathways, offering potential therapeutic benefits.
Area of Science:
- Cell Biology
- Immunology
- Pharmacology
Background:
- Staphylococcus aureus (S. aureus) is a significant bacterial pathogen causing inflammation in humans and animals.
- Mangiferin (MG), a natural flavonoid, exhibits anti-inflammatory, anti-bacterial, and anti-oxidative properties.
- The effects of MG on apoptosis and autophagy induced by S. aureus remain largely unexplored.
Purpose of the Study:
- To investigate the inhibitory effects of Mangiferin (MG) on Staphylococcus aureus (S. aureus)-induced apoptosis and autophagy in RAW264.7 cells.
- To elucidate the underlying molecular mechanisms of MG's protective action against S. aureus infection.
Main Methods:
- RAW264.7 cells were treated with MG and subsequently infected with S. aureus.
- Cell viability, proliferation, protein expression (Bax, Bcl-2, caspase-3, JNK, ERK, p38, LC3, Beclin-1, p62), and apoptosis rates were assessed using MTT, EdU, ELISA, Western blotting, and flow cytometry.
- The role of the JNK signaling pathway was confirmed using specific agonists and inhibitors.
Main Results:
- MG significantly reduced S. aureus-induced apoptosis and autophagy in RAW264.7 cells.
- MG downregulated active caspase-3 and Bax, while upregulating Bcl-2, thereby alleviating apoptosis.
- MG inhibited autophagy by decreasing LC3-II/LC3-I and Beclin-1 levels and increasing p62 expression, mediated through the JNK signaling pathway.
Conclusions:
- Mangiferin (MG) demonstrates protective effects against S. aureus-induced apoptosis and autophagy in RAW264.7 cells.
- The protective mechanism involves the inhibition of the JNK/Bax-dependent signaling pathway.
- MG holds potential as a therapeutic agent against pathological cell damage caused by S. aureus infections.
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