Mangiferin might protect RAW264.7 cells from S. aureus-induced apoptosis. - GreenMedInfo Summary
Mangiferin Inhibits Apoptosis and Autophagy Induced byin RAW264.7 Cells.
J Inflamm Res. 2020 ;13:847-857. Epub 2020 Nov 3. PMID: 33177860
Jun Xu
Purpose: Staphylococcus 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-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(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. MG alleviated-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-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-induced apoptosis and autophagy via inhibiting JNK/Bax-dependent signal pathway. Therefore, MG may be a potential agent against pathological cell damage inducedinfection.