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Updated: Jun 16, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
Phosphoinositide 3-kinase/Akt and nuclear factor-kappaB are involved in Staphylococcus aureus-induced apoptosis in
Jia-he Wang1, Yi-jun Zhou, Li Tian
1Department of Geriatrics, Shengjing Hospital, China Medical University, Shenyang 110004, China. cmuwjh@126.com
Objective:
To explore the mechanisms involved in Staphylococcus aureus (S. aureus) invading human monocytic U937 cells.
Methods:
S. aureus were added to U937 cells at multiplicity of infections (MOI) of 20:1 for 0, 15, 30, 60, and 90 minutes, respectively. Cell apoptosis was analyzed with Hoechst 33258 staining and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry analysis. Akt and nuclear factor-kappaB (NF-kappaB) activities were detected by Western blotting.
Results:
Infection of U937 cells with S. aureus induced rapid cell death in a time-dependent manner, and the cells displayed characteristic features of apoptosis. S. aureus-induced apoptosis was associated with a prominent downregulation of activated (phosphorylated) Akt and NF-kappaB. The inhibition of phosphorylated Akt by LY294002 led to the inhibition of NF-kappaB in a dose-dependent manner. Inhibition of Akt with LY294002 caused further increase in apoptosis of U937 cells.
Conclusions:
S. aureus can stimulate the apoptosis of U937 cells. S. aureus induces apoptosis of U937 cells by inhibiting Akt-regulated NF-kappaB.
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