Inflammopharmacology · 2026
Integrated network pharmacology and experimental investigation of the potential therapeutic effect of β-sitosterol in systemic lupus erythematosus.
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Gibo Rikngam, Chetia Purbajit, Kom George Hmangte, Talukdar Apurba
Аннотация
BACKGROUND: Systemic lupus erythematosus (SLE) is a chronic autoimmune condition characterized by immunological dysregulation, inflammation, and oxidative stress, affecting multiple organs. The need for safer therapeutic alternatives is highlighted by the substantial side effects and inconsistent effectiveness of current treatments. The current study employed integrated computational and experimental methods to examine the potential effects of β-sitosterol against pristane induced SLE.
METHODS: Network pharmacology, Molecular docking and MD simulations were conducted to discover possible molecular targets of β-sitosterol in SLE. Antioxidant and anti-inflammatory assays were assessed though in vitro experiments. SLE was induced in BALB/c mice by administration of pristane, followed by treatment with β-sitosterol (100, 200, and 400 mg/kg, p.o.) or prednisone (10 mg/kg). Progression of the disease was evaluated through proteinuria, behavioral assessment, paw edema, hematological parameters, cytokine quantification, radiographic and histopathological analysis.
RESULTS: 68 common BS-SLE targets were identified by network pharmacology, where TNF-α, PPARG, and MAPK3 emerged as major hub proteins with stable interaction demonstrated by docking and molecular dynamics. β-sitosterol demonstrated considerable antioxidant and anti-inflammatory properties in vitro and showed a favorable acute safety profile at 300 mg/kg, while one mortality was observed at 2000 mg/kg. In in vivo experiments, β-sitosterol substantially diminished proteinuria, serum creatinine, BUN, TNF-α, IL-6, paw oedema, and joint inflammation, while improving anxiety-like behavior, motor coordination, and hematological parameters. Considerable protection against kidney, brain and joint tissue injury was demonstrated by histopathological investigations, especially at 400 mg/kg.
CONCLUSIONS: These findings suggest that β-sitosterol may mitigate lupus-associated inflammation and multiorgan injury through the modulation of inflammatory and metabolic pathways predicted by network pharmacology. The integrated computational and experimental evidence supports further mechanistic investigation and translational studies rather than establishing β-sitosterol as a definitive therapeutic agent for SLE.
METHODS: Network pharmacology, Molecular docking and MD simulations were conducted to discover possible molecular targets of β-sitosterol in SLE. Antioxidant and anti-inflammatory assays were assessed though in vitro experiments. SLE was induced in BALB/c mice by administration of pristane, followed by treatment with β-sitosterol (100, 200, and 400 mg/kg, p.o.) or prednisone (10 mg/kg). Progression of the disease was evaluated through proteinuria, behavioral assessment, paw edema, hematological parameters, cytokine quantification, radiographic and histopathological analysis.
RESULTS: 68 common BS-SLE targets were identified by network pharmacology, where TNF-α, PPARG, and MAPK3 emerged as major hub proteins with stable interaction demonstrated by docking and molecular dynamics. β-sitosterol demonstrated considerable antioxidant and anti-inflammatory properties in vitro and showed a favorable acute safety profile at 300 mg/kg, while one mortality was observed at 2000 mg/kg. In in vivo experiments, β-sitosterol substantially diminished proteinuria, serum creatinine, BUN, TNF-α, IL-6, paw oedema, and joint inflammation, while improving anxiety-like behavior, motor coordination, and hematological parameters. Considerable protection against kidney, brain and joint tissue injury was demonstrated by histopathological investigations, especially at 400 mg/kg.
CONCLUSIONS: These findings suggest that β-sitosterol may mitigate lupus-associated inflammation and multiorgan injury through the modulation of inflammatory and metabolic pathways predicted by network pharmacology. The integrated computational and experimental evidence supports further mechanistic investigation and translational studies rather than establishing β-sitosterol as a definitive therapeutic agent for SLE.