Introduction
Inflammation is a protective physiological response, but its chronic manifestation leads to adverse health outcomes. Current anti-inflammatory treatments often have significant side effects, necessitating safer alternatives. Mitragyna parvifolia, a medicinal plant, has demonstrated anti-inflammatory potential, though its mechanisms remain underexplored. The current study was designed to explore the anti-inflammatory mechanisms of M parvifolia, emphasising its potential as therapeutic agent for inflammatory diseases.
Methods
This study employed in silico approaches, including network pharmacology, molecular docking, and molecular dynamic simulations, to identify interactions between M parvifolia phytocompounds and inflammatory targets. Experimental validation was conducted using supercritical CO2 leaf extract, evaluated for cytotoxicity, protein denaturation, COX-2 inhibition, and HRBC membrane stabilisation and phytochemical profiling using LC-QTOF-MS analysis.
Results
Thirteen phytocompounds of M parvifolia were found to modulate 97 inflammatory targets, significantly impacting Interleukin-17 and TNF signalling pathways. Molecular docking revealed strong binding of compounds to key targets, including MMP9 and PTGS2, with the MMP9-Corynan-17-ol complex showing the highest stability in simulations. LC-QTOF-MS analysis identified 10 major bioactive constituents, supporting in silico predictions. Experimental assays confirmed low cytotoxicity (>90% cell viability) and demonstrated potent anti-inflammatory effects: 73.71% ± 1.5% inhibition of COX-2 activity, 73.9% ± 0.4% inhibition of protein denaturation, and 75.5% ± 0.83% HRBC membrane stabilisation at maximum concentrations.
Conclusions
M parvifolia exhibits significant anti-inflammatory properties through modulation of key pathways and targets, combined with strong experimental validation of its efficacy and safety. These findings position M parvifolia as a promising candidate for developing natural, safer anti-inflammatory therapies.
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