Mechanistic insights into the anti-neuroinflammatory effects of cassia obtusifolia in Parkinson’s disease: a network pharmacology-based study

TL;DR

This study explores how Cassia obtusifolia may help reduce brain inflammation in Parkinson’s disease through multiple biological pathways.

Contribution

The study provides new mechanistic insights into Cassia obtusifolia’s anti-neuroinflammatory effects using network pharmacology and experimental validation.

Findings

Cassia obtusifolia targets NF-κB, MAPK, and NLRP3 pathways to reduce neuroinflammation.

Rhein, a compound in Cassia obtusifolia, showed strong binding to NF-κB p65 and reduced inflammation in microglial cells.

The compound suppressed inflammatory mediator production and p65 phosphorylation in vitro.

Abstract

Parkinson’s disease (PD) is a chronic neurodegenerative disorder that is closely associated with neuroinflammation, yet effective anti-inflammatory therapies remain limited. This study aimed to elucidate the potential mechanisms of Cassia obtusifolia in mitigating PD-associated neuroinflammatory responses.

Network pharmacology was employed to identify bioactive compounds, candidate targets, and enriched pathways, followed by protein–protein interaction (PPI) analysis and molecular docking. Rhein, a representative compound, was further validated in LPS-induced BV2 microglial cells using CCK-8, NO detection, ELISA, and Western blot assays.

A total of 114 candidate targets were identified, with enrichment highlighting NF-κB, MAPK, and NLRP3 inflammasome pathways. Molecular docking revealed strong binding affinity between rhein and NF-κB p65. In vitro, rhein significantly reduced the production of inflammatory mediators and suppressed p65 phosphorylation in BV2 cells.

Cassia obtusifolia exerts multi-target anti-neuroinflammatory effects, supporting its potential as a therapeutic candidate for PD and providing a foundation for further translational studies.

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