# The Protective Effects of Dendrobine on LPS-Induced Neuroinflammation and Related Mechanisms Based on Microglial M1/M2 Polarization

## TL;DR

Dendrobine reduces neuroinflammation by shifting microglial cells from a harmful to a protective state.

## Contribution

This study reveals DDB's novel ability to modulate microglial M1/M2 polarization in LPS-induced neuroinflammation.

## Key findings

- Dendrobine significantly reduced pro-inflammatory mediators like TNF-α, IL-6, and IL-1β in LPS-induced BV2 cells.
- DDB increased anti-inflammatory markers IL-10 and Arg-1, indicating a shift toward an anti-inflammatory microglial profile.
- DDB decreased M1 markers (iNOS, CD16/32) and increased M2 markers (CD206, Arg-1), suggesting polarization toward M2.

## Abstract

Objectives: Dendrobine (DDB) is one of the active ingredients in Dendrobium and has been reported to have significant neuroprotective properties. Nevertheless, the precise mechanisms underlying its action have not been fully clarified. The microglial imbalance of polarization is regarded as one of the key determinants in the etiology of neurodegenerative conditions, in the contribution of neuroinflammation. The recovery of M1/M2 balance and the inhibition of over-production of the pro-inflammatory effects have become major topics in modern studies of preventing and treating neurodegenerative diseases. Methods: Therefore, the present study aimed to explore the effects of DDB on the Lipopolysaccharide (LPS)-induced neuroinflammatory model in BV2 microglial cells and the potential molecular mechanisms of microglial M1/M2 polarization. Result: The results showed that DDB significantly suppressed Nitric Oxide (NO) release and ROS levels in LPS-induced BV2 cells. ELISA, qPCR, Western blot, and immunofluorescence results indicated that DDB reduced pro-inflammatory mediators Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6), and nterleukin-1 beta (IL-1β) and increased anti-inflammatory mediators Interleukin-10 (IL-10) and Arginase-1 (Arg-1). Consistently, it decreased M1-like markers Inducible Nitric Oxide Synthase (iNOS) and Cluster of Differentiation 16/32 (CD16/32) while increasing M2-like/repair-associated markers (CD206 and Arg-1), suggesting a shift toward a more anti-inflammatory microglial activation profile based on the assessed marker pane. Conclusions: These results suggested that DDB can suppress the production of inflammatory cytokines and modulate microglial polarization, which indicated that DDB can be used as an effective compound in the prevention of neuroinflammation-related disorders.