Narirutin mitigates neuroinflammation following traumatic brain injury and modulates microglial polarization via the JAK2/STAT3 signaling pathway

TL;DR

Narirutin reduces brain inflammation after injury by modulating immune cell activity and signaling pathways in mice.

Contribution

This study is the first to show Narirutin's anti-inflammatory effects in traumatic brain injury via the JAK2/STAT3 pathway.

Findings

Narirutin reduces neuroinflammation by suppressing NLRP3, IL-1β, and IL-6 in TBI models.

Narirutin promotes microglial M2 polarization and inhibits JAK/STAT phosphorylation.

Narirutin improves behavioral outcomes in TBI mice.

Abstract

Traumatic brain injury (TBI) causes irreversible cerebral damage characterized by neuroinflammation and neuronal injury, representing a critical factor contributing to poor prognosis in TBI patients. While existing studies have demonstrated Narirutin’s (Nar) neuroprotective effects in Parkinson’s disease, research on Nar in the context of traumatic brain injury remains markedly limited. This investigation elucidates Nar’s protective mechanisms in murine TBI models.

The behavioral tests of TBI model mice were conducted using the Morris water maze method. HE staining, Nissl staining and immunohistochemistry were performed. Western blotting was used to detect inflammatory indicators, and immunofluorescence was used to detect microglial polarization.

Nar significantly reduced the inflammatory response and abnormal activation of signaling pathways induced by TBI. This effect is achieved by reducing the expression levels of NLRP3, IL-1β, and IL-6, promoting M2 polarization in microglia, and inhibiting the phosphorylation of JAK and STAT within the TBI model.

In conclusion, our research results indicate that Nar can improve neuroinflammation in TBI model mice, demonstrating excellent anti-inflammatory effects and neuroprotective properties, providing potential therapeutic strategies for the clinical treatment of TBI.

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