Pharmacological Network Analysis of the Functions and Mechanism of Quercetin From Jisuikang (JSK) in Spinal Cord Injury (SCI)

Journal of Cellular and Molecular Medicine, 2024 · DOI: https://doi.org/10.1111/jcmm.70269 · Published: November 26, 2024

Spinal Cord Injury Pharmacology Immunology

Simple Explanation

This study investigates how Quercetin, a compound from a Chinese herbal formula called Jisuikang (JSK), can protect against inflammation and cell damage in spinal cord injury (SCI). They found that Quercetin can reduce inflammation and promote the polarization of macrophages to M2 type. The researchers used network pharmacology to identify Quercetin as a key component of JSK. They then tested Quercetin on microglial cells (immune cells in the spinal cord) and in a rat model of SCI. The results showed that Quercetin can reduce inflammation and promote the polarization of macrophages to M2 type, which is associated with tissue repair. These effects are partially mediated by IL1R1, a protein involved in inflammation.

Study Duration

Not specified

Participants

Male Sprague–Dawley rats weighing 200–250 g

Evidence Level

Not specified

Key Findings

1
Quercetin, a key ingredient in Jisuikang (JSK), protects microglial cells from LPS-induced inhibition of cell viability and cellular inflammation.
2
Quercetin modulates microglia M1/M2 polarization, inhibiting pro-inflammatory M1 polarization and promoting anti-inflammatory M2 polarization.
3
The protective effects of Quercetin are partially attenuated by IL1R1 overexpression, suggesting that IL1R1 plays a role in Quercetin's mechanism of action.

Research Summary

This study investigated the protective effects of quercetin, a compound found in the Chinese herbal formula Jisuikang (JSK), on spinal cord injury (SCI). The research used network pharmacology to identify quercetin as a key active ingredient and then examined its effects in vitro using microglial cells and in vivo using a rat SCI model. The results demonstrated that quercetin protects against LPS-induced cell viability inhibition and cellular inflammation in microglial cells. It also modulates microglia M1/M2 polarization, inhibiting pro-inflammatory M1 polarization and promoting anti-inflammatory M2 polarization. Furthermore, in an SCI rat model, quercetin improved histopathological alterations, reduced local inflammation, and facilitated M2 macrophage polarization. These beneficial effects were partially attenuated by IL1R1 overexpression, suggesting that IL1R1 plays a role in quercetin's mechanism of action.

Practical Implications

Drug Development

Quercetin could be developed as a therapeutic agent for SCI, potentially as an alternative or adjunct to current treatments.

Dietary Supplementation

Increased intake of quercetin-rich foods might offer a protective effect against neuroinflammation in individuals at risk of SCI.

Personalized Medicine

Understanding the role of IL1R1 in quercetin's mechanism of action could lead to personalized treatment strategies based on individual IL1R1 expression levels.

Study Limitations

1
Use of a non-cell-specific lentiviral vector for IL1R1 overexpression.
2
Lack of a detailed compositional analysis of the JSK formula.
3
Whether other JSK active ingredients could synergistically interact with quercetin still needs investigation.

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