Introduction Inflammation and joint damage are hallmarks of rheumatoid arthritis (RA), a chronic autoimmune disease. Objectives This study investigated the anti-arthritic efficacy and mechanisms of Syringic acid (SA), a natural phenolic compound, in a Complete Freund's Adjuvant (CFA)-induced arthritis rat model. Methods Arthritis was induced in Wistar rats, which were then orally treated with SA (50, 100, 200 mg/kg) or prednisolone for 28 days. Paw swelling, arthritic index, body weight, motor functions, cytokine levels (Nuclear factor kappa B (NF-κB), Tumor necrosis factor alpha (TNF-α), Interleukin-6 (IL-6), Interleukin-1 beta (IL-1β)), antioxidant enzyme activities, histopathology, and radiological changes were assessed. Molecular docking studies were also performed. Results SA significantly reduced paw swelling and arthritic index, improved body weight and motor functions, and modulated inflammatory cytokines (NF-κB, TNF-α, IL-6, IL-1β) and oxidative stress markers dose-dependently. Histopathological and radiological analyses confirmed SA's protective effects on joint integrity. Docking studies showed strong binding affinities of SA to NF-κB and TNF-α. SA exhibits significant anti-inflammatory and anti-arthritic properties in CFA-induced RA, modulating cytokine pathways and reducing oxidative stress. Conclusion These findings suggest SA's potential as a therapeutic agent for RA, warranting further clinical investigation.<Table Float="No" ID="Taba"> <tgroup cols="2"> <colspec align="left" colname="c1" colnum="1" /> <colspec align="left" colname="c2" colnum="2" /> <tbody> <row> <entry align="left" nameend="c2" namest="c1"> Key Points • Syringic acid (SA) modulated key pro-inflammatory cytokines (NF-κB, TNF-α, IL-6, IL-1β) and enhanced antioxidant enzyme activities. • Molecular docking demonstrated strong binding of SA with NF-κB and TNF-α, supporting its immunomodulatory role. • The findings highlight SA’s potential as a natural immunomodulator for RA, warranting further clinical exploration. </entry> </row> </tbody> </tgroup> </Table> Graphical abstract

Protective effects of Syringic acid on joint inflammation and damage in a rat model of rheumatoid arthritis

期刊论文
发表日期：

2026年3月6日

查看全文

Pankaj Singh,
Siddhi Bagwe Parab,
Afreen Khan,
Gaurav Doshi

摘要

Introduction

Inflammation and joint damage are hallmarks of rheumatoid arthritis (RA), a chronic autoimmune disease.

Objectives

This study investigated the anti-arthritic efficacy and mechanisms of Syringic acid (SA), a natural phenolic compound, in a Complete Freund's Adjuvant (CFA)-induced arthritis rat model.

Methods

Arthritis was induced in Wistar rats, which were then orally treated with SA (50, 100, 200 mg/kg) or prednisolone for 28 days. Paw swelling, arthritic index, body weight, motor functions, cytokine levels (Nuclear factor kappa B (NF-κB), Tumor necrosis factor alpha (TNF-α), Interleukin-6 (IL-6), Interleukin-1 beta (IL-1β)), antioxidant enzyme activities, histopathology, and radiological changes were assessed. Molecular docking studies were also performed.

Results

SA significantly reduced paw swelling and arthritic index, improved body weight and motor functions, and modulated inflammatory cytokines (NF-κB, TNF-α, IL-6, IL-1β) and oxidative stress markers dose-dependently. Histopathological and radiological analyses confirmed SA's protective effects on joint integrity. Docking studies showed strong binding affinities of SA to NF-κB and TNF-α. SA exhibits significant anti-inflammatory and anti-arthritic properties in CFA-induced RA, modulating cytokine pathways and reducing oxidative stress.

Conclusion

These findings suggest SA's potential as a therapeutic agent for RA, warranting further clinical investigation.

Key Points

• Syringic acid (SA) modulated key pro-inflammatory cytokines (NF-κB, TNF-α, IL-6, IL-1β) and enhanced antioxidant enzyme activities.

• Molecular docking demonstrated strong binding of SA with NF-κB and TNF-α, supporting its immunomodulatory role.

• The findings highlight SA’s potential as a natural immunomodulator for RA, warranting further clinical exploration.

Graphical abstract