Emodin for pulmonary fibrosis: a systematic review and meta-analysis of efficacy and molecular mechanisms

TL;DR

This study reviews and analyzes how emodin, a compound, may help treat pulmonary fibrosis by reducing inflammation and fibrosis in animal models.

Contribution

The study provides a systematic review and meta-analysis of emodin's anti-fibrotic effects and mechanisms in animal models of pulmonary fibrosis.

Findings

Emodin significantly reduces fibrosis severity, inflammation, and oxidative stress in animal models.

It mitigates collagen deposition and epithelial-mesenchymal transition, key factors in fibrosis progression.

Variations in dosing and animal species contribute to study heterogeneity.

Abstract

This systematic review and meta-analysis aimed to evaluate emodin’s therapeutic efficacy in animal models of pulmonary fibrosis (PF) and summarize its anti-fibrotic mechanisms, providing a theoretical basis for the application of emodin in the clinical treatment of fibrosis.

A comprehensive literature search was conducted across 4 major international databases and 4 Chinese databases through July 2025. Study quality was assessed using the SYRCLE risk of bias tool. The mean difference (MD) or standardized mean difference (SMD) with 95% confidence intervals (CIs) was used to evaluate emodin’s effects on fibrosis severity, histopathological damage, inflammation, oxidative stress, and epithelial-mesenchymal transition (EMT).

Meta-analysis revealed emodin significantly attenuated PF across multiple scales [Szapiel score: SMD = −1.73, 95% CI: −2.02 to −1.43; Ashcroft score: SMD = −3.10, 95% CI: −4.40 to −1.79; fibrotic area: SMD = −4.97, 95% CI: −7.87 to −2.08]. Emodin substantially reduced hydroxyproline content (SMD = −1.91, 95% CI: −2.42 to −1.41) and collagen deposition, while improving alveolitis (SMD = −1.89, 95% CI: −2.21 to −1.57) and lung coefficients (SMD = −1.35, 95% CI: −2.06 to −0.65). Emodin also mitigated inflammation by reducing pulmonary levels of IL-6 (SMD = −3.86, 95% CI: −6.21 to −1.51), IL-1β (SMD = −3.21, 95% CI: −4.90 to −1.53), and TNF-α (SMD = −3.31, 95% CI: −3.96 to −2.67). Additionally, it attenuated oxidative stress and inhibited EMT by elevating SOD activity (SMD = 4.69, 95% CI: 3.59 to 5.80) while decreasing MDA (SMD = −3.58, 95% CI: −4.48 to −2.68) and TGF-β levels (SMD = −2.72, 95% CI: −3.41 to −2.02).

Emodin effectively alleviates PF through reducing collagen deposition, attenuating inflammation, suppressing oxidative stress, and inhibiting EMT. Subgroup analyses indicated that heterogeneity across studies was partly attributable to variations in dosing regimens and animal species. Further investigation into the anti-fibrotic properties of emodin is warranted to facilitate its therapeutic development.

CRD420251131483, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251131483.

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