Leonurine microcomposite depots alleviate endometriosis and rheumatoid arthritis via shared anti-inflammatory cascades

Shiyu Meng, Jingyi Zhong, Yi Xiao, Xican Zhang, Zhuang Tang, Zhiling Song, Xiaoxue Yang, Yi Zhun Zhu, Xiaolin Wang, Hui Guo
In: International Journal of Pharmaceutics: X · 2026 · vol. 12 , pp. 100690 · doi:10.1016/j.ijpx.2026.100690 · W7222783504
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Leonurine microcomposite depots alleviate endometriosis and rheumatoid arthritis by suppressing inflammatory cytokines to restore autophagy, apoptosis, and bone homeostasis with an excellent safety profile.

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Abstract

Chronic inflammatory diseases, such as endometriosis (EMS) and rheumatoid arthritis (RA), share a common pathogenic hallmark driven by a hyperinflammatory microenvironment. Nonetheless, long-acting therapeutic platforms capable of concurrently addressing these disparate disorders remain rarely explored. Herein, we developed a leonurine microcrystal-encapsulated microcomposite depot (Leo-micro@MD) capable of effectively mitigating inflammation, thereby reversing the progression of both EMS and RA. Systemic formulation optimization yielded an optimized Leo-micro@MD formulation with high drug loading and a sustained, burst-free release profile extending over 18 days, markedly reducing administration frequency. Mechanistically, Leo-micro@MD suppresses key upstream inflammatory cytokines, thereby branching into distinct downstream therapeutic pathways tailored to each disorder. In EMS, this reduction attenuated estrogen-ERα signaling and restored progesterone receptor B (PRB) expression, subsequently reactivating LC3B-mediated autophagy and Bax/Bcl-2-dependent apoptosis to eradicate ectopic lesions. Concurrently, in an adjuvant-induced arthritis rat model, this anti-inflammatory cascade attenuates synovial hyperplasia, rescues bone mineral density and trabecular architecture, and re-establishes articular matrix homeostasis, as confirmed by micro-CT and comprehensive histopathology. Importantly, these disease-modifying effects are achieved with an excellent systemic safety profile, with no detectable hepatotoxicity, nephrotoxicity, or immune organ damage. Collectively, this study provides a robust and translatable controlled-release strategy for the comprehensive management of chronic inflammatory diseases.

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