ArticleEndocrine, metabolic & immune disorders drug targets2026
Therapeutic Potential of Phellodendrine/ Atractylenolide-I Combination in Rheumatoid Arthritis: Targeting Neutrophil Apoptosis through LTB4/BLT1 Pathway Suppression
Article in Endocrine, metabolic & immune disorders drug targets, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionTo investigate the therapeutic effects of rheumatoid arthritis (RA) Phellodendrine and Atractylenolide-I (PHE/ATL-1) on RA and their mechanisms.
methodsIn this study, first clinical experiments were conducted to investigate whether the delayed neutrophil apoptosis in the course of RA was related to the Leukotriene B4 (LTB4)/ Leukotriene B4 receptor 1 (BLT1) pathway, and then the effects of PHE/ATL-1 inhibition of the LTB4/BLT1 pathway to promote neutrophil apoptosis to inhibit inflammation were evaluated in vitro, as well as the in vivo effects of PHE/ATL-1 on the collagen-induced arthritis (CIA) model.
resultsClinical studies revealed elevated BLT1 expression in RA neutrophils, impairing apoptosis and exacerbating inflammation. In vitro, PHE/ATL-1 restored neutrophil apoptosis and reduced inflammation by inhibiting the LTB4/BLT1 pathway. The CIA mouse model further confirmed PHE/ATL-1's therapeutic potential in alleviating arthritis symptoms. DISCUSSION: PHE/ATL-1 ameliorates RA through LTB4/BLT1 pathway inhibition, reversing neutrophil apoptosis delay and attenuating inflammation. Clinical evidence of upregulated BLT1 in RA neutrophils and therapeutic efficacy in both in vitro and CIA models establishes PHE/ATL-1 as a compelling RA treatment candidate requiring clinical validation.
conclusionThese findings suggest that PHE/ATL-1 may serve as a potential therapeutic agent for RA treatment.
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