Saroglitazar Ameliorates Pulmonary Fibrosis Progression in Mice by Suppressing NF-κB Activation and Attenuating Macrophage M1 Polarization.

ABSTRACT: Background and Objectives: Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease with limited therapeutic options. Current therapies (pirfenidone, nintedanib) exhibit modest efficacy and significant side effects, underscoring the need for novel strategies targeting early pathogenic drivers. Saroglitazar (SGZ), a dual PPARα/γ agonist with anti-inflammatory properties approved for diabetic dyslipidemia, has not been explored for IPF. We aimed to investigate SGZ's therapeutic potential in pulmonary fibrosis and elucidate its mechanisms of action. Materials and Methods: Using a bleomycin (BLM)-induced murine pulmonary fibrosis model, we administered SGZ therapeutically. A histopathological assessment (H&E, Masson's trichrome, collagen I immunofl

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC12299589 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature