ArticleEndocrine, metabolic & immune disorders drug targets2026
Paricalcitol Attenuates Bleomycin-induced Pulmonary Fibrosis: Insights from Immunohistochemical and Molecular Genetic Analysis.
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
introductionPulmonary fibrosis is a progressive disease marked by excessive fibrotic transformation of lung tissue. Paricalcitol, a selective vitamin D receptor (VDR) agonist, has shown promise in reducing fibrosis in experimental models, primarily due to its anti-inflammatory and anti-fibrotic properties. This study evaluates the therapeutic effects of paricalcitol on bleomycin-induced pulmonary fibrosis in a rat model. MATERIALS AND
methodsFifty-four male Wistar rats were randomly assigned to three groups: a control group, a bleomycin-induced pulmonary fibrosis group (PF), and a bleomycin-induced pulmonary fibrosis group with paricalcitol treatment (PF+P). Pulmonary fibrosis was induced via intratracheal bleomycin instillation, and paricalcitol was administered every two days to the PF+P group. Effects were assessed through histopathological, immunohistochemical, and molecular genetic analyses, including mRNA expression levels of inflammatory and fibrotic markers at 10, 20, and 30 days.
resultsParicalcitol treatment significantly reduced fibrosis severity, with the Aschoff score decreasing on day 30 to 2.50±0.63 compared with 5.88±0.52 in untreated PF rats (p = 0.02). The number of CD80+ M1 macrophages was reduced on day 10 (29.9±3.8 vs 64.2±5.2, p = 0.001), while CD163+ M2 macrophages were increased (30.7±2.7 vs 21.7±2.8, p = 0.03) compared to the control group. Paricalcitol also decreased TGF-β1 expression on day 30 (47.1±5.3 vs 70.8±7.1, p = 0.03) and MMP-9 on day 20 (28.9±2.5 vs 76.4±4.7, p < 0.001). DISCUSSION: The present study investigates the effects of paricalcitol, a selective vitamin D receptor (VDR) agonist, on bleomycin-induced pulmonary fibrosis, revealing notable reductions in inflammatory and fibrotic markers. Our findings indicate that paricalcitol treatment (PF+P group) significantly attenuates fibrosis severity, as observed through histopathological, immunohistochemical, and molecular genetic analyses.
conclusionParicalcitol markedly reduces fibrosis severity, as shown through histopathological, immunohistochemical, and molecular genetic analyses. The treatment decreased the expression of key fibrotic and inflammatory markers, including TGF-β, MMP9, IL-1β, and TNF-α, and shifted macrophage polarization toward an anti-inflammatory M2 phenotype. These findings suggest paricalcitol's potential in modulating the immune response and highlight its therapeutic promise.
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