Skip to main content
Fig. 1 | Arthritis Research & Therapy

Fig. 1

From: Prolactin blocks the expression of receptor activator of nuclear factor κB ligand and reduces osteoclastogenesis and bone loss in murine inflammatory arthritis

Fig. 1

The long prolactin (PRL) receptor isoform increases in the joints and PRL reduces the systemic levels of C-reactive protein and TNFα and the expression of transcription factors and cytokines related to T helper 17 (Th17) cells and regulatory T cells in the joints of rats subjected to polyarticular adjuvant-induced arthritis (AIA). Osmotic minipumps delivering PRL were positioned (or not positioned) 3 days before the intradermal injection of complete Freund’s adjuvant (CFA) to induce AIA in rats. All evaluations were performed 21 days after injection of CFA. a Serum PRL levels, b ankle circumference, and c quantitative real-time PCR (qRT-PCR) quantification of Tnfa, Il1b, Il6, and Ifng mRNA levels in ankle joints. d qRT-PCR and western blot evaluation of PRL receptor (Prlr) long (Long) and short (Short) isoform mRNA and long PRL receptor protein (PRLR Long), respectively. Bars show the quantification of PRLR Long/β-Tubulin by densitometry (n = 3). e C-reactive protein (CRP) and f TNFα levels in serum. g qRT-PCR quantification of the mRNA levels of the Th17-cell-related transcription factors, Rora and Rorc, and cytokine genes Il17a, Il21, Il22, and Il23 in the ankle joints. h qRT-PCR quantification of the mRNA levels of the regulatory-T-cell-related transcription factor Foxp3 and cytokine genes Ebi3, Il12a, Tgfb1, Il10 in the ankle joints. Values are means ± SEM (n = 5–12). *P < 0.05, **P < 0.01, ***P < 0.001, n.s. non-significant

Back to article page