Baicalin alleviates collagen‑induced arthritis and suppresses TLR2/MYD88/NF‑κB p65 signaling in rats and HFLS‑RAs.

Abstract

Baicalin is a flavonoid isolated from the root of Scutellaria baicalensis with anti-inflammatory, antioxidant and antiapoptotic pharmacological properties. However, the therapeutic effect of baicalin on rheumatoid arthritis (RA) is not completely understood. The present study aimed to explore the therapeutic potential and mechanisms underlying baicalin in collagen-induced arthritis (CIA) model rats. CIA was induced in male SD rats. The hind paw thickness and severity of joint injury were monitored to assess the onset of arthritis. At 28 days after the initial immunization, different doses of baicalin were administered once daily via oral gavage for 40 days. The radiologic and pathological alterations were examined using X-ray, and hematoxylin and eosin staining, respectively. ELISA was employed to measure the serum levels of proinflammatory cytokines. Reverse transcription-quantitative PCR and western blotting were conducted to determine the expression of toll-like receptor (TLR)2, myeloid differentiation factor 88 (MYD88) and NF-κB p65. Baicalin treatment noticeably alleviated radiographic and histologic abnormalities in the hind paw joints of CIA model rats in a dose-dependent manner. The serum levels of proinflammatory cytokines were significantly decreased in baicalin-treated CIA model rats compared with vehicle-treated CIA model rats. The mRNA expression levels of TLR2 and MYD88, as well as the protein expression levels of TLR2, MYD88 and NF-κB p65 were significantly decreased by baicalin treatment in the synovial tissue of CIA model rats and human RA fibroblast-like synoviocytes. The results suggested that baicalin may exert a beneficial effect on CIA, which may be mediated by inhibiting the TLR2/MYD88/NF-κB signaling pathway.