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.

Baicalin Inhibits Inflammation in Rats with Chronic Obstructive Pulmonary Disease by the TLR2/MYD88/NF-κBp65 Signaling Pathway

“…Li et al found that the TLR2/MYD88/NF-κB signaling pathway reduced pulmonary fibrosis [33]. In addition, Bai et al found that BA may promote collagen-induced arthritis by inhibiting the TLR2/MYD88/NF-κB signaling pathway [34]. In our study, when giving BA treatment, it could reduce the levels of TLR2, MYD88, TNF-α, and IL-1β mRNA, thereby reduce the expressions of MYD88, p-NF-κBp65/NF-κBp65, TLR4, and TLR2, indicating that BA could downregulate the TLR2/ MYD88/NF-κBp65 signaling pathway, which is similar to the BA inhibiting TLR2/MYD88/NF-κB signaling pathway to reduce inflammation in fever rats [15,35].…”

Baicalein Induces Apoptosis of Rheumatoid Arthritis Synovial Fibroblasts through Inactivation of the PI3K/Akt/mTOR Pathway

“…BAI is a traditional Chinese herbal medicine with anti-inflammatory and antioxidant activities [ 23 , 24 ]. However, the therapeutic effect of BAI on RA is not fully understood [ 25 ]. Tang et al found that BAI may be a candidate drug for treatment of RA and the biological function of the grouping network related to the pathogenesis of RA is clarified.…”

Natural medicines of targeted rheumatoid arthritis and its action mechanism

“…( 53 ) showed that baicalin treatment could reduce joint inflammation in CIA rats, which was related to that baicalin could inhibit the expression of NF-κB p65 protein in synovial tissue and FLSs, and down-regulate NF-κB p65 acetylation by increasing Sirt1. Studies ( 54 , 55 ) have shown that the anti-RA effect of baicalin is related to the down-regulation of pro-inflammatory factors (TNF-α, IL-1β, and IL-6) and inflammatory markers (MMP-2, MMP-9, iNOS, and COX-2), the induction of monocyte apoptosis in synovial fluid of CIA mice, and the inhibition of JAK1/STAT3 and TLR2/MYD88/NF-κB p65 signal transduction. The above studies have shown that Baicalin has anti-RA activity.…”