Abstract
Context: Rheumatoid arthritis (RA) is a common systemic auto-immune disease, which is characterized by chronic and symmetry synovial inflammation. Crocin has been reported to exhibit anti-inflammatory effects in animal models.Objective: This study investigates the anti-inflammatory and anti-arthritic effects of crocin on type II collagen-induced arthritis (CIA) in Wistar rats.Materials and methods: The CIA rat model was established and randomly divided into five groups with or without crocin treatment (10, 20 or 40 mg/kg), which was started on day 21 after arthritis induction and persisted for 36 days. The symptoms and molecular mechanisms of CIA and crocin-treated CIA rats were compared and investigated.Results: CIA rats presented severe RA symptoms, including high arthritis score, paw swelling, joint inflammation, bone erosion, chondrocyte death, cartilage destruction, enhanced expressions of matrix metalloproteinase (MMP) and pro-inflammatory cytokines. However, crocin could mitigate these symptoms. Crocin (40 mg/kg) exhibited the most efficient therapeutic function on CIA rats: the histological scores of joint inflammation, bone erosion, chondrocyte death, cartilage surface erosion, and bone erosion of CIA rats receiving 40 mg/kg crocin treatment were comparable to the normal rats. MMP-1, -3 and -13 protein expression levels of CIA rats with 40 mg/kg crocin treatment were decreased to levels similar to normal rats. Moreover, crocin could also inhibit the expression of TNF-α, IL-17, IL-6 and CXCL8 in serum and ankle tissues of CIA rats.Conclusions: In summary, crocin exhibits therapeutic potential for RA, by mitigating the symptoms and inhibiting the pro-inflammatory factor expression.
Highlights
Rheumatoid arthritis (RA) is a common systemic auto-immune disease characterized by chronic and symmetry synovial inflammation, which potentially leads to irreversible joint destruction (Nakken et al 2017)
As RA has been reported to be associated with major histocompatibility complex (MHC) class II genes (Griffiths et al 1992; Rosloniec et al 1996), it is speculated that T cells play an essential role in the pathogenesis of RA, which is supported by experimental evidence: mice with CD4 deficiency were less susceptible to collagen-induced arthritis (CIA) compared to wild-type mice (Ehinger et al 2001)
Our results indicated that after the initial crocin administration, arthritis scores decreased in CIA rats compared to the control group (Figure 1(A))
Summary
Rheumatoid arthritis (RA) is a common systemic auto-immune disease characterized by chronic and symmetry synovial inflammation, which potentially leads to irreversible joint destruction (Nakken et al 2017). Most auto-immune diseases result from targeting of autologous proteins by auto-reactive T cells and antibodies in both human and animal models (Cho et al 2007). Type II collagen (CII) is one of the major auto-antigens in human RA, as the incidences of anti-CII antibodies and CIIspecific T cells are relatively high (Kim et al 1999, 2000). Type II collagen-induced arthritis (CIA) animal models have been widely used to study human RA, as they demonstrate that auto-immunity to CII can lead to auto-immune arthritis, with symptoms such as bone erosion, cartilage destruction and synovial joints (Cho et al 2007). Studies support the essential role of Th17 in CIA, where antibody neutralizing the endogenous IL-17 or IL-22 deletion could alleviate RA symptoms (Lubberts et al 2004; Geboes et al 2009; Kelchtermans et al 2009)
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