Vitexin alleviates inflammation and enhances apoptosis through the regulation of the JAK/STAT/SOCS signaling pathway in the arthritis rat model

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory and autoimmune disorder. RA is progressive and needs long-term treatment. Vitexin is a naturally-occurring flavonoid that is identified in various plant sources. Vitexin is demonstrated to produce antioxidant effects with numerous pharmacological activities. This experimental in vivo study assessed the antiarthritic and apoptotic role of a natural plant extract, vitexin, on RA. Collagen-induced arthritis (CIA) rat model Sprague Dawley males were grouped into five sets with six rats each: control, CIA, CIA + vitexin (10 mg/kg bw), CIA + Methotrexate (1 mg/kg bw), and vitexin (10 mg/kg bw) alone.The body weight, organ weight, biochemical assay, inflammatory enzymes, apoptosis, and cytokines levels were evaluated and compared among groups. Janus kinase (JAK)/signal transducer and activator of transcription (STAT)/suppressors of cytokine signaling (SOCS) levels and histopathology of ankle joints were also studied and compared. Significance was considered at a p < 0.05. Vitexin (10 mg/kg bw) significantly reduced the inflammatory enzyme markers, interleukin (IL)-1β, IL-6, IL-17, IL-4, IL-10, tumor necrosis factor-α, interferon-γ, and iNOS levels in arthritis rats (p < 0.05). Vitexin significantly improved collagen-induced arthritic histological changes (p < 0.05). Vitexin also reduced JAK/STAT expressions associated with inflammation and significantly increased elevated SOCS levels (p < 0.05). Aberration in apoptosis, inflammatory mediators, C-reactive protein, and rheumatoid factor levels in the arthritic rats reverted to normal with vitexin. These results emphasize that vitexin possesses anti-inflammatory and apoptotic activity via the regulation of JAK/STAT/SOCS signaling in CIA in a rat model. Hence, vitexin is a promising auxiliary drug for RA treatment.

Natural anti‐inflammatory products for osteoarthritis: From molecular mechanism to drug delivery systems and clinical trials

“…Furthermore, Vitexin also suppresses OA chondrocyte apoptosis via regulation of ER stress (Xie et al, 2018). Although the specific mechanism by which Vitexin regulates apoptosis in OA chondrocytes remains to be elucidated, recent studies have explored the relevant mechanisms under RA conditions and demonstrated that Vitexin has anti‐inflammatory and apoptotic activities by modulating JAK/STAT/SOCS signaling in a collagen‐induced arthritis rat model (Zhang, Ning, & Wang, 2022). Kong et al (2017) reported the promoting effect of the JAK/STAT/SOCS signaling pathway on IL‐10 production, which is well known as an anti‐inflammatory cytokine, and demonstrated that the activation of JAK/STAT/SOCS signaling also could be found in OA chondrocytes.…”

Vitexin Regulates Heat Shock Protein Expression by Modulating ROS Levels Thereby Protecting against Heat-Stress-Induced Apoptosis

“…It can also increase the expression of epidermal growth factor in chickens on the 6th, 10th, and 15th day of heat stress, thereby reducing stressinduced intestinal mucosal damage [10][11][12][13][14]. As a natural polyphenol, vitexin, which is present in high concentrations in mung beans, hawthorn, and other foods, has a strong antioxidant activity [15] and has been widely used for the prevention and treatment of various diseases because of its functional and pharmacological activities [16]. It was shown that vitexin could alleviate heat-stress-induced apoptosis by upregulating antioxidant enzyme activities and endoplasmic reticulum-stress-mediated autophagy [17]; however, whether vitexin can relieve apoptosis induced by heat stress by regulating the ROS level and the heat shock protein expression has not been investigated.…”