Abstract
Gouty arthritis (GA) is an inflammatory disease owing to the accumulation of monosodium urate (MSU) in joints, leading to redness and burning pain. In this study, the effect of Zisheng Shenqi Decoction (ZSD) on a rat model of MSU-induced GA was investigated. ZSD obviously diminished the right paw thickness, the degree of the swelling of the paw, and the infiltration of the inflammatory cell, as well as cartilage erosion, and widened the joint space in MSU-treated rats. Besides, MSU remarkably elevated the release of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-18; however, ZSD treatment dose dependently lowered these levels and resulted in a significant decrease in articular elastase activity. Also, ZSD administration increased the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) but declined malondialdehyde (MDA) and nitrogen monoxide (NO) contents. Importantly, western blotting analysis revealed that NOD-like receptor protein 3 (NLRP3), cleaved caspase-1, IL-1β, nuclear factor-E2-related factor 2 (Nrf2) in the cytoplasm, phosphorylated mammalian target of rapamyclin (p-mTOR), and p62 expressions were downregulated, whereas the levels of nuclear Nrf2, phosphorylated AMP-activated protein kinase (p-AMPK), Beclin-1, and LC3II/I were upregulated by ZSD. Immunofluorescence assay indicated that ZSD evidently promoted nuclear translocation of LC3. Taken together, ZSD inhibited inflammation and oxidative stress and facilitated autophagy through the activation of the AMPK pathway and suppression of the mTOR signaling pathway, demonstrating its potential for preventing and curing GA.
Highlights
Excessive alcohol intake, obesity, type 2 diabetes mellitus, hypertension, metabolic syndrome, chronic kidney disease, and the use of medications are capable of increasing the risk of gout [1]
We demonstrated that Zisheng Shenqi Decoction (ZSD) could activate the AMP-activated protein kinase (AMPK) signaling pathway and inhibit the mammalian target of the rapamyclin pathway to promote autophagy in a rat model of Gouty arthritis (GA)
The monosodium urate (MSU)-mediated rats developed the swelling of the right paw, whereas pretreatment with ZSD obviously attenuated this process (Figure 1(b))
Summary
Obesity, type 2 diabetes mellitus, hypertension, metabolic syndrome, chronic kidney disease, and the use of medications are capable of increasing the risk of gout [1]. Gout is a metabolic disease involved in joint pain, fatigue, and high fever, second only to diabetes in China [2, 3]. Gouty arthritis (GA) is an acute inflammatory response caused by formation and precipitation of monosodium urate (MSU) crystals in the articular and Evidence-Based Complementary and Alternative Medicine surrounding joints with high disability rate, which is the most common first clinical manifestation in gout [4]. Varieties of proinflammatory indicators such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-18 release are exacerbated through the deposition of MSU crystals, thereby resulting in intense pain and swelling, as well as articular inflammation [5]. Mast cells, monocytes/macrophages, and neutrophils take part in gouty inflammatory response. Colchicine, corticosteroids, and nonsteroidal anti-inflammatory drugs (NSAIDs) have been widely utilized for the treatment of GA, they still have some side effects containing renal toxicity, gastritis, and gastrointestinal bleeding [8, 9]. erefore, it is vital to seek for novel and curative drugs to prevent and treat GA
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