Abstract
Objectives The Selaginella moellendorffii prescription (SMP) consists of S. moellendorffii Herba (SM), Smilacis glabrae Rhizoma (SGR), and Plantaginis Semen (PS). It has been commonly used to treat hyperuricemia and acute gouty arthritis as a hospital preparation. This study was aimed at investigating the best compatibility ratio of SMP on hyperuricemia and gouty arthritis and getting better insight of the possible mechanism. Methods. In vitro, anti-inflammatory activity of SMP was evaluated by lipopolysaccharide (LPS) induced RAW264.7 cells. The release of nitric oxide (NO) was screened by Griess assay, and NF-κB p65 and NLRP3 proteins expression was examined by immunofluorescence assay. Then, the levels of creatinine (Cr), blood urea nitrogen (BUN), and uric acid (UA) were detected in mice induced by potassium oxonate, and the paw oedema, inflammatory mediators, and histological examination were analyzed in rats induced by monosodium urate (MSU). HPLC method was employed to investigate the chemical profile of this preparation. Results. In vitro, SMP-3 (the ratio of SMP:SGR:PS was 3:1:1) exhibited the most potent anti-NO production activity without obvious toxicity. This anti-inflammatory effect was associated with suppression of NF-κB p65 nuclear translocation and NLRP3 protein expression. In animal experiments, the levels of BUN and Cr in SMP-3 group were lower than other extract groups, and the level of UA was also remarkably decreased by SMP-3 in hyperuricemic mice (P<0.01). Besides, SMP-3 extract was able to prevent the paw edema, reduce gouty joint inflammatory features, and decrease the levels IL-1β, PGE-2, IL-8, and NO in gouty arthritis rats. Furthermore, 6-C-β-D-xylopyranosyl-8-C-β-D-glucopyranosyl, apigenin, and astilbin were identified from SMP-3 extract. Conclusions In summary, SMP-3 may be a potential therapeutic agent for the prevention of hyperuricemic and gout.
Highlights
Gout is the chronic inflammatory arthritis which is caused by hyperuricemia and the deposition of monosodium urate (MSU) crystals in the articular cavity [1]
Hyperuricemia is defined as uric acid (UA) level > 7.0 mg/dL, which derives from the increase in purine metabolism and impairment of renal excretion of UA [3, 4]
According to the theory of Chinese medicine, excessive internal dampness and phlegm turbidity are the key cause of hyperuricemia [23]
Summary
Gout is the chronic inflammatory arthritis which is caused by hyperuricemia and the deposition of MSU crystals in the articular cavity [1]. Hyperuricemia is the most dominant factor in gout occurrence and clearly associated with a variety of comorbidities, including cardiovascular diseases [5], chronic kidney disease [6], and urolithiasis and metabolic syndrome [3]. The drugs used for gout treatment include allopurinol (ALL), probenecid, colchicine (COL), interleukin-1 (IL-1) inhibitors, glucocorticoids, and other anti-inflammatory drugs [8, 9]. These drugs are generally effective, they will increase the risk of ADR in some patients who have preexisting renal, liver, gastrointestinal, and cardiovascular diseases [10, 11]
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