S-allyl cysteine (SAC) is known for its various beneficial effects such as neuroprotection and immunomodulation. The beneficial effect of SAC against gout has not been explored. The present study aims to describe the two roles of SAC: (1) inhibitory effect against xanthine oxidase (XO) enzyme activity; and (2) anti-inflammatory property against MSU crystal-induced gouty inflammation in rat. The inhibitory effect of SAC against bovine XO enzyme activity was determined in vitro. In silico analysis was carried out to determine the intermolecular interaction between SAC and bovine XO. MSU crystal was injected in the right paw of the rat to induce gouty inflammation. SAC (40 mg/kg body weight) and colchicine (positive control; 1 mg/kg body weight) was given for 3 days. At the end of the treatment, the oxidative stress, antioxidant parameters and mitochondrial function were determined in the ankle joint tissue. The concentration of inflammatory cytokines such as TNF-α and IL-1β was measured in the serum using ELISA. SAC inhibited (IC₅₀ value, 33 μg/ml) XO enzyme activity in a competitive mode with corresponding Ki value of 4 μg/ml. In silico analysis predicted the interaction of SAC with the amino acids such as Arg880, Phe798, Phe914 and Phe1009 of XO enzyme. The root mean square deviation, root mean square fluctuation and free energy calculation values confirmed the stable SAC-XO interaction. The inhibition of SAC on XO enzyme activity in in vivo was further confirmed by silkworm model. SAC through reducing oxidative stress, enhancing antioxidants, protecting mitochondrial function has shown anti-inflammatory effect against MSU crystal-induced gout which was observed as reduced level of inflammatory markers in the serum. The medicinal potential of SAC as a preventive agent through its XO inhibitory property as well as curative agent through its anti-inflammatory property against gout has been understood from the present study.

S-烯丙基半胱氨酸（SAC）因其各种有益作用而闻名，例如神经保护和免疫调节。尚未探讨SAC对痛风的有益作用。本研究旨在描述SAC的两个作用：（1）对黄嘌呤氧化酶（XO）酶活性的抑制作用；（2）抗MSU晶体引起的痛风性炎症的抗炎特性。测定了SAC对牛XO酶活性的抑制作用。在计算机上进行了分析，以确定SAC和牛XO之间的分子间相互作用。将MSU晶体注射到大鼠的右爪中，以引起痛风性炎症。给予SAC（40 mg / kg体重）和秋水仙碱（阳性对照； 1 mg / kg体重）3天。在治疗结束时，确定踝关节组织中的氧化应激，抗氧化剂参数和线粒体功能。使用ELISA测量血清中炎性细胞因子如TNF-α和IL-1β的浓度。SAC以竞争模式抑制（IC ₅₀值为33μg/ ml）XO酶活性，相应的Ki值为4μg/ ml。在计算机上分析预测了SAC与XO酶的氨基酸如Arg880，Phe798，Phe914和Phe1009的相互作用。均方根偏差，均方根波动和自由能计算值证实了SAC-XO相互作用稳定。家蚕模型进一步证实了SAC在体内对XO酶活性的抑制作用。SAC通过降低氧化应激，增强抗氧化剂，保护线粒体功能显示出对MSU晶体诱发的痛风的抗炎作用，这被认为是血清中炎症标记物水平的降低。通过本研究已经理解了SAC通过其XO抑制特性作为预防剂以及通过其对痛风的抗炎特性而作为治疗剂的医学潜力。