Department of Pharmacology, School of Basic and Life Science, Hainan Medical University, Haikou, 571199, China.
HMC Cancer Institute, The First Affiliated Hospital of Hainan Medical University, Haikou, China.
BMC Complement Med Ther. 2021 Jul 20;21(1):202. doi: 10.1186/s12906-021-03364-5.
Gout is initiated by the precipitation of monosodium urate (MSU) crystals within the joints and soft tissues, and it can eventually cause acute or chronic arthritis. MSU crystals trigger, amplify, and maintain a strong inflammatory response through promoting proinflammatory activity. In this study, the therapeutic effects of Stephania hainanensis (S. hainanensis) total alkaloid (SHA) were tested and evaluated on MSU-induced acute gouty arthritis in a mouse model.
After oral administration of SHA (10 or 20 mg/kg) or the antigout medicine colchicine (0.5 mg/kg) once daily for 3 consecutive days, MSU crystals suspended in saline (2.5 mg/50 μl) were intradermally injected into the right paw of the mice. Then, SHA and colchicine were administered for another 2 days. During this period, swelling of the ankle and clinical scores were measured at 12, 24, and 48 h postinjection. After the mice were euthanized, inflammatory cytokine expression and paw tissue inflammation-related gene and protein expression, and a histopathological analysis was performed.
SHA had obvious therapeutic effects on MSU-induced acute gouty arthritis in mice. SHA alleviated ankle swelling and inhibited the production of cytokines, such as IL-1β and TNF-α. In addition, NLRP3, Caspase-1 and IL-1β, which are activated by MSU were also suppressed by SHA. The histological evaluation showed that SHA relieved the infiltration of inflammation around the ankle.
These results suggest that SHA is capable of anti-inflammatory activities and may be useful for treating gouty arthritis.
痛风是由单钠尿酸盐(MSU)晶体在关节和软组织中的沉淀引发的,最终可导致急性或慢性关节炎。MSU 晶体通过促进前炎性活性引发、放大和维持强烈的炎症反应。在这项研究中,我们测试和评估了海南蒌总碱(SHA)对 MSU 诱导的小鼠急性痛风性关节炎模型的治疗效果。
连续 3 天每天口服 SHA(10 或 20mg/kg)或秋水仙碱(抗痛风药,0.5mg/kg)一次后,将 MSU 晶体混悬于生理盐水中(2.5mg/50μl),皮内注射于小鼠右后足。然后,再给予 SHA 和秋水仙碱连续 2 天。在此期间,于注射后 12、24 和 48h 测量踝关节肿胀和临床评分。处死小鼠后,进行炎症细胞因子表达、爪组织炎症相关基因和蛋白表达以及组织病理学分析。
SHA 对 MSU 诱导的小鼠急性痛风性关节炎具有明显的治疗作用。SHA 减轻了踝关节肿胀并抑制了细胞因子(如 IL-1β 和 TNF-α)的产生。此外,SHA 还抑制了 MSU 激活的 NLRP3、Caspase-1 和 IL-1β。组织学评价表明 SHA 缓解了踝关节周围炎症的浸润。
这些结果表明 SHA 具有抗炎活性,可能对痛风性关节炎的治疗有用。