Sulfasalazine is a sulfonamide drug [1]. Sulfasalazine can inhibit the NF-κB pathway and reduce cytokine release, thereby regulating immune responses [2]. Sulfasalazine is commonly used to treat inflammatory bowel disease and rheumatoid arthritis [3-4].
In Jurkat T-lymphocytes, Sulfasalazine (0.2mM, 0.5mM, 1mM, 2mM; 24h) induces cell apoptosis [5]. In endothelial cells, Sulfasalazine (0.125mM, 24h) inhibits tritiated thymidine incorporation and cell proliferation [6]. In RBL5 cells, Sulfasalazine (1.25mM, 24h) inhibits NF-κB/Rel activation in mouse T lymphocytes [7].
In ICR mice, Sulfasalazine (250mg/kg, 500mg/kg, 1000mg/kg; po; 4 weeks) significantly increased serum levels of ALT, ALP and TBIL [8]. In DSS-Induced ulcerative colitis mice, Sulfasalazine (30mg/kg, 60mg/kg; ip; 7d) can inhibit colon length and mucosal inflammatory infiltration [9]. In middle cerebral artery occlusion mice, Sulfasalazine (5mg/kg, 10mg/kg; iv; single injection) could reduce the infarct size and improve neuro-motor function [10].
References:
[1]. Goldman P, Peppercorn MA. Sulfasalazine. New England Journal of Medicine. 1975 Jul 3; 293(1): 20-23.
[2]. Wahl C, Liptay S, Adler G, et al. Sulfasalazine: a potent and specific inhibitor of nuclear factor kappa B. The Journal of clinical investigation. 1998 Mar 1; 101(5): 1163-1174.
[3]. Peppercorn MA. Sulfasalazine: pharmacology, clinical use, toxicity, and related new drug development. Annals of Internal Medicine. 1984 Sep 1; 101(3): 377-386.
[4]. Plosker GL, Croom KF. Sulfasalazine: a review of its use in the management of rheumatoid arthritis. Drugs. 2005 Sep; 65: 1825-1849.
[5]. Liptay S, Fulda S, Schanbacher M, et al. Molecular mechanisms of sulfasalazine‐induced T‐cell apoptosis. British Journal of Pharmacology. 2002 Nov; 137(5): 608-620.
[6]. Sharon P, Drab EA, Linder JS, et al. The effect of sulfasalazine on bovine endothelial cell proliferation and cell cycle phase distribution: comparison with olsalazine, 5-aminosalicylic acid, and sulfapyridine. The Journal of laboratory and clinical medicine. 1992 Jan 1; 119(1): 99-107.
[7]. Liptay S, Bachem M, Hacker G, et al. Inhibition of nuclear factor kappa B and induction of apoptosis in T‐lymphocytes by sulfasalazine. British journal of pharmacology. 1999 Dec; 128(7): 1361-1369.
[8]. Li YC, Shen JD, Lu SF, et al. Transcriptomic analysis reveals the mechanism of sulfasalazine-induced liver injury in mice. Toxicology Letters. 2020 Mar 15; 321: 12-20.
[9]. Shin MR, Kim KJ, Kim SH, et al. Comparative Evaluation between Sulfasalazine Alone and in Combination with Herbal Medicine on DSS‐Induced Ulcerative Colitis Mice. BioMed Research International. 2017; 2017(1): 6742652.
[10]. Li X, Ding H, Jing J, et al. Sulfasalazine improves neuronal function in mice with ischemic stroke by inhibiting the STING/NF-κB pathway. Naunyn-Schmiedeberg's Archives of Pharmacology. 2025 May; 398(5): 5797-5810.
Sulfasalazine是一种磺胺类药物 [1]。Sulfasalazine可以抑制NF-κB通路并减少细胞因子释放，从而调节免疫反应 [2]。Sulfasalazine常用于治疗炎症性肠病和类风湿性关节炎 [3-4]。
在Jurkat T淋巴细胞中，Sulfasalazine（0.2mM、0.5mM、1mM、2mM；24h）诱导细胞凋亡 [5]。在内皮细胞中，Sulfasalazine（0.125mM；24h）抑制氚化胸苷的掺入和细胞增殖 [6]。在RBL5细胞中，Sulfasalazine（1.25mM；24h）抑制小鼠T淋巴细胞中的NF-κB/Rel活化 [7]。
在ICR小鼠中，Sulfasalazine（250mg/kg、500mg/kg、1000mg/kg；po；4周）显著升高血清ALT、ALP和TBIL水平 [8]。在DSS诱发的溃疡性结肠炎小鼠中，Sulfasalazine（30mg/kg、60mg/kg；ip；7d）可抑制结肠长度和粘膜炎症浸润 [9]。在大脑中动脉闭塞小鼠中，Sulfasalazine（5mg/kg、10mg/kg；iv；单次注射）可缩小梗死面积并改善神经运动功能 [10]。