Diclofenac Potassium is a potent, non-selective cyclooxygenase (COX) inhibitor, with IC₅₀ values of 4nM and 1.3nM for human COX-1 and COX-2, respectively, in CHO cells, and 5.1μM and 0.84μM for ovine COX-1 and COX-2, respectively[1][2]. Diclofenac Potassium is a nonsteroidal anti-inflammatory drug (NSAID) widely used in clinical practice for its anti-inflammatory, analgesic, and antipyretic effects[3].
In vitro, Diclofenac Potassium (10-200mM; 24-72h) inhibited the proliferation of HepG2 and Hep3B cells in a dose-dependent manner. After 48h of treatment at 50mM, the inhibition rates are 40.47% and 54.49% for HepG2 and Hep3B cells, respectively, with IC₅₀ values of 70.54mM and 48.39mM[4]. Diclofenac Potassium (10-200mM; 24-72h) also upregulated COX-2 mRNA expression in both cell lines[4]. Diclofenac Potassium (0-60μM, 24-48h) dose-dependently inhibited neurite outgrowth and neuronal differentiation of neural stem cells (NSCs), and induced NSC death via activation of the caspase signaling cascade[3].
In vivo, Administration of Diclofenac Potassium (3mg/kg; twice daily for 5 days; p.o.) in male SD rats disrupted gastrointestinal integrity, resulting in a significant increase in fecal ⁵¹Cr excretion[1]. Oral Diclofenac Potassium (3mg/kg/d) for 15 days significantly reduced edema by day 3 and exhibited anti-hyperalgesic effects by day 9 in the rat model of repeated arthritis[5].
References:
[1] Riendeau D, Percival MD, Boyce S, et al. Biochemical and pharmacological profile of a tetrasubstituted furanone as a highly selective COX-2 inhibitor. Br J Pharmacol. 1997;121(1):105-117.
[2] Labib MB, Sharkawi SMZ, El-Daly M. Design, synthesis of novel isoindoline hybrids as COX-2 inhibitors: Anti-inflammatory, analgesic activities and docking study. Bioorg Chem. 2018;80:70-80.
[3] Kudo C, Kori M, Matsuzaki K, et al. Diclofenac inhibits proliferation and differentiation of neural stem cells. Biochem Pharmacol. 2003;66(2):289-295.
[4] Chen NN, Wu SG. Nan Fang Yi Ke Da Xue Xue Bao. 2006;26(6):814-817.
[5] Peter-Szabo, Mihaly et al. “Quantitative characterization of a repeated acute joint inflammation model in rats.” Clinical and experimental pharmacology & physiology vol. 34,5-6 (2007): 520-6.
Diclofenac Potassium是一种强效的非选择性环氧化酶（COX）抑制剂，在CHO细胞中对人源COX-1和COX-2的IC₅₀值分别为4nM和1.3nM；对羊源COX-1和COX-2的IC₅₀值分别为5.1μM和0.84μM[1][2]。Diclofenac Potassium是一种非甾体抗炎药（NSAID），因其具有抗炎、镇痛和解热作用而被广泛应用于临床[3]。
体外实验中，Diclofenac Potassium（10-200mM；24-72h）以剂量依赖性方式抑制HepG2和Hep3B细胞的增殖。在50mM处理48h后，对HepG2和Hep3B细胞的抑制率分别为40.47%和54.49%，其IC₅₀值分别为70.54mM和48.39mM[4]。Diclofenac Potassium（10-200mM；24-72h）还上调了这两种细胞系中的COX-2 mRNA表达水平[4]。Diclofenac Potassium（0-60μM；24-48h）以剂量依赖的方式抑制神经干细胞（NSCs）的神经突起生长及向神经元的分化，并通过激活caspase信号级联反应诱导NSCs死亡[3]。
体内实验中，Diclofenac Potassium（3mg/kg；每日两次连续5天；口服）在雄性SD大鼠中可破坏胃肠道完整性，导致粪便中⁵¹Cr排泄显著增加[1]。口服Diclofenac Potassium（3mg/kg/天）连续15天在反复关节炎大鼠模型中于第3天显著减轻水肿，在第9天表现出抗痛觉作用[5]。