Moxifloxacin

Moxifloxacin is a fourth-generation, broad-spectrum 8-methoxyfluoroquinolone antibacterial agent. Moxifloxacin inhibits the activity of bacterial DNA topoisomerase II (DNA gyrase) and topoisomerase IV, thereby blocking bacterial DNA replication and transcription processes, ultimately leading to bacterial death. Moxifloxacin can be used in research related to respiratory tract infections, skin and skin structure infections, intra-abdominal infections, and tuberculosis (especially drug-resistant tuberculosis)^[1-4].

In vitro, Moxifloxacin (5-50μg/ml) was co-treated with TNF-α (50ng/ml) in cystic fibrosis bronchial epithelial cell lines IB3 and C38 cells for 48 hours. Moxifloxacin significantly inhibited the secretion of IL-8 and IL-6; Moxifloxacin (5-20μg/ml) was co-treated with TNF-α (50ng/ml) in IB3 and C38 cells for 15-60 minutes. Moxifloxacin significantly inhibited the activation of ERK1/2, JNK, and NF-κB^[5]. Moxifloxacin (0.05-1mg/ml) was used to treat immortalized human corneal endothelial cells (B4G12 cells) for 24-72 hours. Moxifloxacin induced dose-dependent cytotoxicity, increased reactive oxygen species generation and autophagy, activated caspase 2, 3, 8 pathways and induced apoptosis^[6].

In vivo, Moxifloxacin (12.5, 25, 50mg/kg; once daily) was orally administered to Wistar mice for 7 days. Moxifloxacin significantly increased serum creatinine, cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglyceride, urea levels and aspartate transaminase, alanine transaminase, alkaline phosphatase activities, while decreasing total bilirubin levels in mice^[7]. Moxifloxacin (100mg/kg; twice daily) was intraperitoneally injected into C57BL/6N mice for 2 days. Moxifloxacin significantly reduced the numbers and concentrations of total immune cells, neutrophils, and inflammatory mediators (KC, IL-1β, IL-17A) in the lungs after infection with live or heat-killed bacteria^[8].

References:
[1] Balfour JA, Wiseman LR. Moxifloxacin. Drugs. 1999 Mar;57(3):363-73; discussion 374.
[2] Al Omari MM, Jaafari DS, Al-Sou'od KA, Badwan AA. Moxifloxacin hydrochloride. Profiles Drug Subst Excip Relat Methodol. 2014;39:299-431.
[3] Miravitlles M, Anzueto A. Moxifloxacin: a respiratory fluoroquinolone. Expert Opin Pharmacother. 2008 Jul;9(10):1755-72.
[4] Khan F, Ismail M, Khan Q, et al. Moxifloxacin-induced QT interval prolongation and torsades de pointes: a narrative review. Expert Opin Drug Saf. 2018 Oct;17(10):1029-1039.
[5] Blau H, Klein K, Shalit I, et al. Moxifloxacin but not ciprofloxacin or azithromycin selectively inhibits IL-8, IL-6, ERK1/2, JNK, and NF-kappaB activation in a cystic fibrosis epithelial cell line. Am J Physiol Lung Cell Mol Physiol. 2007 Jan;292(1):L343-52.
[6] Park JH, Kim M, Chuck RS, et al. Evaluation of moxifloxacin-induced cytotoxicity on human corneal endothelial cells. Sci Rep. 2021 Mar 18;11(1):6250.
[7] Ukpo GE, Ebuehi OA, Kareem AA. Evaluation of Moxifloxacin-induced Biochemical Changes in Mice. Indian J Pharm Sci. 2012 Sep;74(5):454-7.
[8] Beisswenger C, Honecker A, Kamyschnikow A, et al. Moxifloxacin modulates inflammation during murine pneumonia. Respir Res. 2014 Jul 17;15(1):82.

Moxifloxacin是一种第四代、具有广谱抗菌活性的8-甲氧基氟喹诺酮类抗菌药。Moxifloxacin通过抑制细菌DNA拓扑异构酶Ⅱ（DNA旋转酶）和拓扑异构酶Ⅳ的活性，阻断细菌DNA复制与转录过程，最终导致细菌死亡。Moxifloxacin可用于呼吸道感染、皮肤及皮肤结构感染、腹腔内感染以及结核病（尤其是耐药结核病）的相关研究^[1-4]。

在体外，Moxifloxacin（5-50μg/ml）与TNF-α（50ng/ml）同时处理囊性纤维化支气管上皮细胞系IB3和C38细胞48小时。Moxifloxacin显著抑制IL-8和IL-6的分泌；Moxifloxacin（5-20μg/ml）与TNF-α（50ng/ml）同时处理IB3和C38细胞15-60分钟。Moxifloxacin显著抑制ERK1/2、JNK和NF-κB的激活^[5]。Moxifloxacin（0.05-1mg/ml）处理永生化人角膜内皮细胞（B4G12细胞）24-72小时。Moxifloxacin产生剂量依赖性的细胞毒性，增加活性氧生成和自噬，激活caspase 2、3、8通路并诱导细胞凋亡^[6]。

在体内，Moxifloxacin（12.5、25、50mg/kg；每日一次）口服给药于Wistar小鼠，连续7天。Moxifloxacin显著增加了小鼠的血清肌酐、胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、甘油三酯、尿素水平以及天冬氨酸转氨酶、丙氨酸转氨酶、碱性磷酸酶活性，同时降低了总胆红素水平^[7]。Moxifloxacin（100mg/kg；每天两次）腹腔注射于C57BL/6N小鼠，连续两天。Moxifloxacin显著减少了感染活菌或热灭活细菌后肺部总免疫细胞、中性粒细胞以及炎症介质（KC、IL-1β、IL-17A）的数量和浓度^[8]。