Ciprofloxacin (Bay-09867) hydrochloride monohydrate, a robust orally active topoisomerase IV inhibitor, induces damage to mitochondrial and nuclear DNA, resulting in mitochondrial dysfunction and ROS production. It exhibits anti-proliferative effects and promotes apoptosis, and is recognized as a potent fluoroquinolone antibiotic with substantial antibacterial properties[1].[2].[3].[4].
体内研究
When administered intraperitoneally at 30 mg/kg over 24 hours, Ciprofloxacin (Bay-09867) hydrochloride monohydrate offers protection against Y. pestis in a BALB/c murine model of pneumonic plague[3].
Ciprofloxacin (Bay-09867) hydrochloride monohydrate, given intragastrically at 100 mg/kg daily for four weeks in C57BL/6J mice, accelerates aortic root enlargement and increases the risk of aortic dissection and rupture by lowering LOX levels and enhancing MMP levels and activity in the aortic wall[4].
Additionally, Ciprofloxacin (Bay-09867) hydrochloride monohydrate at the same dosage and duration induces DNA damage, leads to DNA release into the cytosol, and triggers mitochondrial dysfunction and activation of cytosolic DNA sensor signaling, while Ciprofloxacin lactate raises levels of apoptosis and necroptosis in the aortic wall[4].
体外研究
In tendon cells treated with Ciprofloxacin (Bay-09867) hydrochloride monohydrate (5-50 μg/mL; 0-24 h), there is a significant reduction in cell proliferation and a cell cycle halt at the G2/M phase[1].
Ciprofloxacin (Bay-09867) hydrochloride monohydrate demonstrates significant efficacy against Y. pestis and B. anthracis, with MIC90 values of 0.03 μg/mL and 0.12 μg/mL respectively[2].
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