Ofloxacin induces apoptosis in microencapsulated juvenile rabbit chondrocytes by caspase-8-dependent mitochondrial pathway

Sheng, Zhenfeng; Cao, Xiaojuan; Peng, Shuangqing; Wang, Changyong; Li, Qianqian; Wang, Yimei; Liu, Mifeng

doi:10.1016/j.taap.2007.08.025

Cited by 26 publications

(18 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The use of ofloxacin for urinary tract infection treatment has increased in the past decade because this antibiotic has excellent efficacy and increases resistance to older agents, such as trimethoprim and sulfamethoxazole [7]. Some studies have reported that ofloxacin could efficiently inhibit the growth of various tumor cells via induced apoptosis [8,9]. Considerable evidence suggests that ruthenium(II)-polypyridyl complexes can kill tumor cells by interacting with DNA and inducing apoptosis [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Synthesis, characterization and DNA-binding properties of Ru(II) complexes coordinated by ofloxacin as potential antitumor agents

Wang

Zeng

et al. 2015

Journal of Coordination Chemistry

View full text Add to dashboard Cite

Three Ru complexes coordinated by oxfloxacin, [Ru(L) 2 (OFX)]Cl·2H 2 O (L = bpy, 1; dmbpy, 2; phen, 3; and OFX = ofloxacin), were synthesized and characterized. These complexes can inhibit the growth of cervical cancer HeLa cells efficiently. Furthermore, these three complexes exhibited excellent binding affinities with DNA, as confirmed by spectroscopy methods and viscosity experiments. Therefore, the synthesized Ru(II) complexes have excellent DNA-binding abilities with potential applications in cancer chemotherapy.

show abstract

Section: Introductionmentioning

confidence: 99%

Synthesis, characterization and DNA-binding properties of Ru(II) complexes coordinated by ofloxacin as potential antitumor agents

Wang

Zeng

et al. 2015

Journal of Coordination Chemistry

View full text Add to dashboard Cite

show abstract

“…On the other hand, different sensitivities of non-cancer cells were found on quinolone treatment by some authors (Aranha et al ., 2003; Xiao et al ., 2008; Wang et al ., 2008; Al-Trawneh et al ., 2010; Huang et al ., 2011; Forezi et al ., 2014).…”

Section: Discussionmentioning

confidence: 99%

“…They are inductors of DNA damage, cell cycle arrest and apoptotic and autophagic cell death (Chang et al ., 2009; Hadjeri et al ., 2004; Sheng et al ., 2008). …”

Section: Introductionmentioning

confidence: 99%

Original Article. Study of the cytotoxic/toxic potential of the novel anticancer selenodiazoloquinolone on fibroblast cells and 3D skin model

Jantová

Topoľská

Janošková

et al. 2016

Interdisciplinary Toxicology

View full text Add to dashboard Cite

The new synthetically prepared quinolone derivative 7-ethyl 9-ethyl-6-oxo-6,9-dihydro[1,2,5]selenadiazolo [3,4-h]quinoline-7-carboxylate (E2h) showed in our previous study cytotoxic effects towards tumor cells and immunomodulatory activities on RAW 264.7 cell line murine macrophages. E2h may have a potential use as a novel chemotherapeutic agent with immunomodulatory properties and the ability to induce apoptotic death of cancer cells. The aim of the present study was to examine the antiproliferative/cytotoxic activities of E2h on human non-cancer fibroblast BHNF-1 cells and reconstructed human epidermis EpiDerm™. Further the effects of E2h on tissue structure and morphology were examined. Cytotoxic/toxic studies showed that selenadiazoloquinolone is not toxic on normal human fibroblast cells BHNF-1 and dimensional skin constructs EpiDerm™. Evaluation of morphological changes in EpiDerm™ showed no change in the construction and morphology of skin tissue treated by E2h compared to control.

show abstract

“…QNT4 binds the reversible complex between DNA and topoisomerase II, preventing the dissociation of the DNA-topoisomerase II complex and thereby inducing DNA damage [22,23] . It has been reported that one of the key responses of fluoroquinolone-induced DNA damage is the expression of tumor suppressor protein p53, causing apoptosis of the treated cells [24,25] . The results of this study showed that QNT4 induced cell apoptosis, which was accompanied by the up-regulation of p53 protein level in a dose-dependent manner, suggesting that the activation of the p53 pathway may be involved in the apoptotic process of SMMC-7721 cells.…”

Section: Wwwchinapharcom Shi Zy Et Almentioning

confidence: 99%

Piperonal ciprofloxacin hydrazone induces growth arrest and apoptosis of human hepatocarcinoma SMMC-7721 cells

Shi

Kang

et al. 2012

Acta Pharmacol Sin

View full text Add to dashboard Cite

Aim: To investigate the cytotoxic effects of piperonal ciprofloxacin hydrazone (QNT4), a novel antibacterial fluoroquinolone derivative, against human hepatocarcinoma SMMC-7721 cells. Methods: Human hepatocarcinoma cells (SMMC-7721), human breast adenocarcinoma cells (MCF-7) and human colon adenocarcinoma cells (HCT-8) were tested. The effects of QNT4 on cell proliferation were examined using MTT assay. Cell apoptosis was determined using Hoechst 33258 fluorescence staining, TUNEL assay and agarose gel electrophoresis. The topoisomerase II activity was measured using agarose gel electrophoresis with the DNA plasmid pBR322 as the substrate. Mitochondrial membrane potential (∆ψm) was measured using a high content screening imaging system. Protein expression of caspase-9, caspase-8, caspase-3, p53, Bcl-2, Bax, and cytochrome c was detected with Western blot analysis. Results: Treatment with QNT4 (0.625-10 μmol/L) potently inhibited the proliferation of the cancer cells in time-and dose-dependent manners (the IC 50 value at 24 h in SMMC-7721 cells, MCF-7 cells and HCT-8 cells was 2.956±0.024, 3.710±0.027, and 3.694±0.030 μmol/L, respectively). Treatment of SMMC-7721 cells with QNT4 (0.2146, 2.964, and 4.600 μmol/L) for 24 h dose-dependently increased the percentage of apoptotic cells, elicited characteristic DNA "ladder" bands, and decreased the mitochondrial membrane potential. QNT4 dose-dependently increased topoisomerase II-mediated DNA breaks while inhibiting DNA relegation, thus keeping the DNA in fragments. Treatment of SMMC-7721 cells with QNT4 significantly increased cytochrome c in the cytosol, and decreased cytochrome c in the mitochondrial compartment. QNT4 (3-7.39 μmol/L) significantly increased the protein expression of p53, Bax, caspase-9, caspase-3, and the cleaved activated forms of caspase-9 and caspase-3 in SMMC-7721 cells. In contrast, the expression of Bcl-2 was decreased, while caspase-8 had no significant change. Conclusion: QNT4 induced the apoptosis of SMMC-7721 cells via inhibiting topoisomerase II activity and modulating mitochondrialdependent pathways.

show abstract

Ofloxacin induces apoptosis in microencapsulated juvenile rabbit chondrocytes by caspase-8-dependent mitochondrial pathway

Cited by 26 publications

References 42 publications

Synthesis, characterization and DNA-binding properties of Ru(II) complexes coordinated by ofloxacin as potential antitumor agents

Synthesis, characterization and DNA-binding properties of Ru(II) complexes coordinated by ofloxacin as potential antitumor agents

Original Article. Study of the cytotoxic/toxic potential of the novel anticancer selenodiazoloquinolone on fibroblast cells and 3D skin model

Piperonal ciprofloxacin hydrazone induces growth arrest and apoptosis of human hepatocarcinoma SMMC-7721 cells

Contact Info

Product

Resources

About