Katson mitä PubMed sanoo fluorokinoneista ja MMP-entsyymeistä. Suoran assosiaation vastauksia en saa, mutta katson mitä jäi seulaani.
https://www.ncbi.nlm.nih.gov/pubmed/?term=Fluorokinolones+%3B+MMPs
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1. ENROFLOXACIN , MARBOFLOXACIN
Siengdee P, Euppayo T, Buddhachat K, Chomdej S, Nganvongpanit K.
J Vet Pharmacol Ther. 2016 Oct;39(5):439-51. doi: 10.1111/jvp.12305. Epub 2016 Mar 11.Abstract
Fluoroquinolones
(FQs) are frequently used for septic arthritis. Increased antibacterial
activity has been associated with mammalian cell cytotoxicity that may
increase the risk of developing osteoarthritis. This study compared the
direct effects of two different FQs, enrofloxacin (Enro) and
marbofloxacin (Mar), on normal primary canine chondrocytes and
inflammatory-stimulated chondrocytes, in addition to their
administration in combination with hyaluronan (HA). Cell viability, cell
apoptosis, s-GAG production, and expression patterns of inflammatory,
extracellular matrix
(ECM) component and protease genes were measured. Enro co-culturing
with HA could modify s-GAG synthesis compared with the negative control
group. Co-treatment with both FQs and HA significantly decreased cell
viability and induced more total apoptotic cell death compared with the
negative control and pre-IL-1β-stimulated group. Enro regulated
IL-1β-stimulated cells to overexpress IL-1β, TNF, and MMP3, whereas Mar
induced upregulation of PTGS2 and NFKB1 and enhanced the expression of
ECM component genes HAS1, COL2A1, and ACAN as well as TIMP1 and MMP9.
Simultaneous use of HA with Enro can effectively reduce the expression
of IL-1β, TNF, and MMP3 in pre-IL-1β-stimulated chondrocytes. These
results suggest the beneficial effects of HA in reducing the adverse
effects of Enro treatment at the transcriptional level.
2. LEVOFLOXACIN
Bai ZL, Chen Q, Yang SD, Zhang F, Wang HY, Yang DL, Ding WY.
Med Sci Monit. 2014 Nov 8;20:2205-12. doi: 10.12659/MSM.892610. Abstract BACKGROUND:
Fluoroquinolones
are in wide clinical use as safe and effective antibiotics. Articular
cartilage, tendons, and epiphyseal growth plates have been recognized as
targets of fluoroquinolone-induced connective tissue toxicity. However,
the effects of fluoroquinolones on annulus fibrosus (AF) cells are still unknown. MATERIAL/METHODS: The
main objective of this study was to investigate the effects of
levofloxacin, a typical fluoroquinolone antibiotic drug, on rat AF cells
in vitro. Rat annulus fibrosus (RAF) cells were treated with
levofloxacin at different concentrations (0, 10, 20, 30, 40, 60, 80, and
90 μg/ml) and were assessed to determine the possible cytotoxic effects
of levofloxacin. Inverted phase-contrast microscopy was used to
accomplish the morphological observation of apoptosis of treated cells.
Western blot and real-time quantitative RT-PCR (qPCR) was used to
explore the expression of active caspase-3 and MMP-3. Flow cytometry was
used to measure the apoptotic incidences. RESULTS:
Our study showed that levofloxacin, with concentrations at 30, 60, and 90 μg/ml, induced dose-dependent RAF cell apoptosis and higher expression of caspase-3 and MMP-3. More apoptotic cells were observed by inverted phase-contrast microscopy. Moreover, levofloxacin increased the activity of caspase-3, and it also reduced cell viability with different concentrations ranging from 10 to 80 μg/ml.CONCLUSIONS:
Our study results suggest that levofloxacin has cytotoxic effects on RAF cells, characterized by enhancing apoptosis and reducing cell viability, and indicate a potential toxic effect of fluoroquinolones on RAF cells.
Our study showed that levofloxacin, with concentrations at 30, 60, and 90 μg/ml, induced dose-dependent RAF cell apoptosis and higher expression of caspase-3 and MMP-3. More apoptotic cells were observed by inverted phase-contrast microscopy. Moreover, levofloxacin increased the activity of caspase-3, and it also reduced cell viability with different concentrations ranging from 10 to 80 μg/ml.CONCLUSIONS:
Our study results suggest that levofloxacin has cytotoxic effects on RAF cells, characterized by enhancing apoptosis and reducing cell viability, and indicate a potential toxic effect of fluoroquinolones on RAF cells.
3. FLEROXACIN
Fox AJ, Schär MO, Wanivenhaus F, Chen T, Attia E, Binder NB, Otero M, Gilbert SL, Nguyen JT, Chaudhury S, Warren RF, Rodeo SA.
Am J Sports Med. 2014 Dec;42(12):2851-9. doi: 10.1177/0363546514545858. Epub 2014 Aug 20.
Reverse transcriptase quantitative polymerase chain reaction (RTqPCR) analysis revealed a 30-fold increase in expression of matrix metalloproteinase (MMP)-3, a 7-fold increase in MMP-13, and a 4-fold increase in tissue inhibitor of metalloproteinases
(TIMP)-1 in the Pre/Postop group compared with the other groups. The
appearance of the healing enthesis in all treated animals was
qualitatively different than that in controls. The tendons were friable
and atrophic. All 3 treated groups showed significantly less
fibrocartilage and poorly organized collagen at the healing enthesis
compared with control animals. There was a significant difference in the
mode of failure, with treated animals demonstrating an intrasubstance
failure of the supraspinatus tendon during testing. In contrast, only 1
of 10 control samples failed within the tendon substance. The healing
enthesis of the Pre/Postop group displayed significantly reduced
ultimate load to failure compared with the Preop, Postop, and control
groups. There was no significant difference in load to failure in the
Preop group compared with the Postop group. Pre/Postop animals
demonstrated significantly reduced cross-sectional area compared with
the Postop and control groups. There was also a significant reduction in
area between the Preop and control groups. CONCLUSION:
In this preliminary study, fluoroquinolone treatment negatively influenced tendon healing. CLINICAL RELEVANCE:
In this preliminary study, fluoroquinolone treatment negatively influenced tendon healing. CLINICAL RELEVANCE:
These
findings indicate that there was an active but inadequate repair
response that has potential clinical implications for patients who are
exposed to fluoroquinolones before tendon repair surgery. © 2014 The Author(s). KEYWORDS:
fleroxacin; fluoroquinolone; rotator cuff repair; tendinopathy; tendon healing
4. MOXIFLOXACIN and antimycobacterial drugs (TBC)
Singh S, Kubler A, Singh UK, Singh A, Gardiner H, Prasad R, Elkington PT, Friedland JS.
Antimicrob Agents Chemother. 2014 Aug;58(8):4657-65. doi: 10.1128/AAC.02141-13. Epub 2014 Jun 2. Abstract
Tuberculosis is characterized by extensive destruction and remodelling of the pulmonary extracellular matrix (ECM). Stromal cell-derived matrix metalloproteinases (MMPs) are implicated in this process and may be a target for adjunctive immunotherapy. We hypothesized that MMPs
are elevated in bronchoalveolar lavage fluid of tuberculosis patients
and that antimycobacterial agents may have a modulatory effect on MMP
secretion.
Concentrations of MMP-1, -2, -3, -7, -8, and -9 were elevated in the bronchoalveolar lavage fluid from tuberculosis patients compared to those in bronchoalveolar lavage fluid from patients with other pulmonary conditions.
There was a positive correlation between MMP-3, MMP-7, and MMP-8 and a chest radiological score of cavitation and parenchymal damage.
Respiratory epithelial cell-derived MMP-3 was suppressed by moxifloxacin, rifampicin, and azithromycin in a dose-dependent manner. Respiratory epithelial cell-derived MMP-1 was suppressed by moxifloxacin and azithromycin, whereas MMP-9 secretion was only decreased by moxifloxacin. In contrast, moxifloxacin and azithromycin both increased MMP-1 and -3 secretion from MRC-5 fibroblasts, demonstrating that the effects of these drugs are cell specific. Isoniazid (INH) did not affect MMP secretion. In conclusion, MMPs are elevated in bronchoalveolar lavage fluid from tuberculosis patients and correlate with parameters of tissue destruction. Antimycobacterial agents have a hitherto-undescribed immunomodulatory effect on MMP release by stromal cells.
Free PMC Article
Concentrations of MMP-1, -2, -3, -7, -8, and -9 were elevated in the bronchoalveolar lavage fluid from tuberculosis patients compared to those in bronchoalveolar lavage fluid from patients with other pulmonary conditions.
There was a positive correlation between MMP-3, MMP-7, and MMP-8 and a chest radiological score of cavitation and parenchymal damage.
Respiratory epithelial cell-derived MMP-3 was suppressed by moxifloxacin, rifampicin, and azithromycin in a dose-dependent manner. Respiratory epithelial cell-derived MMP-1 was suppressed by moxifloxacin and azithromycin, whereas MMP-9 secretion was only decreased by moxifloxacin. In contrast, moxifloxacin and azithromycin both increased MMP-1 and -3 secretion from MRC-5 fibroblasts, demonstrating that the effects of these drugs are cell specific. Isoniazid (INH) did not affect MMP secretion. In conclusion, MMPs are elevated in bronchoalveolar lavage fluid from tuberculosis patients and correlate with parameters of tissue destruction. Antimycobacterial agents have a hitherto-undescribed immunomodulatory effect on MMP release by stromal cells.
Free PMC Article
5. CIPROFLOXACIN , radioactive exposure, radiation combined ijury
Kiang JG, Fukumoto R.
Health Phys. 2014 Jun;106(6):720-6. doi: 10.1097/HP.0000000000000108.
Exposure to
ionizing radiation alone (radiation injury, RI) or combined with
traumatic tissue injury (radiation combined injury, CI) is a crucial
life-threatening factor in nuclear and radiological accidents. It is
well documented that RI and CI occur at the molecular, cellular, tissue,
and system levels. However, their mechanisms remain largely unclear. It
has been observed in dogs, pigs, rats, guinea pigs, and mice that
radiation exposure combined with burns, wounds, or bacterial infection
results in greater mortality than radiation exposure alone. In this
laboratory, the authors found that B6D2F1/J female mice exposed to 9.75
Gy ⁶⁰Co-γ photon radiation followed by 15% total body surface area
wounds experienced 50% higher mortality (over a 30-d observation period)
compared to irradiation alone. CI enhanced DNA damages, amplified iNOS
activation, induced massive release of pro-inflammatory cytokines,
overexpressed MMPs
and TLRs, and aggravated sepsis that led to cell death. In the present
study, B6D2F1/J mice that received CI were treated with ciprofloxacin
(CIP, 90 mg/kg p.o., q.d. within 2 h after CI through day 21). At day 1,
CIP treatment reduced CI-induced γ-H2AX formation significantly. At day
10, CIP treatment not only reduced cytokine/chemokine concentrations
significantly, including IL-6 and KC (i.e., IL-8 in humans), but also
enhanced IL-3 production compared to vehicle-treated controls. CIP also
elevated red blood cell counts, hemoglobin levels, and hematocrits. At
day 30, CIP treatment increased 45% survival after CI (i.e., 2.3-fold
increase over vehicle treatment). The results suggest that CIP may prove
to be an effective therapeutic drug for CI.
6.
Kim EY, Shin JH, Song HY, Kim JH, Lee EW, Kim WJ, Shin DH, Lee H.
Endoscopy. 2014 Jun;46(6):507-12. doi: 10.1055/s-0034-1365495. Epub 2014 Apr 25.
The silencing effect of the candidate siRNA (termed (MMP-9 siRNA) was evaluated in 9 L rat glial cells. Four groups of rats (n = 10, each group) were used: Eso-S, stent insertion only, comparison; Eso-R, stent insertion plus treatment with MMP-9 siRNA complexed with Chol-R9 for delivery, experimental; Eso-P, stent insertion plus treatment with pCMV-luc complexed with Chol-R9, for confirmation of Chol-R9 delivery effect; and Eso-N, no stent insertion and no treatment, controls. All rats were sacrificed at 3 weeks. The therapeutic efficacy of the MMP-9 siRNA/Chol-R9 complex was assessed. RESULTS:
The most potent MMP-9 siRNA was selected. Compared with the Eso-S group, the Eso-R group showed significantly less tissue hyperplasia with a lower percentage of granulation tissue and smaller granulation tissue area, and also significantly lower MMP-9 level. CONCLUSIONS:
MMP-9 siRNA/Chol-R9 is effective for inhibiting stent-induced tissue hyperplasia in a rat esophageal model.
7. QUINOLONES, LEVOFLOXACIN
Wang L, Wu Y, Tan Y, Fei X, Deng Y, Cao H, Chen B, Wang H, Magdalou J, Chen L.
J Appl Toxicol. 2014 Aug;34(8):870-7. doi: 10.1002/jat.2903. Epub 2013 Jul 1.
Quinolones have
been reported to induce adverse effects on articular cartilage, tendons
and ligaments. However, the effects of quinolones on menisci have not
been revealed. The present study was to test the effects of levofloxacin
on meniscus cells in vitro. Rabbit meniscus cells were administrated
with different concentrations of levofloxacin (0, 14, 28, 56, 112 and
224 µm) for 24 or 48 h, and cell viability and apoptosis were measured.
The mRNA expression levels of matrix
metalloproteinase (MMP)-1, MMP-3, MMP-13, tissue inhibitors of
metalloproteinase (TIMP)-1, TIMP-3, Col1a1, Bcl-2, caspase-3 and
inducible nitric oxide were analyzed by real-time polymerase chain
reaction. Active caspase-3 was detected by immunocytochemical assay,
while protein expression levels of MMP-3 and MMP-13 were measured by
Western blotting assay. After treatment with levofloxacin for 48 h, cell
viability was decreased from dose of 28 to 224 µm in a
concentration-dependent manner. An increase of apoptotic cells was
observed by flow cytometry. Active caspase-3 protein expression level
was also increased. The mRNA level of Bcl-2 was decreased and levels of
MMP-1, MMP-3 and MMP-13 in experimental groups were higher than those of
controls. The protein levels of MMP-3 and MMP-13 were increased.
Moreover, the mRNA levels of TIMP-3 and col1a1 were decreased. A
dose-dependent increase of inducible nitric oxide mRNA expression level
was also observed. Our results suggested the cytotoxic effects of
levofloxacin on meniscus cells through induction of apoptosis and
unbalanced MMPs/TIMPs expression. These side effects might result in meniscus extracellular matrix
degradation and meniscal lesion. Thus, quinolones should be used
cautiously on patients who perform athletic activities or undergo
surgical meniscus repair.
Copyright © 2013 John Wiley & Sons, Ltd. KEYWORDS:
apoptosis; extracellular matrix degradation; levofloxacin; matrix metalloproteinases; meniscus cell
8. OFLOXACIN (OFLOX)
Goto K, Imaoka M, Goto M, Kikuchi I, Suzuki T, Jindo T, Takasaki W.
Toxicol Lett. 2013 Feb 4;216(2-3):124-9. doi: 10.1016/j.toxlet.2012.11.017. Epub 2012 Nov 29.
9. LEVOFLOXACIN
Tan Y, Lu K, Deng Y, Cao H, Chen B, Wang H, Magdalou J, Chen L.
Toxicol Appl Pharmacol. 2012 Dec 1;265(2):175-80. doi: 10.1016/j.taap.2012.10.003. Epub 2012 Oct 12.
10. CIPROFLOXACIN , Systemic sclerosis, Lungfibrosis
Bujor AM, Haines P, Padilla C, Christmann RB, Junie M, Sampaio-Barros PD, Lafyatis R, Trojanowska M.
Int J Mol Med. 2012 Dec;30(6):1473-80. doi: 10.3892/ijmm.2012.1150. Epub 2012 Oct 5.
Systemic sclerosis
(SSc) is characterized by fibrosis of the skin and internal organs. The
present study was undertaken to examine the effects of ciprofloxacin, a
fluoroquinolone antibiotic implicated in matrix
remodeling, on dermal and lung fibroblasts obtained from SSc patients.
Dermal and lung fibroblasts from SSc patients and healthy subjects were
treated with ciprofloxacin. Western blotting was used to analyze protein
levels and RT-PCR was used to measure mRNA expression. The
pharmacologic inhibitor UO126 was used to block Erk1/2 signaling. SSc
dermal fibroblasts demonstrated a significant decrease in collagen type I
mRNA and protein levels after antibiotic treatment, while healthy
dermal fibroblasts were less sensitive to ciprofloxacin, downregulating
collagen only at the protein levels. Connective tissue growth factor
(CCN2) gene expression was significantly reduced and matrix
metalloproteinase 1 (MMP1) levels were enhanced after ciprofloxacin
treatment to a similar extent in healthy and SSc fibroblasts.
Ciprofloxacin induced Erk1/2 phosphorylation, and Erk1/2 blockade
completely prevented MMP1 upregulation. However, Smad1 and Smad3
activation in response to TGFβ was not affected. The expression of
friend leukemia integration factor 1 (Fli1), a transcriptional repressor
of collagen, was increased after treatment with ciprofloxacin only in
SSc fibroblasts, and this was accompanied by a decrease in the levels of
DNA methyltransferase 1 (Dnmt1). Similar effects were observed in
SSc-interstitial lung disease (ILD) lung fibroblasts. In summary, our
study demonstrates that ciprofloxacin has antifibrotic actions in SSc
dermal and lung fibroblasts via the downregulation of Dnmt1, the
upregulation of Fli1 and induction of MMP1 gene expression via an
Erk1/2-dependent mechanism. Thus, our data suggest that ciprofloxacin
may be an attractive therapy for SSc skin and lung fibrosis.
11. NADIFLOXACIN
Hosoda S, Komine M, Karakawa M, Tsuda H, Ohtsuki M.
J Dermatol. 2012 Oct;39(10):855-7. doi: 10.1111/j.1346-8138.2011.01466.x. Epub 2012 Jan 4. No abstract available.
- PMID:
- 22220987
12. NORFLOXACIN, CIPROFLOXACIN, LOMEFLOXACIN, SPARFLOXACIN, GATIFLOXACIN, MOXIFLOXACIN
Effect of fluoroquinolones on the expression of matrix metalloproteinase in debrided cornea of rats.
Sharma C, Velpandian T, Baskar Singh S, Ranjan Biswas N, Bihari Vajpayee R, Ghose S.
Toxicol Mech Methods. 2011 Jan;21(1):6-12. doi: 10.3109/15376516.2010.529183. Epub 2010 Nov 9.
13. CIPROFLOXACIN, Achilles tendon
Tsai WC, Hsu CC, Chen CP, Chang HN, Wong AM, Lin MS, Pang JH.
J Orthop Res. 2011 Jan;29(1):67-73. doi: 10.1002/jor.21196.
Ciprofloxacin-induced tendinopathy and tendon rupture
have been previously described, principally affecting the Achilles
tendon. This study was designed to investigate the effect of
ciprofloxacin on expressions of matrix metalloproteinases
(MMP)-2 and -9, tissue inhibitors of metalloproteinase (TIMP)-1 and -2
as well as type I collagen in tendon cells. Tendon cells intrinsic to
rat Achilles tendon were treated with ciprofloxacin and then underwent
MTT (tetrazolium) assay. Real-time reverse-transcription polymerase
chain reaction (RT-PCR) and Western blot analysis were used,
respectively, to evaluate the gene and protein expressions of type I
collagen, and MMP-2. Gelatin zymography was used to evaluate the
enzymatic activities of MMP-2 and -9. Reverse zymography was used to
evaluate TIMP-1 and -2. Immunohistochemical staining for MMP-2 in
ciprofloxacin-treated tendon explants was performed. Collagen
degradation was evaluated by incubation of conditioned medium with
collagen. The results revealed that ciprofloxacin up-regulated the
expression of MMP-2 in tendon cells at the mRNA and protein levels.
Immunohistochemistry also confirmed the increased expressions of MMP-2
in ciprofloxacin-treated tendon explants. The enzymatic activity of
MMP-2 was up-regulated whereas that of MMP-9, TIMP-1 or TIMP-2 was
unchanged. The amount of secreted type I collagen in the conditioned
medium decreased and type I collagen was degraded after ciprofloxacin
treatment. In conclusion, ciprofloxacin up-regulates the expressions of
MMP-2 in tendon cells and thus degraded type I collagen. These findings
suggest a possible mechanism of ciprofloxacin-associated tendinopathy.
Free Article
Copyright © 2010 Orthopaedic Research Society.
14. CIPROFLOXACIN, NORFLOXACIN, OFLOXACIN, non-fluorinated quinolone nalidixic acid
Corps AN, Harrall RL, Curry VA, Hazleman BL, Riley GP.
Rheumatology (Oxford). 2005 Dec;44(12):1514-7. Epub 2005 Sep 7.
Fluoroquinolone antibiotics may
cause tendon pain and rupture. We reported previously that the
fluoroquinolone ciprofloxacin potentiated interleukin
(IL)-1beta-stimulated expression of matrix metalloproteinases (MMP)-3 and MMP-1 in human tendon-derived cells. We have now tested additional fluoroquinolones and investigated whether they have a similar effect on expression of MMP-13. METHODS: Tendon cells were incubated for two periods of 48 h with or without fluoroquinolones
and IL-1beta. Total ribonucleic acid (RNA) was assayed for MMP
messenger RNA by relative quantitative reverse transcriptase polymerase
chain reaction, with normalization for glyceraldehyde-3-phosphate
dehydrogenase mRNA. Samples of supernatant medium were assayed for MMP
output by activity assays. RESULTS: MMP-13 was expressed
by tendon cells at lower levels than MMP-1, and was stimulated typically
10- to 100-fold by IL-1beta. Ciprofloxacin, norfloxacin and ofloxacin
each reduced both basal and stimulated expression of MMP-13 mRNA. In
contrast, ciprofloxacin and norfloxacin increased basal and
IL-1beta-stimulated MMP-1 mRNA expression. Both the inhibition of MMP-13
and the potentiation of MMP-1 expression by fluoroquinolones
were accompanied by corresponding changes in IL-1beta-stimulated MMP
output. The non-fluorinated quinolone nalidixic acid had lesser or no
effects. CONCLUSIONS:
Fluoroquinolones (FQs) show contrasting effects on the expression of the two collagenases MMP-1 and MMP-13, indicating specific effects on MMP gene regulation.
Fluoroquinolones (FQs) show contrasting effects on the expression of the two collagenases MMP-1 and MMP-13, indicating specific effects on MMP gene regulation.
15. CIPROFLOXACIN, LEVOFLOXACIN
Sendzik J, Shakibaei M, Schäfer-Korting M, Stahlmann R.
Toxicology. 2005 Aug 15;212(1):24-36.
Antimicrobial therapy with fluoroquinolones
can be associated with tendinitis and other tendon disorders as an
adverse reaction associated with this class of antimicrobials. Here we
investigated aspects of the mechanism of quinolone-induced tendotoxicity
in human tenocytes focussing mainly on the question whether fluoroquinolones
may induce apoptosis. Monolayers of human tenocytes were incubated with
ciprofloxacin or levofloxacin at different concentrations (0, 3, 10, 30
and 100mg/L medium) for up to 4 days. Ultrastructural changes were
studied by electron microscopy, and alterations in synthesis of specific
proteins were determined using immunoblotting. At concentrations, which
are achievable during quinolone therapy, 3mg ciprofloxacin/L medium
significantly decreased type I collagen; similar changes were observed
with 3mg ciprofloxacin or 10mg levofloxacin/L medium for the beta(1)-
integrin receptors. Effects were intensified at higher concentrations
and longer incubation periods. Cytoskeletal and signalling proteins,
such as activated shc or erk 1/2, were significantly reduced by both fluoroquinolones already at 3mg/L. Furthermore, time- and concentration-dependent increases of matrix metalloproteinases
as well as of the apoptosis marker activated caspase-3 were found.
Apoptotic changes were confirmed by electron microscopy: both fluoroquinolones
caused typical alterations like condensed material in the nucleus,
swollen cell organelles, apoptotic bodies and bleb formation at the cell
membrane. Our results provide evidence that besides changes in receptor
and signalling proteins apoptosis has to be considered as a final event
in the pathogenesis of fluoroquinolone-induced tendopathies.
16.CIPROFLOXACIN (Ciloxan, Alcon), OFLOXACIN ( Ocuflox, Allergan), LEVOFLOXACIN (Quixin, Santen)
Reviglio VE, Hakim MA, Song JK, O'Brien TP.
BMC Ophthalmol. 2003 Oct 6;3:10.
Matrix metalloproteinases play an important role in extracellular matrix
deposition and degradation. Based on previous clinical observations of
corneal perforations during topical fluoroquinolone treatment, we
decided to evaluate the comparative effects of various fluoroquinolone
eye drops on the expression of matrix metalloproteinases (MMPs) in cornea. METHODS:
Eighty female Lewis rats were divided into two experimental groups: intact and wounded corneal epithelium. Uniform corneal epithelial defects were created in the right eye with application of 75% alcohol in the center of the tissue for 6 seconds. The treatment groups were tested as follows: 1) Tear drops: carboxymethylcellulose sodium 0.5 % (Refresh, Allergan); 2) Ciprofloxacin 0.3% (Ciloxan, Alcon); 3) Ofloxacin 0.3%(Ocuflox, Allergan); 4) Levofloxacin 0.5%(Quixin, Santen). Eye drops were administered 6 times a day for 48 hours. Rats were sacrificed at 48 hours. Immunohistochemical analysis and zymography were conducted using antibodies specific to MMPs-1, 2, 8 and 9. RESULTS: MMP-1, MMP-2, MMP-8 and MMP-9 expression were detected at 48 hrs in undebrided corneal epithelium groups treated with the topical fluoroquinolones. No statistical difference was observed in quantitative expression of MMPs among ciprofloxacin 0.3%, ofloxacin 0.3%, levofloxacin 0.5%. When the artificial tear group and the fluoroquinolone groups with corneal epithelial defect were compared, increased expression of MMPs was observed as a result of the wound healing process. However, the fluoroquinolone treated group exhibited high statistically significantly levels of MMPs expression. CONCLUSIONS:
Our study provides preliminary evidence that topical application of fluoroquinolone drugs can induce the expression of MMP-1, MMP-2, MMP-8 and MMP-9 in the undebrided corneal epithelium compared to artificial tear eye drops.
Eighty female Lewis rats were divided into two experimental groups: intact and wounded corneal epithelium. Uniform corneal epithelial defects were created in the right eye with application of 75% alcohol in the center of the tissue for 6 seconds. The treatment groups were tested as follows: 1) Tear drops: carboxymethylcellulose sodium 0.5 % (Refresh, Allergan); 2) Ciprofloxacin 0.3% (Ciloxan, Alcon); 3) Ofloxacin 0.3%(Ocuflox, Allergan); 4) Levofloxacin 0.5%(Quixin, Santen). Eye drops were administered 6 times a day for 48 hours. Rats were sacrificed at 48 hours. Immunohistochemical analysis and zymography were conducted using antibodies specific to MMPs-1, 2, 8 and 9. RESULTS: MMP-1, MMP-2, MMP-8 and MMP-9 expression were detected at 48 hrs in undebrided corneal epithelium groups treated with the topical fluoroquinolones. No statistical difference was observed in quantitative expression of MMPs among ciprofloxacin 0.3%, ofloxacin 0.3%, levofloxacin 0.5%. When the artificial tear group and the fluoroquinolone groups with corneal epithelial defect were compared, increased expression of MMPs was observed as a result of the wound healing process. However, the fluoroquinolone treated group exhibited high statistically significantly levels of MMPs expression. CONCLUSIONS:
Our study provides preliminary evidence that topical application of fluoroquinolone drugs can induce the expression of MMP-1, MMP-2, MMP-8 and MMP-9 in the undebrided corneal epithelium compared to artificial tear eye drops.
17. CIPROFLOXACIN,
Ciprofloxacin enhances the stimulation of matrix
metalloproteinase 3 expression by interleukin-1beta in human
tendon-derived cells. A potential mechanism of fluoroquinolone-induced
tendinopathy. Corps AN, Harrall RL, Curry VA, Fenwick SA, Hazleman BL, Riley GP.
Arthritis Rheum. 2002 Nov;46(11):3034-40.
To determine whether the
fluoroquinolone antibiotic ciprofloxacin, which can cause tendon pain
and rupture in a proportion of treated patients, affects the expression
of matrix metalloproteinases (MMPs) in human tendon-derived cells in culture. METHODS:
Cell cultures were derived from 6 separate tendon explants, and were incubated in 6-well culture plates for 2 periods of 48 hours each, with ciprofloxacin (or DMSO in controls) and interleukin-1beta (IL-1beta), alone and in combination. Samples of supernatant medium from the second 48-hour incubation were assayed for MMPs 1, 2, and 3 by Western blotting. RNA was extracted from the cells and assayed for MMP messenger RNA (mRNA) by semiquantitative reverse transcription-polymerase chain reaction, with normalization for GAPDH mRNA. RESULTS:
Unstimulated tendon cells expressed low or undetectable levels of MMP-1 and MMP-3, and substantial levels of MMP-2. IL-1beta induced a substantial output of both MMP-1 and MMP-3 into cell supernatants, reflecting increases (typically 100-fold) in MMP mRNA, but had only minor effects on MMP-2 expression. Ciprofloxacin had no detectable effect on MMP output in unstimulated cells. Preincubation with ciprofloxacin potentiated IL-1beta-stimulated MMP-3 output, reflecting a similar effect on MMP-3 mRNA expression. Ciprofloxacin also potentiated IL-1beta-stimulated MMP-1 mRNA expression, but did not potentiate the output of MMP-1, and had no significant effects on MMP-2 mRNA expression or output. CONCLUSION:
Ciprofloxacin can selectively enhance MMP expression in tendon-derived cells. Such effects might compromise tendon microstructure and integrity.
Free ArticleCell cultures were derived from 6 separate tendon explants, and were incubated in 6-well culture plates for 2 periods of 48 hours each, with ciprofloxacin (or DMSO in controls) and interleukin-1beta (IL-1beta), alone and in combination. Samples of supernatant medium from the second 48-hour incubation were assayed for MMPs 1, 2, and 3 by Western blotting. RNA was extracted from the cells and assayed for MMP messenger RNA (mRNA) by semiquantitative reverse transcription-polymerase chain reaction, with normalization for GAPDH mRNA. RESULTS:
Unstimulated tendon cells expressed low or undetectable levels of MMP-1 and MMP-3, and substantial levels of MMP-2. IL-1beta induced a substantial output of both MMP-1 and MMP-3 into cell supernatants, reflecting increases (typically 100-fold) in MMP mRNA, but had only minor effects on MMP-2 expression. Ciprofloxacin had no detectable effect on MMP output in unstimulated cells. Preincubation with ciprofloxacin potentiated IL-1beta-stimulated MMP-3 output, reflecting a similar effect on MMP-3 mRNA expression. Ciprofloxacin also potentiated IL-1beta-stimulated MMP-1 mRNA expression, but did not potentiate the output of MMP-1, and had no significant effects on MMP-2 mRNA expression or output. CONCLUSION:
Ciprofloxacin can selectively enhance MMP expression in tendon-derived cells. Such effects might compromise tendon microstructure and integrity.
18. ENROFLOXACIN
Effects of enrofloxacin and magnesium deficiency on matrix metabolism in equine articular cartilage.
Davenport CL, Boston RC, Richardson DW.
Am J Vet Res. 2001 Feb;62(2):160-6.
To investigate the effects of enrofloxacin and magnesium deficiency on explants of equine articular cartilage. SAMPLE POPULATION:
Articular cartilage explants and cultured chondrocytes obtained from adult and neonatal horses. PROCEDURE: Full-thickness explants and cultured chondrocytes were incubated in complete or magnesium-deficient media containing enrofloxacin at concentrations of 0, 1, 5, 25, 100, and 500 microg/ml. Incorporation and release of sulfate 35S over 24 hours were used to assess glycosaminoglycan (GAG) synthesis and degradation. An assay that measured binding of dimethylmethylene blue dye was used to compare total GAG content between groups. Northern blots of RNA from cultured chondrocytes were probed with equine cDNA of aggrecan, type-II collagen, biglycan, decorin, link protein, matrix metalloproteinases 1, 3, and 13, and tissue inhibitor of metalloproteinase 1. RESULTS:
A dose-dependent suppression of 35S incorporation was observed. In cartilage of neonates, 35S incorporation was substantially decreased at enrofloxacin concentrations of 25 mg/ml. In cartilage of adult horses, 35S incorporation was decreased only at enrofloxacin concentrations of > or =100 microg/ml. Magnesium deficiency caused suppression of 35S incorporation. Enrofloxacin or magnesium deficiency did not affect GAG degradation or endogenous GAG content. Specific effects of enrofloxacin on steady-state mRNA for the various genes were not observed. CONCLUSION AND CLINICAL RELEVANCE:
Enrofloxacin may have a detrimental effect on cartilage metabolism in horses, especially in neonates.
Articular cartilage explants and cultured chondrocytes obtained from adult and neonatal horses. PROCEDURE: Full-thickness explants and cultured chondrocytes were incubated in complete or magnesium-deficient media containing enrofloxacin at concentrations of 0, 1, 5, 25, 100, and 500 microg/ml. Incorporation and release of sulfate 35S over 24 hours were used to assess glycosaminoglycan (GAG) synthesis and degradation. An assay that measured binding of dimethylmethylene blue dye was used to compare total GAG content between groups. Northern blots of RNA from cultured chondrocytes were probed with equine cDNA of aggrecan, type-II collagen, biglycan, decorin, link protein, matrix metalloproteinases 1, 3, and 13, and tissue inhibitor of metalloproteinase 1. RESULTS:
A dose-dependent suppression of 35S incorporation was observed. In cartilage of neonates, 35S incorporation was substantially decreased at enrofloxacin concentrations of 25 mg/ml. In cartilage of adult horses, 35S incorporation was decreased only at enrofloxacin concentrations of > or =100 microg/ml. Magnesium deficiency caused suppression of 35S incorporation. Enrofloxacin or magnesium deficiency did not affect GAG degradation or endogenous GAG content. Specific effects of enrofloxacin on steady-state mRNA for the various genes were not observed. CONCLUSION AND CLINICAL RELEVANCE:
Enrofloxacin may have a detrimental effect on cartilage metabolism in horses, especially in neonates.
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https://www.ncbi.nlm.nih.gov/pubmed/?term=Fluoroquinolone+in+antibiotic-loaded+Bone+substitute
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Bone void filler substitutes with antibiotics? Are there even FQ???
https://www.ncbi.nlm.nih.gov/pubmed/?term=Fluoroquinolone+in+antibiotic-loaded+Bone+substitute
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The impregnation and antibiotic efficiency of gentamicin and levofloxacin with Healos was investigated in vitro and compared with Healos without an antibiotic additive. These antibiotic-loaded bone graft substitutes were examined without dilution and with 10-fold and 100-fold dilution for activity against spondylodiscitis-causing bacteria on different agar plates using an agar diffusion method. RESULTS:
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The analysis showed that the antimicrobial activity of HA/collagen-saturated antibiotics corresponded to the antimicrobial dilutions. These results should be further analyzed using in vivo studies to determine the remaining antibiotic efficiency after implantation of bone graft substitutes. PMID: 19784617 DOI: 10.1007/s00132-009-1528-1
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The analysis showed that the antimicrobial activity of HA/collagen-saturated antibiotics corresponded to the antimicrobial dilutions. These results should be further analyzed using in vivo studies to determine the remaining antibiotic efficiency after implantation of bone graft substitutes. PMID: 19784617 DOI: 10.1007/s00132-009-1528-1
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