http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
남성일,권택규 대한이비인후과학회 2014 Clinical and Experimental Otorhinolaryngology Vol.7 No.3
Objectives. To investigate the effect of interleukin (IL)-1β on matrix metalloproteinase (MMP)-9 expression in cochlea and regulation of IL-1β-mediated MMP-9 expression by dexamethasone and the molecular and signaling mechanisms in- volved. Methods. House ear institute-organ of Corti 1 (HEI-OC1) cells were used and exposed to IL-1β with/without dexametha- sone. Glucocorticoid receptor antagonist, RU486, was used to see the role of dexamethasone. PD98059 (an extracel- lular signal-regulated kinases [ERKs] inhibitor), SB203580 (a p38 mitogen-activated protein kinases [MAPK] inhibi- tor), SP600125 (a c-Jun N-terminal kinase [JNK] inhibitor) were also used to see the role of MAPKs signaling pathway(s) in IL-1β-induced MMP-9 expression in HEI-OC1 cells. Reverse transcription-polymerase chain reaction and gelatin zymography were used to measure mRNA expression level of MMP-9 and activity of MMP-9, respectively. Results. Treatment with IL-1β-induced the expression of MMP-9 in a dose- and time-dependent manner. IL-1β (1 ng/mL)- induced MMP-9 expression was inhibited by dexamethasone. Interestingly, p38 MAPK inhibitor, SB203580, signifi- cantly inhibited IL-1β-induced MMP-9 mRNA and MMP-9 activity. However, inhibition of JNKs and ERKs had no effect on the IL-1β-induced MMP-9 expression. Conclusion. These results suggest that the pro-inflammatory cytokine IL-1β strongly induces MMP-9 expression via activa- tion of p38 MAPK signaling pathway in HEI-OC1 cells and the induction was inhibited by dexamethasone.
와우 세포주에서 겐타마이신에 의해 유발된 세포자멸사의 특성
남성일,송대규,박성희,이재훈,이우근,김일만,박재식 대한이비인후과학회 2009 대한이비인후과학회지 두경부외과학 Vol.52 No.3
Background and Objectives:Aminoglycoside antibiotics are ototoxic. Understanding of the molecular mechanisms underlying the drug-induced ototoxicity, however, has been hampered by limited cell availability. Recently, HEI-OC1 cells, which are of an immortalized cochlear cell line sensitive to ototoxic drugs, have been derived from the auditory sensory organ. This study was performed to confirm whether cultured HEI-OC1 cells can be used to evaluate aminoglycoside-induced ototoxicity and the effect of antioxidants against aminoglycoside-induced colchlear cell damage. Materials and Method:Gentamicin was administered for 3 days in the media containing HEI-OC1 cells. Results:Cell viability was decreased by gentamicin in a dose-dependent manner. The cell number was decreased by 50% 3 days after the exposure to 2 mM gentamicin. Penicillin did not have any significant effect. Flow cytometric analysis revealed that sub G1 arrest representing cellular apoptosis was accelerated by gentamicin treatment but not by penicillin. Expression of p27Kip1, the cyclin-dependent kinase inhibitor, was exclusively increased by gentamicin. Reactive oxygen species were also increased by gentamicin when compared with those of the control or when penicillin was used. Caspase-3 activity became increased according to the elevation of gentamicin concentrations. N-acetyl cysteine, but not vitamin E or vitamin C, ameliorated cell survival dose-dependently against gentamicin. Conclusion:The present study reveals that the HEI-OC1 cell line is a good model to evaluate gentamicin-induced ototoxicity. The results suggest that gentamicin-induced apoptosis may be, at least partially, linked to the overproduction of a reactive oxygen species called. Nacetyl cysteine, a free radical scavenger, that decreases the gentamicin ototoxicity.
남성일 대한이비인후과학회 2011 대한이비인후과학회지 두경부외과학 Vol.54 No.8
Endolymphatic hydrops (EH) represents a histopathologic finding in which the structures bounding the endolymphatic space are distended by an enlargement of endolymphatic volume. EH primarily involves the cochlear duct and saccule but can involve the utricle and ampullae of the semicircular canals. EH is a consistent finding in patients with Meniere’s disease, however, the reverse is not true. EH may occur as a consequence of a variety of disorders, including DFNA 9, Alport syndrome, serous labyrinthitis, suppurative labyrinthitis, otosyphilis, temporal bone fracture, surgical trauma, neoplasm, immune disorders, otosclerosis, or Paget’s disease. The mechanism of development of hydrops is also unclear. This review provides information to understand the recent pathophysiologic mechanism and causal disoders in EH.