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低强度激光对软骨胶原合成和细胞增殖影响 被引量:4

Effects of low intensity laser irradiation on proliferation and collagen synthesis of chondrocytes in vitro
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摘要 研究了810nm低强度Ga-Al-As半导体激光对兔软骨细胞增殖和胶原合成的影响。取新西兰白兔的关节软骨细胞,用浓度为2%的新生牛血清(NCS)培养媒介培养。激光功率密度分别为1.75、3.50、5.25、7.00和8.75mW/cm2,以连续方式每天照射软骨细胞5min,共5d。分别用四甲基氮唑盐(MTT)法和氯胺T消化法检测细胞的增殖和胶原蛋白合成。结果发现:第8天实验结束时,各激光照射组细胞数量随激光强度线性增加,与无激光照射组的差异有统计学意义(P<0.01),其中最佳照射功率密度为7.00mW/cm2;第8天实验结束时,激光照射组胶原含量显著低于对照组(P<0.01),8.75mW/cm2组与3.50~7.00mW/cm2组有显著差异(P<0.05)。激光照射7.00mW/cm2组与对照组第2、4、6和8天胶原含量的测定表明,照射组胶原含量先增加后降低,其中第6天照射组胶原含量最高,与相应对照组有极显著差异(P<0.01),对照组胶原含量在第6天后急剧增加,第8天与照射组有极显著差异(P<0.01)。研究结果表明,低强度Ga-Al-As半导体激光能促进兔关节软骨细胞的生长,有望成为临床治疗软骨损伤的一种有效方法。 To investigate the potential effects of continuous wave 810 nm low intensity Ga-Al-As laser irradiation(LIGL) on proliferation and collagen synthesis of rabbit articular cartilage cells in vitro. Articular cartilage cells of New Zealand white rabbits were suspended in medium with concentration 2% of newborn calf serum. The chondrocytes were treated by LIGL at 1.75,3.50,5.25,7.00 and 8.75 mW/cm^2 for 5 minutes per day, respectively, for 5 days, and then incubated till the 8th day. The proliferation and collagen synthesis were assessed by a 3-(4,5-dimenthylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) test and hydroxyproline(Hpr) content measurement, respectively. The MTT tests showed that LIGL irradiation significantly promoted chondrocyte proliferation (P〈0.01) ,whose optimal intensity was 7.00 mW/cm^2. The Hpr content tests showed that LIGL irradiation significantly inhibited collagen synthesis (P〈0. 01) at the end of the study. The group of 8.75 mW/cm^2 was significantly different from groups of 3.50,5.25 and 7.00 mW/cm^2 (P〈0.05). Collagen content of the group of 7.00 mW/cm^2 was significantly higher than that without LIGL irradiation at the day of 6th (P〈0.01) ,but significantly lower than that without LIGL irradiation at the day of 8th (P〈0.01). The results show that low intensity GA-Al-As diode 810 nm laser irradiation might promote the proliferation of articular chondrocytes,which might be used to achieve the repair of articular cartilage in clinic.
出处 《光电子.激光》 EI CAS CSCD 北大核心 2008年第1期139-142,共4页 Journal of Optoelectronics·Laser
基金 国家自然科学基金资助项目(60178003,6478048) 广东省卫生厅资助项目(A2003653)
关键词 低强度激光 软骨细胞 增殖 胶原合成 low intensity laser chondrocytes proliferation collagen synthesis
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  • 1Hubbard M J.Articular debridement versus washout for degeneration of the medial femoral condyle.A five-year study[J].J Bone Joint Surg,1996,78(2):217-219.
  • 2Minas T,Nehrer S.Current concepts in the treatment of articular cartilage defects[J].Orthopedics,1997,20(6):5256-538.
  • 3Brittberg M,Lindahl A,Nilsson A,et al.Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation[J].New Engl J Med,1994,331:889-895.
  • 4Rubak J M,Poussa M,Ritsila V.Chondrogenesis in repair of articular cartilage defects by free periosteal grafts in rabbits[J].Acta Orthop Scand,1982,53:181-186.
  • 5Delaney J P,Odriscoll S W,Salter R B.Neochondrogenesis in free intra-articular periosreal autografts in an immobilized and paralyzed limb[J].Clin Orthop Rel Res,1989,248:278-282.
  • 6Eells J T,Henry M M,Summerfelt P,et al.Therapeutic photobiomodulation for methanol-induced retinal toxicity[J].Natl Acad Sci U S A,2003,100(6):3439-3444.
  • 7Shefer G,Oron U,Irintchev A,et al.Skeletalmuscle cell activation by low-energy laser irradiation:a role for the MAPK/ERK pathway[J].J Cell Physiol,2001,187(1):73-80.
  • 8Lubart R,Lavi R,Fiedmann H,et al.Photochemistry and photobiology of light absorption by living cells[J].Photomed Laser Surg,2006,24(2):179-185.
  • 9Duan R,Liu T C Y,Li Y,et al.Signal transduction pathways involved in low intensity He-Ne laser-induced respiratory burst in bovine neutrophils:A potential mechanism of low intensity laser biostimulation[J].Lasers Surg Med,2001,29:174-178.
  • 10Duan R,Zhu L,Liu T C,et al.Light emitting diode irradiation protect against the amyloid beta 25-35 induced apoptosis of PC12 cell in vitro[J].Lasers Surg Med,2003,33:199-203.

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