title: Heme oxygenase-1 modulates degeneration of the intervertebral disc after puncture in Bach 1 deficient mice.
abstract: OBJECTIVE
  Intervertebral disc degeneration is considered to be a major feature of low back pain. Furthermore, oxidative stress has been shown to be an important factor in degenerative diseases such as osteoarthritis and is considered a cause of intervertebral disc degeneration. The purpose of this study was to clarify the correlation between oxidative stress and intervertebral disc degeneration using Broad complex-Tramtrack-Bric-a-brac and cap'n'collar homology 1 deficient (Bach 1-/-) mice which highly express heme oxygenase-1 (HO-1). HO-1 protects cells from oxidative stress.
  
  
  METHODS
  Caudal discs of 12-week-old and 1-year-old mice were evaluated as age-related models. Each group and period, 5 mice (a total of 20 mice, a total of 20 discs) were evaluated as age-related model. C9-C10 caudal discs in 12-week-old Bach 1-/- and wild-type mice were punctured using a 29-gauge needle as annulus puncture model. Each group and period, 5 mice (a total of 60 mice, a total of 60 discs) were evaluated. The progress of disc degeneration was evaluated at pre-puncture, 1, 2, 4, 8 and 12 weeks post-puncture. Radiographic, histologic and immunohistologic analysis were performed to compare between Bach 1-/- and wild-type mice.
  
  
  RESULTS
  In the age-related model, there were no significant differences between Bach 1-/- and wild-type mice radiologically and histologically. However, in the annulus puncture model, histological scoring revealed significant difference at 8 and 12 weeks post-puncture. The number of HO-1 positive cells was significantly greater in Bach 1-/- mice at every period. The apoptosis rate was significantly lower at 1 and 2 weeks post-puncture in Bach 1-/- mice.
  
  
  CONCLUSIONS
  Oxidative stress prevention may avoid the degenerative process of the intervertebral disc after puncture, reducing the number of apoptosis cells. High HO-1 expression may also inhibit oxidative stress and delay the process of intervertebral disc degeneration.
authors: Department of Orthopaedic Surgery, Graduate School of Biomedical Sciences, Hiroshima University, Kasumi, Hiroshima, 734-8551, Japan, xxxhr307@ybb.ne.jp
authors: Ryo
authors: R
authors: Ohta
authors: Nobuhiro
authors: N
authors: Tanaka
authors: Kazuyoshi
authors: K
authors: Nakanishi
authors: Naosuke
authors: N
authors: Kamei
authors: Toshio
authors: T
authors: Nakamae
authors: Bunichiro
authors: B
authors: Izumi
authors: Yuki
authors: Y
authors: Fujioka
authors: Mitsuo
authors: M
authors: Ochi
mesh_terms: D000375:Aging / Q000502:physiology; D000818:Animals; D050976:Basic-Leucine Zipper Transcription Factors / Q000172:deficiency*; D002574:Cervical Vertebrae / Q000293:injuries*; D051547:Heme Oxygenase-1 / Q000378:metabolism*; D055959:Intervertebral Disc Degeneration / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018384:Oxidative Stress / Q000502:physiology*
chemical_list: C486316:Bach1 protein, mouse; D050976:Basic-Leucine Zipper Transcription Factors; D051547:Heme Oxygenase-1