2006 Fiscal Year Final Research Report Summary
Study of the gene therapy with extracorporeal shockwaves for Discogenic low back pain
| Project/Area Number |
17591547
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Chiba University |
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Principal Investigator |
TAKAHASHI Kazuhisa Chiba University, Graduate School of Medicine, Assistant Professor, 大学院医学研究院, 助教授 (20179477)
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| Co-Investigator(Kenkyū-buntansha) |
OHTORI Seiji Chiba University, Hospital, Assistant, 医学部附属病院, 助手 (40361430)
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| Project Period (FY) |
2005 – 2006
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| Keywords | extracorporeal shockwave / Nuclear Factor-kappa Decoy / discogenic low back pain / inflammatory pain / gene therapy |
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| Research Abstract |
Study Design. In vitro and in vivo study of a rat inflammatory pain model using nuclear factor-kappa B (NF-kB) decoy.
Summary and Background Data. Transcription factor NF-kB is reported to play a crucial role in regulating proinflammatory cytokine gene expression. We hypothesized that inhibiting NF-kB gene expression with NF-kB decoy may suppress inflammatory pain.
Methods. NF-kB decoy-FITC was induced in explant culture, endoneurally injected into the sciatic nerve, and its transduction efficiency into DRG measured. For behavioral testing, 12 rats received plantar injections of complete Freund's adjuvant and were divided into three groups : decoy group - single endoneural injection of 10111 of NF-kB decoy (n=4) ; saline group - single endoneural injection of 10μl of saline (n=4) ; and naive group - untreated (n=4). Behavioral testing was performed using von Frey filaments and a Hargreaves device with a heat source.
Results. Total transduction efficiency of NF-kB decoy-FITC was 53.6% in vitro and 20.5% in vivo. No statistical differences were observed with respect to types of cell size distributions of all FITC-positive neurons. In behavioral testing, withdrawal latencies or thresholds significantly differed between the decoy group and the saline group from 2 to 14 days after surgery in the mechanical allodynia experiments, and from 2 to 3 days after surgery in the thermal hyperalgesia experiments.
Conclusions. NF-kB decoy was conveyed and transduced into DRG both in vivo and in vitro. Additionally, NF-kB decoy reduced mechanical allodynia and thermal hyperalgesia in the rat inflammatory pain model, suggesting that inhibition of NF-kB with NF-kB decoy may represent a key mechanism for mediating inflammation or reducing inflammatory pain.
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