BACKGROUND: We intended to clarify the hypothesis that minimally invasive total hip arthroplasty (MI-THA) leads to less tissue damage and inflammatory response than does conventional total hip arthroplasty (C-THA). METHODS: We performed 30 cases of THA between September 2005 and May 2006 and evaluated these cases prospectively. We chose 15 MI-THA cases for the study group and another 15 C-THA cases for the control group. We checked skeletal muscle marker enzymes, such as serum creatinine kinase and aldolase, the pro-inflammatory cytokines, interleukin (IL)-6 and 8, and the anti-inflammatory cytokines, IL-10 and IL-1 receptor antagonist (ra) the day before surgery and at postoperative days 1, 7, and 14. RESULTS: On postoperative days 1 and 3, the study group showed significantly lower serum creatinine kinase, IL-6, IL-10, and IL-1ra values than those in the control group. Additionally, IL-8 was significantly lower on day 7 after surgery. CONCLUSIONS: These data show that MI-THA decreased the release of muscle marker enzymes due to tissue damage immediately after surgery and minimized the inflammatory response related to the surgery during the early postoperative period.
Adult ; Aged ; Aged, 80 and over ; Arthroplasty, Replacement, Hip/*adverse effects ; Biological Markers/blood ; Creatine Kinase/blood ; Female ; Fructose-Bisphosphate Aldolase/blood ; Humans ; Interleukin 1 Receptor Antagonist Protein/blood ; Interleukin-10/blood ; Interleukin-6/blood ; Interleukin-8/blood ; Male ; Middle Aged ; Minimally Invasive Surgical Procedures/adverse effects ; Soft Tissue Injuries/*blood/etiology

BACKGROUND: allergic disease is an inflammatory disease, whose main inflammatory cells are eosinophils, mast cells, and T lymphocytes. From that point, new therapeutic targets on allergic inflammation focusing on them are under investigation. We extracted four isoflavonoids from sophorica japonica such as sophi, orobol, genistin and genistein which are known PTK antagonists. We documented that these iso-flavonoids except genistein had an antagonism on IL-5 and IL-3 in vitro eosinophil activation and also in allergic mouse model sensitized by OA(ovualbumin). Their common action is due to the common beta chains. GM-CSF also share common beta chains, through which it activates eosinophils. OBJECTIVES: From the above results, We observed the antagonistic effects of these compounds on GM-CSF using eosinophil activation in vitro. METHODS: LTC4 which was detected by RIA and ECP by UniCAP were activation markers. RESULTS: Among those compounds, sophi was the most potent antagonist on GM-CSF induced LTC4 release and even on degranulation and orobol and genistin also had antagonism on them but genistein an antagonist of PTK did not show any antagonistic effects. CONCLUSION: From these results, We concluded these three iso-flavonoids were GM-CSF antagonists and the mechanism might not be through PTK signaling.
Animals ; Eosinophils ; Genistein ; Granulocyte-Macrophage Colony-Stimulating Factor ; Inflammation ; Interleukin-3 ; Interleukin-5 ; Leukotriene C4 ; Mast Cells ; Mice ; T-Lymphocytes

BACKGROUND: Allergic disease is an inflammatory disease, whose main inflammatory cells are eosinophils, mast cells, and T lymphocytes. From that point, new therapeutic targets on allergic inflammation focusing on them are under investigation. We extracted four isoflavonoids from Sophorica japonica such as sophi, orobol, genistin, and genistein which has been known as PTK antagonist. We documented those three iso-flavonoids except genistein had an anti-inflammatory effect as potent as dexamethasone on carageen-induced ear model. Also they had antagonism on the Y-16 cell line, whose growth is dependent on IL-5. OBJECTIVES: From above results, in this experiment, we tried to find antagonistic effects of those compounds on IL-5 using the inhibition of eosinophil activation and survival in vitro and possibility of anti-allergic medicine. METHODS: LTC4 by RIA and ECP for degranulation by UniCAP(TM), which had been used previously were activation markers. RESULTS: Among those compounds, sophi was the most potent antagonist on IL-5 induced LTC4 release, degranulation, and survival. Orobol and genistin also had antagonism on them, but genistein, an antagonist of PTK didn't show any antagonistic effects. CONCLUSION: From these results, we concluded those three iso-flavonoids were IL-5 antagonist, and the mechanism of it might not be through PTK signaling.
Cell Line ; Dexamethasone ; Ear ; Eosinophils ; Genistein ; Inflammation ; Interleukin-5* ; Leukotriene C4 ; Mast Cells ; T-Lymphocytes