OBJECTIVETo investigate the expression of high mobility group box 1 (HMGB1) in gingival tissues of chronic periodontitis.

METHODSHuman peripheral blood mononuclear cells(PBMC) were stimulated with 1 microg x mL(-1) lipopolysaccharide (LPS) for 24 h or 48 h. Expression and release of HMGB1 were checked by immunofluorescence and enzyme-linked immunosorbent assay (ELISA), respectively. PBMC were stimulated with 100 ng x mL(-1) HMGB1 or 50 ng x mL(-1) tumor necrosis factor-alpha (TNF-alpha), the expressions of TNF-alpha and HMGB1 in the supernatant were studied by ELISA. Gingival tissues and gingival crevicular fluids (GCF) were collected from patients and healthy people. Expression of HMGB1 in gingival tissues and GCF was studied using immunofluorescence and ELISA, respectively.

RESULTSHMGB1 was translocated from nucleus to cytosol in PBMC after LPS stimulation for 24 h. The content of HMGB1 in the supernatant from stimulated cells was significantly higher than that from unstimulated cells after 48 h (P < 0.01). HMGB1 was released by PBMC in response to TNF-alpha stimulation, it also stimulated PBMC to release TNF-alpha (P < 0.01). Translocation of HMGB1 from nucleus to cytosol was also found in infiltrated cells in gingival tissues from patients, and HMGB1 in GCF from patients was significantly higher than that from healthy people P < 0.01).

CONCLUSIONThe results suggest that HMGB1 may play an important role in the pathological progress of chronic periodontitis.

Chronic Periodontitis ; Gingiva ; HMGB1 Protein ; Humans ; Leukocytes, Mononuclear ; Male ; Tumor Necrosis Factor-alpha

Objective To set up an administrative system of altitude knowledge data so as to raise up the retrieval efficiency of altitude knowledge for the scientific research in hospital.Methods ACCESS 2003 was used to create the administrative system.Results Altitude literature resources could be retrieved rapidly.Conclusion The administrative system of altitude knowledge data is simple in structure,easy to operate,fast in rate and convenient to retrieve.Good result is obtained in practice.[Chinese Medical Equipment Journal,2008,29(2):62-63]

OBJECTIVETo investigate the influence of carbon monoxide on the expression of adhesion molecules stimulated by inflammatory cytokines on human gingival fibroblasts.

METHODSHuman gingival fibroblasts were stimulated with 50 ng x mL(-1) tumor necrosis factor (TNF)-alpha and 10 ng x mL(-1) interleukin (IL)-1beta concurrently in the presence or absence of 500 micromol x L(-1) carbon monoxide releasing molecule (CORM). Expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1 at protein and mRNA level was examined by Western blot and reverse transcription polymerase chain reaction (RT-PCR), respectively. Activity of transcription factor NF-kappaB was evaluated by reporter gene assay.

RESULTSExpression of ICAM-1 and VCAM-1 on human gingival fibroblasts increased dramatically after concurrent stimulation of TNF-alpha and IL-1beta, while CORM inhibited the upregulation of ICAM-1 and VCAM-1. CORM decreased the activity of NF-KB stimulated by TNF-alpha and IL-1beta.

CONCLUSIONCarbon monoxide could be a promising way in treating of periodontitis.

Carbon Monoxide ; Cells, Cultured ; Fibroblasts ; Gingiva ; Humans ; Intercellular Adhesion Molecule-1 ; Interleukin-1beta ; NF-kappa B ; RNA, Messenger ; Tumor Necrosis Factor-alpha ; Vascular Cell Adhesion Molecule-1

OBJECTIVETo investigate the mechanism by which carbon monoxide inhibits the expression of adhesion molecules on human gingival fibroblasts (HGF) stimulated with inflammatory cytokines.

METHODSHGF were cultured in vitro, and stimulated with 50 ng x mL tumor necrosis factor-alpha (TNF-alpha) and 10 ng x mL(-1) interleukin-1beta (IL-1beta) concurrently in the presence or absence of carbon monoxide releasing molecule-3 (CORM-3) at 500 micromol x L-1. Expression of phosphorylated extracellular regulated protein kinase (ERK), phosphorylated c-Jun N-terminal kinase (NK) and phosphorylated p38 in mitogen-activated protein kinase(MAPK) pathway was studied by Western blot at 10 min and 20 min, respectively. Nuclear expression of nuclear factor-kappaB (NF-kappaB) was checked by Western blot after 4 h stimulation. In some experiments, cells were prestimulated by 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one (ODQ) for 8 h before cytokine stimulation and the expression of intercellular adhesion molecule-1 (ICAM-1) was checked by Western blot after 24 h.

RESULTSCORM-3 significantly inhibited the phosphorylation of MAPK p38 after 10 min stimulation with cytokines, but had no signifi-cant effect on the phosphorylation of ERK and JNK. CORM-3 significantly inhibited the nuclear expression of NF-KB-p65 on HGF after 4 h stimulation by inflammatory cytokines. The inhibitory effect of CORM-3 on the expression of ICAM-1 was not influenced by guanylate cyclase inhibitor ODQ.

CONCLUSIONThe inhibitory effect of carbon monoxide on the expression of adhesion molecules might be exerted by its inhibitory effect on the NF-kappaB activity and MAPK p38 phosphorylation.

Carbon Monoxide ; Cytokines ; Fibroblasts ; Gingiva ; Humans ; Intercellular Adhesion Molecule-1 ; JNK Mitogen-Activated Protein Kinases ; Mitogen-Activated Protein Kinases ; NF-kappa B ; Phosphorylation ; Tumor Necrosis Factor-alpha

Objective To investigate the protective effect of peroxisome proliferator receptor γcoactivator (PGC)-1αon he-patic ischemia-reperfusion injury .Methods The rat model of hepatic ischemia-reperfusion injury was established .The expression of PGC-1αwas detected by Western blot after 12 hours of reperfusion .The changes of reactive oxygen species(ROS) ,ATP level and serum liver enzyme activity were measured ,and the liver function was evaluated .On the other hand ,PGC-1α lentiviral overexpres-sion vector was constructed and transfected in rat before ischemia-reperfusion .After ischemia-reperfusion ,the expression of PGC-1α,liver ROS ,ATP level were measured by Western blot to explore the protective role of PGC-1αin liver ischemia reperfusion inju-ry .Results The expression of PGC-1α in ischemia-reperfusion liver was significantly lower than that in the control group (P<0 .05) .The level of ROS[(325 .4 ± 70 .9)RLU vs .(108 .5 ± 25 .2)RLU ,P<0 .05] ,the ALT activity in serum [(367 .8 ± 82 .7)U/L vs .(98 .7 ± 16 .8 )U/L ,P<0 .05]in ischemia-reperfusion liver were increased than that in the control group ,whereas liver ATP production was reduced[(6 .1 ± 3 .7)pmol vs .(19 .8 ± 3 .1)pmol ,P<0 .05)] .The expression of PGC-1αin the liver was significantly up-regulated by PGC-1αlentiviral overexpression vector (57 .3 ± 21 .3) U/L vs .(311 .2 ± 25 .8) U/L ,P<0 .05) ,down-regulated ROS[(98 .7 ± 18 .9)RLU vs .(300 .2 ± 45 .6)RLU ,P< 0 .05] and serum glutamic-pyruvic transaminase[(105 .3 ± 21 .3)U/L vs . (311 .2 ± 25 .8)U/L ,P<0 .05)] ,and increased liver ATP production [(17 .3 ± 3 .1)pmol vs .(5 .8 ± 2 .0)pmol ,P<0 .05]in contrast to non-transfected rats .Conclusion PGC-1αcontributes to protect liver ischemia reperfusion injury .