OBJECTIVETo observe effects of acupuncture on serum interleukin-1 (IL-1) and soluble intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in the patient of cerebral infarction.

METHODSEighty-two cases of cerebral infarction were randomly divided into a treatment group treated by balanced muscular tension needling method, and a control group by traditional needling method. The levels of serum IL-1, sICAM-1 and sVCAM-1 were determined with enzyme-linked immunosorbent assay (ELISA).

RESULTSThe levels of serum IL-1, sICAM-1 and sVCAM-1 in the patient of cerebral infarction were significantly higher than those in the healthy persons (P < 0.01); there were positive correlation between sICAM-1 or sVCAM-1 level and IL-1 level (r = 0.743, P < 0.001; r = 0.862, P < 0.001). The three indexes improved to a certain extent in the two groups, with the treatment group superior to the control group (P < 0.01).

CONCLUSIONThe improvement of nervous function by the balanced muscular tension needling method in the patient of cerebral infarction is possibly related with decrease of IL-1, sICAM-1 and sVCAM-1 levels.

OBJECTIVE: To investigate the effect of Quercetin on cell cycle and adhesive molecules of NOD.SCID mice with acule B lymphocytic leuaemia(B-ALL). METHODS: 5×10 Nalm-6(B-ALL cell line) cells were injected into the tail vein of 48 NOD/SCID mice to establish the NOD/SCID mice with B-ALL. After 15 day, the NOD/SCID mice with B-ALL were randomly divided into 3 groups: salive group as control (injection with saline of 0.2 ml/mouse), cyclophos-phamid group (injection with cyclophosphamide of 100µg/kg) and quercetin group(injection with quercetin of 3 mg/kg). After treatment for 21 d, the perecntage of Nalm-6 cells in G1, G2, M and S phases was detected by flow cytonetry; the B lymphocytes Nalm-6 cells, neutrophils and WBC in while blood were counted before and after treatment; the expression of intercellalar. Adhesion molecole-1(FCAIU-1), vascular cell adhesion molecule-1(VCAM-1) and P-selectin was detected by double autibody soundwich method. RESULTS: Compared with level before treatment, the expression of ICAM-1, VCAM-1 and P-selectin decreased after treatment with guercetin, The hemogram showed that the peripheral blood nentrophil level obviously increased, while the levels of B lymphocytes, Nalm-6 cells and WBC count decreased obviously after treatment with guercetin. The cell proliferatim rario in G0/G1 phase decreased, yet the cell proliferation ratio in S and G2/M phases increased after treatment with guercetin. CONCLUSION The guercetin can decrease the intercellular adhesion through inhibition of ICAM-1 expression, and arrests Nalm-6 cells in S and G2/M phases. The guercetin has obviously inhibitory effect on B-ALL cells.
Animals ; Cell Adhesion ; Cell Adhesion Molecules ; Intercellular Adhesion Molecule-1 ; Leukemia, B-Cell ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Quercetin ; Vascular Cell Adhesion Molecule-1

BACKGROUND: Angiotensin II (AngII) and abnormal oscillatory shear stress are highly associated with vascular inflammation including atherosclerosis. However, it is poorly understood how interactions between AngII and shear stress in human aortic endothelial cells (HAEC) are involved in mechanisms by which cellular adhesion molecules are expressed. The purpose of this study was to improve that understanding. METHODS: AngII (10(-7)M for 6 hr) and two-types of shear stress treatments were used: laminar shear stress (LS: unidirectional, 12 dynes/cm2) and oscillatory shear stress (OS: bi-directional, 5 dynes/cm2, 1 Hz) in HAEC. Immunoblotting was used to detect expression of cellular adhesion molecules markers such as vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM1). RESULTS: AngII significantly increased VCAM1 and ICAM1 expression in HAEC that had been reduced due to pretreatment with telmisartan. AngII-LS co-stimulation and AngII-OS co-stimulation significantly increased VCAM1 and ICAM1 expression in HAEC. The expression levels of VCAM1 and ICAM1 were also, significantly reduced when pretreated with telmisartan. However, VCAM1 and ICAM1 expression were significantly reduced under LS and OS stimulation. CONCLUSIONS: Telmisartan may modulate the expressions of VCAM1 and ICAM1 via different types of shear stress in HAEC that are activated by AngII.
Angiotensin II ; Angiotensins ; Atherosclerosis ; Benzimidazoles ; Benzoates ; Endothelial Cells ; Humans ; Immunoblotting ; Inflammation ; Intercellular Adhesion Molecule-1 ; Vascular Cell Adhesion Molecule-1

PURPOSE: To clarify the relationship between aseptic loosening of hip arthroplasty and adhesion molecules on interfacial membrane from revisional hip arthroplasty. MATERIALS AND METHODS: We studied 26 revisional total hip arthroplasties between May 2004 and July 2006, and 15 synovial tissues from hip fractures were selected as the control group. We analyzed the degree of femoral osteolysis by Paprosky's classification. We examined the expression of soluble endothelial leukocyte adhesion molecule-1 (E-selectin), vascular adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) by immunohistochemical staining technique. We compared and analyzed radiologic evaluation and expression of adhesion molecules. RESULTS: Expression of E-selectin was observed in 100%, VCAM-1 in 42.3% and ICAM-1 in 34.6%. Expression of adhesion molecules were increased compared to the control group (p<0.05). The higher the expression of E-selectin, the higher the degree of osteolysis (p=0.023). CONCLUSION: These results showed that adhesion molecules are involved in aseptic loosening of hip arthroplasties, and we proposed that E-selectin may strongly engage in the cascade of aseptic loosening in hip arthroplasty.
Arthroplasty* ; Classification ; E-Selectin ; Hip Fractures ; Hip* ; Intercellular Adhesion Molecule-1 ; Membranes* ; Osteolysis ; Vascular Cell Adhesion Molecule-1

Endothelial activation and subsequent recruitment of inflammatory cells are important steps in atherogenesis. The increased levels of cell adhesion molecules (CAM) have been identified in diabetic vasculatures, but the underlying mechanisms remain unclear. To determine the relationship among vascular production of superoxide, expression of CAM and diabetes, superoxide generation and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E- and P-selectin in the aorta from control (C57BL/6J) and diabetic mice (ob/ob) were measured. In situ staining for superoxide using dihydroethidium showed an increased superoxide production in diabetic aorta, accompanied with an enhanced NAD (P) H oxidase activity. Immunohistochemical analysis revealed that the endothelial expression of ICAM-1 (3.5+/-0.4) and VCAM-1 (3.8+/-0.3) in diabetic aorta was significantly higher than those in control aorta (0.9+/-0.5 and 1.6+/-0.3, respectively), accompanied with the enhanced expression of gp91phox, a membrane subunit of NAD (P) H oixdase. Furthermore, there was a strong positive correlation (r=0.89, P< 0.01 in ICAM-1 and r=0.88, P< 0.01 in VCAM-1) between ICAM-1/VCAM-1 expression and vascular production of superoxide. The present data indicate that the increased production of superoxide via NAD (P) H oxidase may explain the enhanced expression of CAM in diabetic vasculatures.
Animals ; Aorta* ; Atherosclerosis ; Cell Adhesion Molecules* ; Cell Adhesion* ; E-Selectin ; Intercellular Adhesion Molecule-1 ; Membranes ; Mice* ; NAD ; Oxidoreductases ; P-Selectin ; Superoxides* ; Vascular Cell Adhesion Molecule-1

BACKGROUND AND OBJECTIVES: Despite significant improvement in the field of angioplasty, restenosis remains a major obstacle to the long-term success of the procedure. Radiation can effectively inhibit neointimal hyperplasia by causing the arrest of mitosis during cell division and limiting proliferation by reducing the number of regenerating clonal progenitors. Balloon injury could induce the cell adhesion molecule, ICAM-1 and VCAM-1, on SMCs and regenerating endothelial cells (ECs). ICAM-1 and/or VCAM-1 may play a role in the progression of neointimal hyperplasia induced by balloon injury and external radiation may effectively inhibit neointimal hyperplasia by attenuating their expression. The purpose of this study was to examine the effect of external radiation against ICAM-1 and VCAM-1 on neointimal hyperplasia after balloon injury in rat carotid arteries. MATERIAL AND METHODS: A standardized carotid balloon catheter arterial injury was produced in 51 rats and external beam radiation with doses from 5-20 Gy were delivered in 28 rats (radiation treated group) at 24 hours after injury. To investigate the effect of the external radiation on neointimal hyperplasia, the intima area and the intima/medial area of arteries were measured at day 14 after injury. The expressions of ICAM-1 and VCAM-1 at day 2, day 7, and day 10 after injury were studied in control group and radiation treated group by immunohistochemistry. RESULTS: Means of intimal area and intima/medial ratio in radiation treated group were significantly lower than those in control group and significantly reduced with increasing radiation dosage. At day 2 after injury, medial SMCs of injury group extensively expressed ICAM-1, while it was focally expressed with 10 Gy radiation treated group. At day 7 and day 10 after injury, ICAM-1 expression on medial SMCs was attenuated and neointimal ICAM-1 expression was increased. As compared with control group, ICAM-1 expression after radiation was weak and focal just around the internal elastic lamina. At 2 days after injury, medial SMCs moderately expressed VCAM-1, which was weakly and focally expressed with 10 Gy radiation treated group. At day 7 and day 10 after injury, focal expression of VCAM-1 was noted around the internal elastic lamina, but there was no VCAM-1 expression on neointima with radiation. CONCLUSION: External radiation after carotid arterial injury may potentially inhibit SMC proliferation and neointimal hyperplasia, and balloon injury-induced or upregulated expressions of ICAM-1 and VCAM-1 may be attenuated with external radiation.
Angioplasty ; Animals ; Arteries ; Carotid Arteries ; Catheters ; Cell Adhesion* ; Cell Division ; Endothelial Cells ; Hyperplasia* ; Immunohistochemistry ; Intercellular Adhesion Molecule-1* ; Mitosis ; Neointima ; Radiation Dosage ; Rats* ; Vascular Cell Adhesion Molecule-1

The purpose of this study was to assess the expression of ICAM-1, VCAM-1 and PECAM-1 in allergic and chemical conjunctivitis. The allergic and chemical conjunctivitis were induced in C57BL/6 mouse by compound 48/80(C48/80) and 2% characterized clinically by blepharospasm 100%, chemosis 80%, injection AgNO3, respectively. The allergic conjunctivitis was characterized clinically by blepharospasm 100%, chemosis 80%, injection, 40%, mucous discharge 20%, but the chemical conjunctivitis by blepharospasm 80%, chemosis 60%, infection 40% and no mucous discharge at 30 minute after topical application. On the endothelial cells, ICAM-1 was expressed from 1 to 48 hours, VCAM-1 from 6 to 72 hours and PECAM-1 from 1 to 72 hours in allergic conjunctivitis. In chemical conjuctivitis, the expression of ICAM-1 was observed from 6 to 72 hours. The expression of VCAM-1 was observed from 24 and 72 hours. The expression of PECAM-1 was demonstrated from 6 to 72 hours. The expression of cell adhesion molecules, particulary VCAM-1 and PECAM-1, was slighter in chemical conjunctivitis compared to allergic conjunctivitis. In conclusion, experimental allergic and chemical conjunctivitis demonstrate that cell adhesion molecules play a role in part in ocular inflammation and that there are differences between the adhesion molecule expression of two types of confunctivitis.
Animals ; Antigens, CD31 ; Blepharospasm ; Cell Adhesion Molecules ; Conjunctivitis* ; Conjunctivitis, Allergic ; Endothelial Cells ; Inflammation ; Intercellular Adhesion Molecule-1 ; Mice ; Vascular Cell Adhesion Molecule-1

BACKGROUND: Inflammation is a frequent reaction following therapeutic irradiation. Since the upregulation of adhesion molecules on endothelial cell surface is known to be associated with inflammation, the expression of adhesion molecules is an important therapeutic target. METHODS: Treatment of human umbilical endothelial cells (HUVECs) with gamma irradiation (gamma R) induces the expression of adhesion proteins such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Changes in the expression of these proteins on gamma irradiated HUVECs which had been treated previously with allicin were measured by ELISA. RESULTS: In the present study, we demonstrate that allicin inhibits the gamma R induced expression of ICAM-1, VCAM-1, and E-selectin on HUVEC in a dose-dependent manner. Allicin was also found to inhibit thegamma R induced production of nitric oxide (NO). CONCLUSION: These data suggest that allicin has a therapeutic potential for the treatment of various inflammatory disorders associated with increase numbers of endothelial leukocyte adhesion molecules.
Cell Adhesion Molecules ; E-Selectin ; Endothelial Cells* ; Enzyme-Linked Immunosorbent Assay ; Humans* ; Inflammation ; Intercellular Adhesion Molecule-1 ; Nitric Oxide ; Up-Regulation ; Vascular Cell Adhesion Molecule-1

Heparin is a well-known anticoagulant widely used in various clinical settings. Interestingly, recent studies have indicated that heparin also has anti-inflammatory effects on neuroinflammation-related diseases, such as Alzheimer's disease and meningitis. However, the underlying mechanism of its actions remains unclear. In the present study, we examined the anti-inflammatory mechanism of heparin in cultured cerebral endothelial cells (CECs), and found that heparin inhibited the tumor necrosis factor alpha(TNF alpha)-induced and nuclear factor kappa B (NF-kappa B)-dependent expression of adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), which are crucial for inflammatory responses. Heparin selectively interfered with NF-kappa B DNA-binding activity in the nucleus, which is stimulated by TNF alpha. In addition, non-anticoagulant 2,3-O desulfated heparin (ODS) prevented NF-kappa B activation by TNF alpha, suggesting that the anti-inflammatory mechanism of heparin action in CECs lies in heparin's ability to inhibit the expression of cell adhesion molecules, as opposed to its anticoagulant actions.
Alzheimer Disease ; Cell Adhesion Molecules ; Endothelial Cells ; Heparin ; Intercellular Adhesion Molecule-1 ; Meningitis ; NF-kappa B ; Tumor Necrosis Factor-alpha ; Vascular Cell Adhesion Molecule-1

BACKGROUND AND OBJECTIVES: Topical steroid therapy may play an important role in reducing the vascular cell adhesion molecule-1(VCAM-1) expression in the nasal polyp. Various adhesion molecules such as VCAM-1 promote formation of nasal polyp and they show different sensitivity to steroid therapy. Changes in the VCAM-1 expression after a 8-week intranasal steroid treatment were investigated. MATERIALS AND METHODS: The endothelial expression of VCAM-1 in biopsy specimens from the nasal polyps and inferior turbinates was investigated using the immunohistochemical staining in 20 patients with nasal polyposis. Biopsy specimens were obtained before, immediately after and 2 months after treatment with 100g fluticasone propionate in each nostril twice daily. The immunohistochemical activity in pretreatment and posttreatment specimens was analyzed. RESULTS: The VCAM-1 expression was significantly higher in the nasal polyps than in inferior turbinates(p=0.002). Immediately after the treatment, the VCAM-1 expression in the nasal polyps was significantly reduced(p=0.001). But the VCAM-1 expression in nasal polyps returned to the pretreatment level 2 months after the treatment. CONCLUSIONS: Intranasal steroid therapy may have an anti-inflammatory effect on nasal polyps by down regulating the VCAM-1 expression
Biopsy ; Cell Adhesion ; Diethylpropion ; Endothelium, Vascular* ; Humans ; Nasal Polyps* ; Steroids ; Turbinates ; Vascular Cell Adhesion Molecule-1* ; Fluticasone