RESUMEN
<p><b>OBJECTIVE</b>This study observed attenuating effect of hydroxysafflor yellow A (HSYA), an effective ingredient of aqueous extract of Carthamus tinctorius L, on lipopolysaccharide (LPS)-induced endothelium inflammatory injury.</p><p><b>METHODS</b>Eahy926 human endothelium cell (EC) line was used; thiazolyl blue tetrazolium bromide (MTT) test was assayed to observe the viability of EC; Luciferase reporter gene assay was applied to measure nuclear factor-κB (NF-κB) p65 subunit nuclear binding activity in EC; Western blot technology was used to monitor mitogen activated protein kinase (MAPKs) and NF-κB activation. Reverse transcription polymerase chain reaction (RT-PCR) method was applied to observe intercellular cell adhesion molecule-1 (ICAM-1) and E-selectin mRNA level; EC surface ICAM-1 expression was measured with flow cytometry and leukocyte adhesion to EC was assayed with Rose Bengal spectrophotometry technology.</p><p><b>RESULTS</b>HSYA protected EC viability against LPS-induced injury (P <0.05). LPS-induced NF-κB p65 subunit DNA binding (P <0.01) and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor α (IκBα) phosphorylation was inhibited by HSYA. HSYA attenuated LPS triggered ICAM-1 and E-selectin mRNA levels elevation and phosphorylation of p38 MAPK or c-Jun N-terminal kinase MAPK. HSYA also inhibited LPS-induced cell surface ICAM-1 protein expression P <0.01) and leukocyte adhesion to EC (P <0.05).</p><p><b>CONCLUSION</b>HSYA is effective to protect LPS-induced high expression of endothelium adhesive molecule and inflammatory signal transduction.</p>
Asunto(s)
Humanos , Adhesión Celular , Núcleo Celular , Metabolismo , Supervivencia Celular , Chalcona , Química , Farmacología , Usos Terapéuticos , Selectina E , Genética , Metabolismo , Endotelio Vascular , Patología , Regulación de la Expresión Génica , Células Endoteliales de la Vena Umbilical Humana , Metabolismo , Patología , Proteínas I-kappa B , Metabolismo , Inflamación , Quimioterapia , Patología , Molécula 1 de Adhesión Intercelular , Genética , Metabolismo , Leucocitos , Biología Celular , Lipopolisacáridos , Sistema de Señalización de MAP Quinasas , Inhibidor NF-kappaB alfa , Fosforilación , Sustancias Protectoras , Farmacología , Unión Proteica , Quinonas , Química , Farmacología , Usos Terapéuticos , ARN Mensajero , Genética , MetabolismoRESUMEN
OBJECTIVE: To observe the effect of the polyglycol (PEG) modification of trimeric ? peptide(?3) on it’s anti-metastasis ability. METHODS: Using adhesion test to study the effects of ?3 and ?3-PEG on the adhesion of tumor cells to FN. Using artificial basal membrane to study the effects of ?3 and ?3-PEG on the invasion and recombination of basal membrane of tumor cells. RESULTS: Comparing to negative control,?3 and ?3-PEG could both inhibit the adhesion of SMMC-7721 and HCCLM6 tumor cells to FN with time-dependently(P
RESUMEN
Objective To summarize the progress on the injury mechanism of vascular endothelial cells in atherosclerosis.Methods The latest progress was reviewed in recent literatures.Results All kinds of etiological factors have activated NF kappa B and cytokines in the development of atherosclerosis, which lead to expression of cell adhesive molecules and adhesion of monocytes to vascular endothelial cells.A variety of inflammatory mediums are released, which can directly damage endothelial cells.Besides, the inflammatory mediums make monocytes and neutrophils attach to endothelial cells by immune mechanisms, which injure the endothelial cells more severely. Meanwhile the damaged membrance structure leads to the production of AECA which activates the complementary system. Then the vascular endothelial cell injury is aggravated and the development of atherosclerosis accelerated. Conclusion It is very important to recognize the injury mechanism of vascular endothelial cells in the development of atherosclerosis for prevention and treatment of atherosclerosis.
RESUMEN
Objective To explore the effect of hypoxia on the in vitro invasion of lung carcinoma cells and its molecular basis. Methods Small cell lung carcinoma cells(H128) were exposed to hypoxia(5%O 2,5%CO 2,90%N 2) or anoxia(95%N 2,5%CO 2)condition for 48 hours. The invasive ability of the cancer cells was assayed with HABM-HEM model. The expression of E-cadherin and ? 1-integrin on the cells was also assayed by flow cytometry. Results Compared with normoxia group, the invasive ability of the cancer cells increased, the expression of E-cadherin decreased, and the expression of ? 1-integrin increased in hypoxia group. In anoxia group, the invasive ability and the expression of E-cadherin and ? 1-integrin all decreased compared with normoxia group. Conclusions Moderate hypoxia can down-regulate the expression of E-cadherin, up-regulate the expression of ? 1-integrin, and increase the invasion of carcinoma cells. But serious hypoxia can decrease the expression of adhesive molecules and the invasion of the cancer cells.
RESUMEN
Objective: To study the expression of neural cell adhesive molecule (NCAM) and its clinical significance in human astrocytoma. Methods: Expression of NCAM mRNA and its protein (CD56) were detected by in situ hybridization using NCAM antisense complementary RNA probe and by immunohistochemical staining in 40 cases of astrocytoma. Results:Expression of NCAM mRNA and CD56 in 1, 2 grade astrocytoma was significantly higher than that in 3, 4 grade astrocytoma. The expression of NCAM mRNA accorded with the expression of CD56. Conclusion: Expression of NCAM mRNA and CD56 is correlated with the malignant degree of astrocytoma. The high expression of NCAM may be correlated with invasion and metastasis of astrocytomas. It is suggested that the expression of NCAM may be an important clue in assessment of malignancy and invasion of astrocytoma, and it may be a guide for the choice of post operation therapy.