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1.
Chinese Journal of Dermatology ; (12): 726-730, 2013.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-442093

RESUMO

Objective To investigate the effect of chloroform extract of Zingiber mioga Roscoe on human dermal microvascular endothelial cell (HDMEC) expression of cell adhesion molecules and adhesivity to lymphocytes.Methods HDMECs were isolated from human foreskin tissue and subjected to subculture.After several passages,some HDMECs were treated with chloroform extract from Zingiber mioga Roscoe (CFMG) of 200 mg/L for 30 minutes before or after 24-hour stimulation with tumor necrosis factor (TNF)-α or interleukin (IL)-1α.Subsequently,enzyme-linked immunosorbent assay was performed to determine the expression levels of intercellular adhesion molecule-1 (ICAM-1),vascular cell adhesion molecule-1 (VCAM-1) and E-selectin on HDMECs.Both T lymphocytes isolated from venous blood of healthy adults and Ramos Burkitt's lymphoma B cells were labelled with chromium-51 and incubated with the HDMECs for four hours followed by the determination of radiation intensity of lymphocytes adhering to HDMECs using a gamma-counter.Results Compared with 0.2% dimethyl sulfoxide (DMSO),CFMG slightly down-regulated the expression of ICAM-1,VCAM-1 and E-selectin on resting HDMECs (all P > 0.05).In comparison with culture medium,TNF-α enhanced the expressions of ICAM-1,VCAM-1 and E-selectin significantly (all P < 0.01),and IL-1α elevated the expressions of ICAM-1 and E-selectin markedly(both P < 0.01) as well as the expression of VCAM-1 slightly (P > 0.05).The upregulating effects of TNF-α and IL-1α on the expressions of adhesion molecules were notably suppressed by the CFMG treatment prior to the stimulation with TNF-α and IL-1α(all P < 0.01),but not affected by that after the stimulation (all P > 0.05).The adhesivity of HDMECs to T lymphocytes and Ramos cells was slightly decreased by CFMG treatment compared with 0.2% DMSO (both P > 0.05),but was markedly increased by TNF-α and IL-1α compared with the culture medium (both P < 0.01).Conclusions CFMG may play an antiinflammatory role via blocking the up-regulating effect of pre-inflammatory cytokines such as TNF-α and IL-1α on the expression of adherence molecules on HDMECs and,hence,inhibiting inflammatory cell infiltration in tissue.

2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-575270

RESUMO

Objective To compare the morphology and ultrastructure changes of human gastric adenocarcinoma cell line treated by tachyplesin and n-sodium butyrate. Methods Light microscope,scanning electron microscope and transmission electron microscope were used to observe human gastric adenocarcinoma cell line BGC-823 treated by 2.0?mg/L tachyplesin,2.0?mmol/L n-sodium butyrate and 1.0?mg/L tachyplesin in combination with 1.0?mmol/L n-sodium butyrate respectively. Results Light microscope observation showed that BGC-823 cells treated by tachyplesin,n-sodium butyrate and tachyplesin+n-sodium butyrate possessed the similar cell modality as follow: the volume of cell increased,the shape of cell became flat and outspread,nucleo-cytoplasmic ratio decreased,the shape of nucleus was rounde,the number of nucleolus decreased.Scanning electron microscope and transmission electron microscope observation showed that,in the BGC-823 cells which were treated with tachyplesin,n-sodium butyrate and tachyplesin in combination with n-sodium butyrate respectively,microvilli and filopodia reduced,sheed pseudopodia increased,the shape of nucleus became regular,heterochromatin decreased while euchromatin increased,the number of mitochondria increased and its structure appeared consistent,Golgi complex turned to be typical,the amount of rough endoplasmic reticulum increased and that of polyribosome decreased.Conclusion All of these results showed that tachyplesin possessed the similar effects to n-sodium butyrate on changing morphology and ultrastructure of human gastric adenocarcinoma cells and possessed an additive role of inducing tumor cells to differentiate cooperatively with n-sodium butyrate to induce carcinoma cell differentiation.

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