[Role of peroxisome proliferator-activated receptor beta in the inhibitory effect of epidermal growth factor on apoptosis of HaCaT].

Objective: To explore the role of EGF in regulating HaCaT apoptosis through peroxisome proliferator-activated receptor beta (PPARbeta).

Methods: Cultured HaCaT cells were divided into different groups with different additives in culture medium as control (normal culture), TNF-alpha (with addition of 10 ng/mL TNF-alpha), EGF (with addition of 20 ng/mL EGF), EGF + TNF-alpha (cells were treated with 10 ng/mL TNF-alpha for 60 mins after the exposure to 20 ng/mL EGF for 4 hs) groups. Conjugation activity and transcription activity of PPARbeta of HaCaT cells in each group were detected by electrophoretic mobility shift assay (EMSA) and luciferase gene analysis (LGA).

[Role of cell-surface nucleolin in lipopolysaccharide-stimulated expression and secretion of TNF-alpha and IL-1beta].

Objective: To explore the role of cell-surface nucleolin in lipopolysaccharide (LPS)-stimulated expression and secretion of TNF-alpha and IL-1beta in human THP-1 monocytes.

Methods: Immuno-fluorescence assay and Western blot were used to identify the expression of nucleolin on the surface of THP-1 monocytes. Inactivation of nucleolin was induced by anti-nucleolin monoclonal antibody blockage, and the expression and secretion of TNF-alpha and IL-1beta were observed by using reverse transcription polymerase chain reaction (RT-PCR) and enzyme linked immuno-sorbent assay (ELISA)respectively in LPS-mediated human THP-1 monocyte inflammatory model.

[Changes of nucleolin expression and cellular localization during HUVEC apoptosis induced by hydrogen peroxide].

Objective: To investigate the expression and cellular localization of nucleolin C23 during human umbilical vein endothelial cell (HUVEC) apoptosis induced by hydrogen peroxide (H(2)O(2)).

Methods: Apoptosis of HUVEC was induced by exposure to 0.5 mmol/L H(2)O(2) for different periods and detected by flow cytometry and activity of caspase-3.

[Inhibitory effect of epidermal growth factor on apoptosis in HaCaT keratinocytes induced by TNF-alpha].

Objective: To explore the effect of epidermal growth factor (EGF) on apoptosis induced by TNF-alpha and the expression of PPARbeta in HaCaT keratinocytes.

Methods: HaCaT keratinocytes were cultured and randomly divided into A (normal control), B (with treatment of 10 ng/ml TNF-alpha for 24 hours), C (with treatment of 20 ng/ml TNF-alpha for 24 hours), D (with treatment of 10 ng/ml TNF-alpha after 20 ng/ml EGF treatment for 4 hours), E (with treatment of 20 ng/ml TNF-alpha after 20 ng/ml EGF treatment for 4 hours) groups. The apoptosis of HaCaT keratinocytes was observed by flow cytometry.

[The role of PPARbeta in the apoptotic HaCaT keratinocytes induced by TNF-alpha].

Objective: To explore the change of transcription activity and expression of PPARbeta in the apoptotic HaCaT keratinocytes induced by TNF-alpha.

Methods: HaCaT keratinocytes were exposed to different concentration TNF-alpha for 24 hours. Apoptotic morphological changes and percentage of apoptotic nuclei were assayed with Hoechst 33258 staining.

[Study on the antisense oligonucleotide against peroxisome proliferator-activated receptors promoting TNF-alpha mediated apoptosis of HaCat cells].

Objective: To investigate the influence of antisense phosphorothioate oligonucleotides on peroxisome proliferator-activated receptors (PPARbeta) in the TNF-alpha mediated apoptosis of HaCat cells.

Methods: HaCat cells were resuscitated and randomly divided into normal control (without transfection), sham (merely with liposome transfection), scrODN (with transfection of 4 micromol/L PPARbeta scrODN), asODN (with transfection of 4 micromol/L PPARbeta asODN), TNF-alpha with transfection of 10 micromol/L TNF-alpha), scrODN + TNF-alpha with 10 micromol/L TNF-alpha stimulation after transfection of 4 micromol/L PPARbeta scrODN), asODN + TNF-alpha with 10 micromol/L TNF-alpha stimulation after transfection of 4 micromol/L PPARbeta asODN) groups. The mRNA and protein levels of PPARbeta were determined with RT-PCR and Western blotting, respectively.

[Heat shock pretreatment in inhibiting myocardical apoptosis induced by ischemia-reperfusion and its mechanism].

Objective: To explore the mechanisms of myocardial apoptosis during myocardial ischemia-reperfusion injury and to further clarify the molecular mechanisms by which heat shock pretreatment in inhibiting myocardial apoptosis induced by ischemia-reperfusion injury.

Methods: Myocardial ischemia-reperfusion injury was induced by the occlusion of left anterior descending branch of the coronary artery. Apoptosis was evaluated by DNA laddering assay and the activities of caspase 3, 8, or 9 was measured with Caspase Colorimetric Assay Kit.

[Mechanisms of heat shock proteins inhibiting C2C12 cell apoptosis induced by hydrogen peroxide].

Objective: To explore the mechanisms of C2C12 cell apoptosis induced by hydrogen peroxide (H2O2) which is inhibited by heat shock proteins.

Methods: The expression of heat shock proteins in mouse embryonic myogenic cell line, C2C12 cell,was induced by heat shock response. C2C12 cell apoptosis induced by 0.

[Heat shock pretreatment inhibits the release of Smac from mitochondria and decreases H2O2-induced cardiomyocyte apoptosis].

Objective: To explore the effect of heat shock pretreatment on H2O2-induced apoptosis of neonatal rat cardiomyocytes and the release of Smac from mitochondria.

Methods: After heat shock pretreatment (42 degrees C for 1 h), neonatal cardiomyocytes were exposed to H2O2 (0.5 mmol/L) for 6, 12, 24, and 36 h, respectively.