ABSTRACT
La hipoxia es un factor importante que regula el desarrollo placentario y estimula la invasión del trofoblasto y la diferenciación, la angiogénesis y la vasculogénesis. Cuando ocurre la fecundación, la hipoxia a la que está expuesta el blastocisto regula su crecimiento, a la vez que limita el número de células del trofoblasto y el desarrollo placentario posterior, lo cual es clave en el transporte de nutrientes y oxígeno al feto en desarrollo; sin embargo, la hipoxia crónica fetoplacentaria conduce a disfunción vascular placentaria y a la programación intrauterina de enfermedades vasculares y metabólicas, ya que regula, a largo plazo, la expresión de enzimas relacionadas con la vía L-arginina/óxido nítrico en células endoteliales de diferentes lechos vasculares, incluyendo la placenta. Teniendo en cuenta los planteamientos anteriores en la presente investigación se describen los efectos de la hipoxia como noxa durante la vida intrauterina y su influencia en el origen temprano de la obesidad y sus complicaciones.
Hypoxia is an important factor that regulates the placental development and stimulates the invasion of trophoblast as well as differentiation, angiogenesis and vasculogenesis. At the moment of fertilization, hypoxia to which the blastocyte is exposed, regulates its growth, at the same time that it limits the number of trophoblast cells and the posterior placental development, that is essential in the transport of nutrients and oxygen to the developing fetus; however, chronic fetus-placental hypoxia leads to vascular placental dysfunction and to intra-uterine programming of vascular and metabolic diseases, since it regulates, at long term, the expression of enzymes related to the L-arginine/nitric oxide way in endothelial cells of different vascular beds, including placenta. Taking this into account the effects of hypoxia as noxa during intra-uterine life and its influence in the early origin of obesity and its complications are described in the present investigation.
Subject(s)
Fetal Development , Hypoxia , Noxae , Pediatric ObesityABSTRACT
Objective: To investigate the inhibitory effect of nitidine chloride (NC) on human esophageal carcinoma cell line Eca109 and the molecular mechanism of its induction. Methods: CCK-8 method was used to detect the inhibition rate of human esophageal cancer Eca109 cells with different concentrations of NC and different intervention time. According to the result of CCK-8 method, the experiment was divided into four groups, and the concentrations of NC in each group were 0, 5, 10, and 15 μmol/L, respectively, and the drug action time was 48 h. The apoptotic rate was detected by flow cytometry with Annexin V-FITC/PI double staining. The mRNA expressions of Caspase-3, Caspase-9, and Noxa were detected by qRT-PCR. The expressions of cleaved Caspase-3 and Bcl-2, p53, and Noxa protein levels were detected by Western blotting. Results: NC had inhibitory effect on Eca109 cells in a certain range of time and dose-dependent manner. Flow cytometry showed that NC at 5 μmol/L mainly induced early apoptosis (P < 0.01); NCs at 10 and 15 μmol/L mainly induced late apoptosis (P < 0.01). qRT-PCR results showed that the mRNA expression of Caspase-3, Caspase-9 and Noxa was increased with the increase of NC concentration, of which 10 and 15 μmol/L group increased significantly. The results of Western blotting showed that the protein levels of cleaved Caspase-3, p53, and Noxa were both increased with the increase of NC concentration (P < 0.01), but the increase of Noxa was not significant in 5 μmol/L group (P < 0.01). The expression of Bcl-2 protein was decreased with the increase of NC concentration, and which was significantly higher in 10 and 15 μmol/L groups (P < 0.05, P < 0.01). Conclusion: The inhibitory effect of NC on human esophageal carcinoma Eca109 cells is mainly through apoptosis. The apoptosis of NC induced of Eca109 cells is associated with increased expression of p53 and Noxa, downregulation of Bcl-2, and activation of Caspase-3.
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Purpose To explore the correlation of Noxa gene with clinical pathology and its effect on proliferation and apoptosis of HepG2 cells.Methods Noxa protein in 100 hepatocellular carcinoma tissues and 100 paracancerous tissues were detected by imnunohistochemical technique,clinicopathological parameters and follow-up data were statistically analyzed.The recombinant eukaryotic expression plasmid pIRES2-EGFP-Noxa was transiently transfected into HepG2 cells with lipofectamine.Both Noxa mRNA and protein were detected by RT-PCR and Western blot respectively.The inhibition of cell proliferation was evaluated by MTT assay.The cell apoptosis was detected by flow cytometry (FCM).Results Immunohistochemistry showed that in tumor tissue of hepatocellular carcinona the positive rate of Noxa protein expression was 50％,while it was 78％ in cancer adjacent normal mucosal tissue,with statistically significant difference (P ＜ 0.05).The expression of Noxa was related to TNM staging and the tumor differentiation.Exotic Noxa gene was expressed successfully in HepG2 cells after transfected with lipofectamine.The expression of Noxa mRNA and protein of HepG2 cells was significantly up-regulated after transfected 24 h,48 h and 72 h (P ＜ 0.05).MTT assay showed that the Noxa expression inhibited HepG2 cell proliferation in a time-dependent manner for 24 h,48 h and 72 h (P ＜ 0.05),which was significantly different from that of the control group (P ＜ 0.05).Apoptosis rate after transfected 24 h,48 h and 72 h was (15.5 ± 0.9)％,(24.6 ±0.8) ％ and (35.4 ±0.7) ％,respectively.There were significant difference between Noxa and the control group (P ＜ 0.05).Conclusion The expression of Noxa in hepatocellular carcinoma tissue is closely related to TNM stage and the tumor differentiation.Noxa gene overexpression is able to effectively inhibit the proliferation and promote the apoptosis of HepG2 cell line.
ABSTRACT
A maioria das escolas da rede brasileira de ensino possui estabelecimentos que distribuem alimentos cuja qualidade higiênica pode ser questionada. Tal situação desperta preocupação, visto que os consumidores desses alimentos são frequentemente mais susceptíveis a doenças de origem alimentar. O objetivo deste estudo foi analisar a existência de contaminação microbiana em copo de liquidificador e placa de corte em cantinas de escolas públicas do Guará - Distrito Federal. Trata-se de um estudo de caráter exploratório realizado em 10 cantinas de escola públicas. A coleta das amostras foi realizada através da técnica do swab e analisado em laboratório a existência de micro-organismos Aeróbios Mesófilos, Coliformes termotolerantes, e Staphylococcus aureus. Verificou-se que as amostras apresentaram a existência de micro-organismos, necessitando de melhor controle das condições higienicossanitárias para garantir a qualidade de vida e prevenção de doenças transmitidas por alimentos.
Most schools in the Brazilian school system has establishments that distribute food whose hygienic quality can be questioned. This situation raises concern, since the consumers of these foods are often more susceptible to food-borne illness. The objective of this study was to analyze the existence of microbial contamination in a blender bowl and cutting board in public schools canteens of Guara - Federal District. It is an exploratory study conducted in 10 public school canteens. The collection of samples was performed by the swab technique and analyzed in the laboratory the existence of mesophilic aerobic, coliforms thermotolerant, and Staphylococcus aureus microorganisms. It was found that the samples showed the presence of microorganisms, requiring better control of sanitary conditions to maintain quality of life and prevention of foodborne illness.
Subject(s)
School Feeding , Food Hygiene , Communicable Disease Control , Noxae , Staphylococcus aureus , Brazil , Food Contamination , Cooking and Eating Utensils , MealsABSTRACT
PURPOSE: The purpose of this study is to understand the mechanism of apoptosis occurring on a cultured human lens epithelial cell line after exposure to ultraviolet (UV) light. We intended to confirm the presence of cellular toxicity and apoptosis and to reveal the roles of p53, caspase 3 and NOXA in these processes. METHODS: Cells were irradiated with an ultraviolet lamp. Cellular toxicity was measured by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Hoechst staining and fluorescent anti-caspase 3 antibodies were used for apoptosis investigation. The quantities of p53, caspase 3, and NOXA were measured by Western blotting for to investigate the apoptosis pathway. RESULTS: Cellular toxicity on the human lens epithelium markedly increased with time after UV exposure. On Hoechst staining, we found that apoptosis also remarkably increased after exposure to ultraviolet light, compared with a control group. In the immunochemical study using anti-caspase 3 antibodies, active caspase 3 significantly increased after exposure to ultraviolet light. On Western blotting, p53 decreased, while caspase 3 and NOXA increased. CONCLUSIONS: Exposure of cultured human lens epithelial cell lines to ultraviolet light induces apoptosis, which promotes the expression of NOXA and caspase 3 increases without increasing p53. This may suggest that UV induced apoptosis is caused by a p53-independent pathway in human lens epithelial cells.