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1.
Int J Mol Med ; 44(3): 903-912, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31524225

RESUMO

Silicon is one of the most widely used chemical materials, and the increasing use of silica nanoparticles (SNs) highlights the requirement for safety and biological toxicity studies. The damaging and adverse effects of SNs on human hepatocytes remain largely unknown, as do the mechanisms involved. In the present study, the mechanisms underlying SN­induced toxicity in the human hepatocyte cell line HL­7702 were investigated. An MTT assay revealed that following exposure to SNs in the concentration range of 25­200 µg/ml, the viability of HL­7702 cells decreased, and the viability decreased further with increasing exposure time. SNs induced a delay in the S and G2/M phases of the cell cycle, and also induced DNA damage in these cells. Western blot and flow cytometry analyses revealed that cell death was mediated by mitochondrial damage and the upregulated expression of a number of pro­apoptotic proteins. In conclusion, exposure to SNs led to mitochondrial and DNA damage, resulting in apoptosis­mediated HL­7702 cell death. The study provided evidence for the cellular toxicity of SNs, and added to the growing body of evidence regarding the potential damaging effects of nanoparticles, indicating that caution should be exercised in their widespread usage.


Assuntos
Apoptose , Hepatócitos/metabolismo , Nanopartículas , Dióxido de Silício , Biomarcadores , Ciclo Celular , Linhagem Celular , Sobrevivência Celular , Dano ao DNA , Metaloproteinases da Matriz/metabolismo , Nanopartículas/efeitos adversos , Nanopartículas/química , Dióxido de Silício/química
2.
Iran J Public Health ; 48(4): 722-729, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31110983

RESUMO

Background: In order to generate data on the burden of foodborne diseases in Shandong Province, we aimed to use the case monitoring data of foodborne diseases from 2016 to 2017 to estimate. Methods: Data were obtained from the foodborne disease surveillance reporting system with dates of onset from Jan 1, 2016, to Dec 31, 2017, in Shandong, China. Results: The places of food exposure were categorized by settings as follows: private home, catering facility, collective canteens, retail markets, rural banquets and other. Exposed food is divided into 23 categories. Overall incidence rate and proportions by exposure categories, age, and sex-specific incidence rates were calculated and sex proportions compared. Approximately 75.00% of cases who had at least one exposure settings were in private homes. The most frequently reported exposed food was a variety of food (meaning more than two kinds of food). The two-year average incidence rate was 75.78/100,000, sex-specific incidence rate was much higher for females compared to males (78.23 vs. 74.69 cases per 100,000 population). An age-specific trend was observed in the cases reported (Chi-Square for linear trend, χ2=4.39, P=0.036<0.05). Conclusion: A preliminary estimate of 14 million cases of foodborne diseases in Shandong province each year. Future studies should focus on cross-sectional and cohort studies to facilitate the assessment of the distribution and burden of foodborne disease of the population in Shandong. Considering strengthening the burden of foodborne diseases in foodborne disease surveillance is also a feasible way.

3.
Toxicol Lett ; 310: 7-13, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30978436

RESUMO

Silicosis is a kind of chronic and incurable lung fibrotic disease with pathogenesis and molecular mechanisms largely unknown. Mounting evidence suggests that long non-coding RNAs (lncRNAs) are involved in the pathogenesis of silicosis. However, how many lncRNAs involved in the pulmonary fibrosis remains to be elucidated. In this study, Wistar rats were exposed to silicon dioxide by an improved tracheal intubation method. Rats in the control group were treated with normal saline solution. Results showed that 28 days after exposure, there were significant differences in body weight and lung coefficient of rats treated with silica compared with control rats. The formation of lung fibrosis in silica-induced rats was confirmed by histologic examination. We then investigated the lncRNAs expression changes in lung tissues of silica-exposed rats and compared that with the rats in the control group using microarray. The results indicated that silica exposure leads to altered expression profile in 682 lncRNAs (300 upregulated and 382 downregulated). Seventy-three ceRNA pairs were acquired by predicted analysis. Kyoto Encyclopedia of Genes and Genomes pathway and Gene Ontology analyses were used to predict the biological pathway and functional classification of lncRNAs. The results showed that silica exposure affected 13 lncRNAs pathways. The functional classification mainly involved in protein binding, cell shape and extracellular exosome. This study indicated that alteration of lncRNAs may play a role in silica-induced pulmonary fibrosis through regulation of expressions of functional genes in lungs of rat. Our results provide more insights into the mechanism of silicosis.


Assuntos
Perfilação da Expressão Gênica/métodos , Pulmão/efeitos dos fármacos , Análise de Sequência com Séries de Oligonucleotídeos , Fibrose Pulmonar/genética , RNA Longo não Codificante/genética , Dióxido de Silício/toxicidade , Silicose/genética , Animais , Regulação da Expressão Gênica/efeitos dos fármacos , Redes Reguladoras de Genes/efeitos dos fármacos , Pulmão/metabolismo , Pulmão/patologia , Fibrose Pulmonar/induzido quimicamente , Fibrose Pulmonar/metabolismo , Fibrose Pulmonar/patologia , RNA Longo não Codificante/metabolismo , Ratos Wistar , Silicose/metabolismo , Silicose/patologia , Fatores de Tempo , Transcriptoma/efeitos dos fármacos
4.
Exp Ther Med ; 17(3): 2247-2255, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30867709

RESUMO

Previous studies have demonstrated that bone marrow mesenchymal stem cell (BMSC) transplantation is a promising treatment strategy for pulmonary fibrosis. Although encouraging results have been obtained using animal models of bleomycin (BLM)-induced pulmonary fibrosis, it is evident that transplantation of BMSCs at various time-points after BLM administration has produced different results in terms of treatment efficacy. To shed light on the potential utility of BMSCs for the treatment of lung disease, the present study performed a meta-analysis to estimate the efficacy of BMSCs in animal models of BLM-induced pulmonary fibrosis, and compare early transplantation (BMSCs injected on the same day after administration of BLM) with late transplantation (BMSCs injected on the 14th day after administration of BLM). Relevant studies were retrieved from the MEDLINE, PubMed, Chinese Knowledge Infrastructure and WanFang databases using a comprehensive search approach. A total of 6 studies involving 228 model rats were included. Meta-analysis indicated that early BMSC transplantation was able to prevent or reduce BLM-induced alveolitis and pulmonary fibrosis, while late BMSC transplantation was able to reduce alveolitis, but there was no significant evidence regarding improvement of pulmonary fibrosis. Although BMSC therapy was identified to be generally beneficial in rodent models of BLM-induced pulmonary fibrosis, the efficacy of early transplantation appears to be more satisfactory; overall, the efficacy of transplantation of BMSCs at the acute inflammatory phase was more effective compared with that at the chronic fibrosis stage. Of note, regarding alveolitis and pulmonary fibrosis scores after late transplantation of BMSCs, the sensitivity analysis revealed that the scores were less stable; thus, this result must be interpreted with caution. Furthermore, the quality and methodology of the included studies was comparatively low. Therefore, higher-quality and more rigorous studies are required to validate the results of the present meta-analysis in the future.

5.
Int J Mol Med ; 43(3): 1229-1240, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30628656

RESUMO

Diseases of the cardiac system caused by silicon dioxide exposure have captured wide public attention. Upon entering the blood circulation, ultrafine particles have the potential to influence cardiomyocytes, leading to myocardial ischemia or even cardiac failure, and the molecular mechanisms remain to be completely elucidated. In this study, the toxicity of ultrafine particles on cardiomyocytes from rats exposed to silica nanoparticles was observed. Rats were randomly divided into a normal saline control group and three exposure groups (2, 5 and 10 mg/kg·body weight) that were intratracheally treated with 60­nm silica nanoparticles. Alterations in body weight, routine blood factors and myocardial enzymes, histopathological and microstructural alterations, apoptosis and the expression of apoptosis­associated proteins were assessed at the end of the exposure period. The silicon levels in the heart and serum, and myocardial enzymes in exposed rats were significantly increased in a dose­dependent manner. In addition, exposure to the silica nanoparticles caused notable histological and ultrastructural alterations in the hearts of these animals. Furthermore, a significant apoptotic effect was observed in the exposure groups. The present data suggest that silica nanoparticles may enter the circulatory system through the lungs, and are distributed to the heart causing cardiovascular injury. Silica nanoparticle­induced apoptosis via the mitochondrial pathway may serve an important role in observed cardiac damage.


Assuntos
Apoptose , Mitocôndrias/metabolismo , Miócitos Cardíacos/metabolismo , Nanopartículas , Dióxido de Silício , Animais , Proteínas Reguladoras de Apoptose/genética , Proteínas Reguladoras de Apoptose/metabolismo , Biomarcadores , Expressão Gênica , Imuno-Histoquímica , Masculino , Miócitos Cardíacos/ultraestrutura , Nanopartículas/química , Nanopartículas/ultraestrutura , Ratos , Dióxido de Silício/química
6.
Med Sci Monit ; 24: 8639-8646, 2018 Nov 29.
Artigo em Inglês | MEDLINE | ID: mdl-30488879

RESUMO

BACKGROUND The composition of the intestinal microbiota and its effect on septic shock patients in the intensive care unit (ICU) is unknown. In the present study we explored the hypothesis that bacterial diversity is decreased in septic shock patients and that this diversity may be improved by use of probiotics or enteral nutrition. MATERIAL AND METHODS A total of 15 stool samples were collected prospectively from septic shock patients in the ICU, while 15 samples from healthy subjects served as controls. Bacterial DNA was submitted for 16S rDNA gene sequencing. The relationship between intestinal microbiota and prognosis was evaluated. RESULTS Significantly lower bacterial diversity was found in septic shock patients compared with healthy subjects (p<0.05). However, there was no difference in bacterial diversity in the presence or absence of probiotics (p=0.59), enteral nutrition (p=0.59), or in-hospital death (p=0.93) in septic shock patients. A high abundance of Proteobacteria and Fusobacteria was observed in most septic shock patients, whereas low abundance was observed in healthy subjects (mean relative proportion: 23.71% vs. 3.53%, p<0.05; 1.27% vs. 0.12%, p=0.59). CONCLUSIONS Bacterial diversity was decreased, and 1 or 2 rare bacterial species were overgrown in septic shock patients. Bacterial diversity was not improved by use of probiotics or enteral nutrition. The small sample size of our study limits the interpretation of results.


Assuntos
Microbioma Gastrointestinal/fisiologia , Choque Séptico/microbiologia , Adulto , Idoso , Bactérias/isolamento & purificação , Fezes/microbiologia , Feminino , Humanos , Unidades de Terapia Intensiva , Masculino , Pessoa de Meia-Idade , Projetos Piloto , Probióticos/uso terapêutico , Prognóstico , Choque Séptico/fisiopatologia
7.
Stem Cell Res Ther ; 9(1): 311, 2018 11 14.
Artigo em Inglês | MEDLINE | ID: mdl-30428918

RESUMO

BACKGROUND: Pulmonary fibrosis induced by silica dust is an irreversible, chronic, and fibroproliferative lung disease with no effective treatment at present. Previous studies have shown that early intervention with bone marrow mesenchymal stem/stromal cells (BMSCs) has positive effect on anti-pulmonary fibrosis caused by silica dust. However, early intervention using BMSCs is not practical, and the therapeutic effects of BMSCs advanced intervention on pulmonary fibrosis have rarely been reported. In this study, we investigated the effects of advanced transplantation (on the 28th day after exposure to silica suspension) of BMSCs on an established rat model of pulmonary fibrosis. METHODS: Sprague Dawley (SD) rats were randomly divided into four groups including (1) control group (n = 6) which were normally fed, (2) silica model group (n = 6) which were exposed to silica suspension (1 mL of 50 mg/mL/rat), (3) BMSC transplantation group (n = 6) which received 1 mL BMSC suspension (2 × 106 cells/mL) by tail vein injection on the 28th day after exposure to silica suspension, and (4) BMSC-CM (conditioned medium) transplantation group (n = 6) which received CM from the same cell number by tail vein injection on the 28th day after exposure to silica suspension. On the 56th day after exposure to silica suspension, we used computed tomography (CT), hematoxylin and eosin (H&E), and Masson's trichrome staining to evaluate the changes in lung tissue. We examined the expression of epithelial-mesenchymal transition (EMT) and Wnt/ß-catenin pathway-related proteins in lung tissue using immunohistochemistry and western blotting. RESULTS: Successful construction of a pulmonary fibrosis model was confirmed by H&E and Masson's trichrome staining on the 28th day after exposure to silica suspension. On the 56th day after exposure, pulmonary CT examination showed a relieving effect of BMSCs on silica-induced pulmonary fibrosis which was confirmed by H&E and Masson's trichrome staining. Treatment of BMSCs increased the expression of epithelial marker proteins including E-cadherin (E-cad) and cytokeratin19 (CK19) and reduced the expression of fibrosis marker proteins including Vimentin (Vim) and α-Smooth actin (α-SMA) after exposure to silica suspension. Furthermore, we found that Wnt/ß-catenin signaling pathway is abnormally activated in silica-induced pulmonary fibrosis, and exogenous transplantation of BMSCs may attenuate their expression. CONCLUSIONS: BMSC transplantation inhibits the EMT to alleviate silica-induced pulmonary fibrosis in rats and the anti-fibrotic effect potentially by attenuating Wnt/ß-catenin signaling. ᅟ: ᅟ.


Assuntos
Células da Medula Óssea/citologia , Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais/citologia , Fibrose Pulmonar/induzido quimicamente , Fibrose Pulmonar/metabolismo , Via de Sinalização Wnt , Animais , Proliferação de Células , Ciclina D1/metabolismo , Transição Epitelial-Mesenquimal , Glicogênio Sintase Quinase 3 beta/metabolismo , Hidroxiprolina/metabolismo , Pulmão/diagnóstico por imagem , Pulmão/patologia , Masculino , Fosforilação , Fibrose Pulmonar/diagnóstico por imagem , Fibrose Pulmonar/patologia , Ratos Sprague-Dawley , Dióxido de Silício , Suspensões , Tomografia Computadorizada por Raios X , beta Catenina/metabolismo
8.
Medicine (Baltimore) ; 97(45): e13142, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30407341

RESUMO

Foodborne disease is a major public health concern in both developed and developing countries. China has established a nationwide Foodborne Disease Outbreak Surveillance System (FDOSS) for collection and periodic reporting of data on the occurrence and causes of foodborne disease outbreaks in China. Each provincial Centers for Disease Control and Prevention (CDC) conducts the system working.We reviewed foodborne disease outbreaks that occurred during 2011 to 2016 in Shandong Province from the FDOSS. The Wilcoxon test was used to compare the median number of ill persons in outbreaks. All data analysis was performed using Epi Info 7.During 2011 to 2016, Shandong CDC received reports of 1043 foodborne disease outbreaks, resulting in 8078 illnesses, 2442 hospitalizations, and 17 deaths. There were a median of 69 outbreaks annually [interquartile range (IQR) 10-342], resulting in 335 to 3824 illnesses each year. The median outbreak size was 3 persons (IQR 2-7). Hotels (including cruise ships, hotpot restaurants, barbecue shops) were the most common setting. Among the 744 (71.3%) outbreaks with an implicated food or contaminated ingredient reported, 704 (94.6%) could be assigned to one of 17 predefined commodity categories. Of the 280 outbreaks with a known etiology, 117 (41.8%) were caused by poisonous plants and animals and their toxins, 39 (13.9) were caused by nitrite, and 27 (9.6%) were caused by vibrio parahaemolyticus. Of the 491 (47.1%) outbreaks with at least a contributing factor to cause outbreak, 168 (34.2%) were caused by improper processing, and 100 (20.4) were caused by inedible and misuse.Timely investigation, disposal and reporting of foodborne disease outbreaks provides information that might help FDOSS to make full use of efficiency and FDOSS should be continued and strengthened even more in Shandong Province, such as an increase in diagnostic laboratory capacities.


Assuntos
Surtos de Doenças/estatística & dados numéricos , Doenças Transmitidas por Alimentos/epidemiologia , China/epidemiologia , Doenças Transmitidas por Alimentos/mortalidade , Hospitalização/estatística & dados numéricos , Humanos , Fatores de Risco
9.
IUBMB Life ; 70(10): 961-968, 2018 10.
Artigo em Inglês | MEDLINE | ID: mdl-30207631

RESUMO

Orexin A is a multifaceted peptide produced in hypothalamus. We examined the effect of orexin A on vascular endothelial cells. Our study showed that orexin A had a profound inhibitory effect against endothelial inflammation by oxidized low-density lipoprotein (ox-LDL) in endothelial cells. Orexin A partially suppressed ox-LDL-induced monocytes THP-1 cells attachment to endothelial cells by limiting expression of vascular molecules including VCAM-1, ICAM-1, and E-selectin. Mechanistically, orexin A ameliorated endothelial dysfunction by reducing MAP kinase p38 and NF-κB activation via its receptor-OX1R. Orexin A suppressed phosphorylation of MAP kinase p38 and the NF-κB cascade kinases IKKα and IκBα, and prevented the shuttle of p65 protein into nuclear. Additionally, we reported that OX1R was expressed in HUVECs. Silence of OX1R completely abolished the inhibitory function of orexin in attachment of THP-1 cells. Collectively, our data suggest that orexin A ameliorated endothelial dysfunction under inflammatory stimuli. © 2018 IUBMB Life, 70(10):961-968, 2018.


Assuntos
Inflamação/genética , NF-kappa B/genética , Receptores de Orexina/genética , Orexinas/genética , Selectina E/genética , Células Endoteliais/metabolismo , Células Endoteliais/patologia , Ensaio de Imunoadsorção Enzimática , Regulação da Expressão Gênica/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana , Humanos , Inflamação/patologia , Molécula 1 de Adesão Intercelular/genética , Lipoproteínas LDL/antagonistas & inibidores , Monócitos/metabolismo , Monócitos/patologia , Receptores de Orexina/efeitos dos fármacos , Fosforilação/efeitos dos fármacos , Transdução de Sinais/genética , Molécula 1 de Adesão de Célula Vascular/genética , eIF-2 Quinase/genética , Proteínas Quinases p38 Ativadas por Mitógeno/genética
10.
Medicine (Baltimore) ; 97(30): e11720, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-30045338

RESUMO

BACKGROUND: At present, occupational noise exposure has become one of the risk factors of occupational workers and attracted serious concerned of most of occupational disease researchers. To assess associations of occupational noise exposure and cardiovascular disease by meta-analysis. METHODS AND ANALYSIS: Results from primary studies about occupational noise and cardiovascular disease (2000-2017) were retrieved from literatures, which were conducted in China only. Both random and fixed effect model were used to calculate pooled odds ratio (OR) and their corresponding 95% confidence interval (CI). Review Manager and Stata software were used to perform data analysis. This study followed the Preferred Reporting Items for Systematic Reviews and Meta-Analysis statements. RESULTS: After applying stringent inclusion and exclusion criteria, 4771 exposures and 3068 controls from 11 primary studies were used to analyze the relationship between occupational noise exposure and cardiovascular disease. The risk of developing high blood pressure for workers exposed to noise is 2.55 times higher than the controls (I = 52%, 95% CI: 1.94-3.36), and electrocardiograph (ECG) abnormality is 2.27 times higher than the control groups (I = 22%, 95% CI: 1.96-2.62). The bias analysis suggested that there is publication bias, but it didn't affect the conclusions from trim test. CONCLUSION: The impact of high-intensity noise exposure on the worker's cardiovascular system is much greater than that of the unexposed control group, and the effect on hypertension of the exposed group is greater than that of the ECG.


Assuntos
Doenças Cardiovasculares/epidemiologia , Ruído Ocupacional/efeitos adversos , Exposição Ocupacional/efeitos adversos , Doenças Cardiovasculares/diagnóstico , China/epidemiologia , Eletrocardiografia , Humanos , Hipertensão/epidemiologia , Doenças Profissionais/diagnóstico , Doenças Profissionais/epidemiologia , Fatores de Risco
11.
Stem Cell Res Ther ; 9(1): 110, 2018 04 19.
Artigo em Inglês | MEDLINE | ID: mdl-29673394

RESUMO

BACKGROUND: Silicosis has been topping the list of high-incidence occupational diseases in developing countries and cannot be completely cured. Recent advances in stem cell research have made possible the treatment of various diseases including lung fibrosis. The application of stem cell therapy in occupational diseases, in particular the use of adipose-derived mesenchymal stem cells (AD-MSCs) in treatment of silicosis, has not yet been reported. The aim of the study is to explore the intervening effect of silica-induced lung fibrosis in rats. METHODS: In this study, we investigated the anti-pulmonary fibrosis effects of the transplantation of AD-MSCs in rats in which lung fibrosis was induced by oral tracheal intubation with silica suspension. Twenty rats were divided into four groups: control group (n = 5), exposure group (n = 5), vehicle group (n = 5) and treatment group (n = 5). AD-MSCs were given to rats after exposure to silica for 24 h. Twenty-eight days after AD-MSC transplantation, we examined the organ coefficient, inflammatory cytokines, apoptosis, pathological and fibrotic changes in lung tissue. RESULTS: Results showed that exposure to silica for 28 days induced an increase of the lung coefficient with significant pulmonary fibrosis. Treatment with AD-MSC transplantation led to a remissive effect on pulmonary fibrosis. We found that after AD-MSC transplantation the inflammatory response decreased and Caspase-3 protein expression significantly decreased with a significant increase of the Bcl-2/Bax ratio. CONCLUSIONS: Anti-inflammatory and anti-apoptosis of AD-MSCs may play important roles in their anti-pulmonary fibrosis effect. Our data suggest that transplantation of AD-MSCs holds promise for potential interference in the formation of silicosis through regulating inflammatory and apoptotic processes.


Assuntos
Anti-Inflamatórios/uso terapêutico , Terapia Baseada em Transplante de Células e Tecidos/métodos , Células-Tronco Mesenquimais/metabolismo , Fibrose Pulmonar/terapia , Silicose/terapia , Animais , Anti-Inflamatórios/farmacologia , Apoptose , Modelos Animais de Doenças , Masculino , Fibrose Pulmonar/patologia , Ratos , Ratos Sprague-Dawley , Silicose/complicações
12.
Int J Nanomedicine ; 12: 2179-2188, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28356735

RESUMO

Gap junction intercellular communication (GJIC) between cardiomyocytes is essential for synchronous heart contraction and relies on connexin-containing channels. Connexin 43 (Cx43) is a major component involved in GJIC in heart tissue, and its abnormal expression is closely associated with various cardiac diseases. Silica nanoparticles (SNPs) are known to induce cardiovascular toxicity. However, the mechanisms through which GJIC plays a role in cardiomyocytes apoptosis induced by SNPs remain unknown. The aim of the present study is to determine whether SNPs-decreased GJIC promotes apoptosis in rat cardiomyocytes cell line (H9c2 cells) via the mitochondrial pathway using CCK-8 Kit, scrape-loading dye transfer technique, Annexin V/PI double-staining assays, and Western blot analysis. The results showed that SNPs elicited cytotoxicity in H9c2 cells in a time- and concentration-dependent manner. SNPs also reduced GJIC in H9c2 cells in a concentration-dependent manner through downregulation of Cx43 and upregulation of P-Cx43. Inhibition of gap junctions by gap junction blocker carbenoxolone disodium resulted in decreased survival and increased apoptosis, whereas enhancement of the gap junctions by retinoic acid led to enhanced survival but decreased apoptosis. Furthermore, SNPs-induced apoptosis through the disrupted functional gap junction was correlated with abnormal expressions of the proteins involved in the mitochondrial pathway-related apoptosis such as Bcl-2/Bax, cytochrome C, Caspase-9, and Caspase-3. Taken together, our results provide the first evidence that SNPs-decreased GJIC promotes apoptosis in cardiomyocytes via the mitochondrial pathway. In addition, downregulation of GJIC by SNPs in cardiomyocytes is mediated through downregulation of Cx43 and upregulation of P-Cx43. These results suggest that in rat cardiomyocytes cell line, GJIC plays a protective role in SNPs-induced apoptosis and that GJIC may be one of the targets for SNPs-induced biological effects.


Assuntos
Apoptose/efeitos dos fármacos , Comunicação Celular , Junções Comunicantes/metabolismo , Mitocôndrias/metabolismo , Miócitos Cardíacos/citologia , Nanopartículas/química , Transdução de Sinais/efeitos dos fármacos , Dióxido de Silício/farmacologia , Animais , Comunicação Celular/efeitos dos fármacos , Linhagem Celular , Junções Comunicantes/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Nanopartículas/ultraestrutura , Ratos , Fatores de Tempo , Tretinoína/farmacologia
13.
Stem Cells Int ; 2015: 516215, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26294918

RESUMO

The mechanisms behind the repairing effects of the cotransplantation of olfactory ensheathing cells (OECs) with bone marrow mesenchymal stromal cells (BMSCs) have not been fully understood. Therefore, we investigated the effects of the cotransplantation of OECs with BMSCs on antiapoptotic effects in adult rats for which the models of SCI are induced. We examined the changes in body weight, histopathological changes, apoptosis, and the expressions of apoptosis-related proteins after 14 days and 28 days after transplantation. We also assessed animal locomotion using BBB test. We found that treatment with OECs and BMSCs had a remissive effect on behavioral outcome and histopathological changes induced SCI. Furthermore, we observed the significant antiapoptotic effect on cotransplant treated group. In addition, cotransplantation of OECs with BMSCs was found to have more significant repairing effect than that of OECs or BMSCs alone. Furthermore, the recovery of hind limb could be related to antiapoptotic effect of OECs and BMSCs through downregulating the apoptotic pathways. Finally, our data suggested the cotransplantation of OECs with BMSCs holds promise for a potential cure after SCI through the ability to incorporate into the spinal cord.

14.
Artigo em Inglês | MEDLINE | ID: mdl-25461676

RESUMO

Glycogen synthase kinase-3 (GSK-3) is a key protein kinase involved in numerous cellular processes, including embryonic development, protein synthesis, glycogen metabolism, mitosis and apoptosis. However, our knowledge of Schizothorax prenanti GSK-3 is very limited. In this study, we cloned and characterized the S. prenanti GSK3ß gene. Using qPCR, we found that the GSK3ß gene was widely expressed in eleven tissues of S. prenanti and had especially high expression levels in the liver and brain. Moreover, we screened and sequenced more than 100 positive clones to identify the alternative transcripts of GSK3ß. Five novel isoforms of GSK3ß were identified in different S. prenanti tissues; these were different from the GSK3ß isoforms previously reported in the other species. We named the five transcripts as GSK3ß1, GSK3ß2, GSK3ß3, GSK3ß4 and GSK3ß5. These consisted of 1266, 1153, 902, 836 and 654 base pairs, respectively. Our studies provide useful information for further research on the S. prenanti GSK3ß gene.


Assuntos
Processamento Alternativo , Cyprinidae/metabolismo , Quinase 3 da Glicogênio Sintase/genética , Quinase 3 da Glicogênio Sintase/metabolismo , Transcriptoma , Animais , Encéfalo/metabolismo , Cyprinidae/genética , Quinase 3 da Glicogênio Sintase/química , Glicogênio Sintase Quinase 3 beta , Fígado/metabolismo , Especificidade de Órgãos , Filogenia
15.
Int J Clin Exp Med ; 8(11): 20002-13, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26884912

RESUMO

AIMS: To investigate the mechanisms of α-zearalanol (Zeranol)-induced male reproductive toxicity, the effects of Zeranol on spermatogenesis and sex hormone levels of male mice were studied. METHODS: Forty healthy sexually mature male Kunming mice were randomly divided into four groups. The mice were mock-treated or treated with Zeranol 25, 50 or 100 mg/kg via oral gavage for 35 days. The epididymal sperms were counted and their morphology and motility were analyzed. The testicles were examined by light and electron microscopy. The levels of serum/testicular testosterone (T), serum follicle stimulating hormone (FSH) and serum luteinizing hormone (LH) were determined by radioimmunoassay. RESULTS: Zeranol decreased the epididymal sperm count and sperm motility in a dose depend manner. While there were not significant differences in the sperm malformation rates between the Zeranol treated groups and the control group. Furthermore, Zeranol could decrease the weight and the organ coefficient of the seminal vesicles and the testicles and lead to significant pathological changes of the testicles. Zeranol could also decrease the levels of serum T, FSH, LH as well as the levels of testicular T of male mice. CONCLUSIONS: Zeranol induced reproductive toxicity in adult male mice. It could damage spermatogenesis via its direct effects on the testicles and interfere with sex hormone levels of male mice through its effects on the hypothalamic-pituitary-testicular axis.

16.
PLoS One ; 8(4): e61346, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23593469

RESUMO

This study aimed to evaluate the acute toxicity of intravenously administrated amorphous silica nanoparticles (SNPs) in mice. The lethal dose, 50 (LD50), of intravenously administrated SNPs was calculated in mice using Dixon's up-and-down method (262.45±33.78 mg/kg). The acute toxicity was evaluated at 14 d after intravenous injection of SNPs at 29.5, 103.5 and 177.5 mg/kg in mice. A silicon content analysis using ICP-OES found that SNPs mainly distributed in the resident macrophages of the liver (10.24%ID/g), spleen (34.78%ID/g) and lung (1.96%ID/g). TEM imaging showed only a small amount in the hepatocytes of the liver and in the capillary endothelial cells of the lung and kidney. The levels of serum LDH, AST and ALT were all elevated in the SNP treated groups. A histological examination showed lymphocytic infiltration, granuloma formation, and hydropic degeneration in liver hepatocytes; megakaryocyte hyperplasia in the spleen; and pneumonemia and pulmonary interstitial thickening in the lung of the SNP treated groups. A CD68 immunohistochemistry stain indicated SNPs induced macrophage proliferation in the liver and spleen. The results suggest injuries induced by the SNPs in the liver, spleen and lungs. Mononuclear phagocytic cells played an important role in the injury process.


Assuntos
Nanopartículas/administração & dosagem , Nanopartículas/toxicidade , Dióxido de Silício/administração & dosagem , Dióxido de Silício/toxicidade , Testes de Toxicidade Aguda , Animais , Antígenos CD/metabolismo , Antígenos de Diferenciação Mielomonocítica/metabolismo , Peso Corporal/efeitos dos fármacos , Hidrodinâmica , Imuno-Histoquímica , Injeções Intravenosas , Dose Letal Mediana , Camundongos , Camundongos Endogâmicos ICR , Nanopartículas/ultraestrutura , Especificidade de Órgãos/efeitos dos fármacos , Tamanho da Partícula , Silício/metabolismo , Espectrofotometria Atômica , Eletricidade Estática , Distribuição Tecidual/efeitos dos fármacos
17.
Cardiovasc Toxicol ; 13(3): 194-207, 2013 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-23322373

RESUMO

The purpose of this work was to investigate the cardiovascular toxicity of different sizes and different dosages of silica nanoparticles in Wistar rats. The three silica nanoparticles (30, 60, and 90 nm) and one fine silica particles (600 nm) at three doses of 2, 5, and 10 (mg/Kg bw) were used in the present experiment. After intratracheal instillation for a total of 16 times, concentration of Si in hearts and serum was measured by inductively coupled plasma optical emission spectrometer. The hematology parameters were analyzed by an automated hematology analyzer, and the inflammatory reaction, oxidative stress, endothelial dysfunction, and the myocardial enzymes in serum were measured by kits. Our results showed intratracheal-instilled silica nanoparticles could pass through the alveolar-capillary barrier into systemic circulation. Concentration of Si in the heart and serum depended on the particles size and dosage. The levels of reactive oxygen species (ROS) at 5, 10 mg/Kg bw of the three silica nanoparticles were higher than the fine silica particles. Blood levels of inflammation-related high-sensitivity C-reactive protein and cytokines such as interleukin-1beta (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor-alpha were increased after exposure to three silica nanoparticles at 10 mg/Kg bw. Moreover, the levels of IL-1ß and IL-6 at 10 mg/Kg bw of silica nanoparticles (30 nm) were higher than the fine silica particles. Significant decrease in superoxide dismutase, glutathione peroxidase and significant increase in malondialdehyde were observed at 10 mg/Kg bw of the three silica nanoparticles. A significant decrease in nitric oxide (NO) production was induced which coincided with the reduction of nitric oxide synthase (NOS) activity and the excessive generation of ROS in rats. The levels of intercellular adhesion molecule-l and vascular cell adhesion molecule-l elevated significantly after exposure to three silica nanoparticles at 10 mg/Kg bw, which are considered as early steps of endothelial dysfunction. We conclude that cardiovascular toxicity of silica nanoparticles could be related to the particles size and dosage. Oxidative stress could be involved in inflammatory reaction and endothelial dysfunction, all of which could aggravate cardiovascular toxicology. In addition, endothelial NO/NOS system disorder caused by nanoparticles could be one of the mechanisms for endothelial dysfunction.


Assuntos
Doenças Cardiovasculares/induzido quimicamente , Nanopartículas/toxicidade , Dióxido de Silício/toxicidade , Animais , Biomarcadores/sangue , Contagem de Células Sanguíneas , Coagulação Sanguínea/efeitos dos fármacos , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/patologia , Relação Dose-Resposta a Droga , Endotélio Vascular/efeitos dos fármacos , Indicadores e Reagentes , Mediadores da Inflamação/metabolismo , Intubação Intratraqueal , Masculino , Microscopia Eletrônica de Transmissão , Miocárdio/enzimologia , Miocárdio/metabolismo , Nanopartículas/administração & dosagem , Nanopartículas/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Tamanho da Partícula , Ratos , Ratos Wistar , Dióxido de Silício/administração & dosagem , Dióxido de Silício/metabolismo
18.
Toxicol In Vitro ; 25(8): 1619-29, 2011 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-21723938

RESUMO

Amorphous silica nanoparticles are widely applied in many fields. But the adverse effects of silica nanoparticle exposure were unclear. The present study investigated the cytotoxicity and mitochondrial damage of silica nanoparticles exposure in hepatocellular carcinoma cell line (HepG2). The cells were treated with 43 nm non-modified amorphous silica nanoparticles which dispersed in serum-free DMEM at concentrations of 0, 25, 50, 100 and 200 µg/mL for 3 and 24 h. The results showed that the silica nanoparticles could lead to increasing cellular reactive oxygen species (ROS) production for 3 and 24 h exposure. Moreover, the oxidative stress induced by the particles could play an important role of the mitochondrial membrane damage and the cell apoptosis. It indicated that apoptosis through mitochondrial pathway mediated by oxidative stress was a potential mechanism of cytotoxicity induced by silica nanoparticles. The particles could enter the cells through different pathways and dispersed in cytoplasm and deposited inside mitochondria. Mitochondria were the major organelles for the cytotoxicity of silica nanoparticles exposure. Mitochondrial damage was related to the oxidative stress and the direct injurious effect of nanoparticles. It can be considered as the potential mechanism for the cytotoxic effects of amorphous silica nanoparticles.


Assuntos
Apoptose/efeitos dos fármacos , Mitocôndrias/efeitos dos fármacos , Nanopartículas/toxicidade , Estresse Oxidativo , Dióxido de Silício/toxicidade , Caspase 3/metabolismo , Linhagem Celular Tumoral , Citocromos c/metabolismo , Humanos , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Microscopia Eletrônica de Transmissão , Mitocôndrias/fisiologia , Mitocôndrias/ultraestrutura , Nanopartículas/ultraestrutura , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Proteína X Associada a bcl-2/metabolismo
19.
Toxicol In Vitro ; 25(7): 1343-52, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-21575712

RESUMO

The purpose of this study is to compare the potential cytotoxicity induced by amorphous silica particles with different sizes. The effects of one fine particle (498 nm) and three nanoparticles (68, 43, and 19 nm) on cultured human hepatoma (HepG2) cells were investigated by detecting morphological changes, cell viability, cytomembrane integrity, DNA damage, cell cycle distribution, and apoptosis after the cells were treated with 100 µg/mL of four silica particles for 24h. The results indicated that in HepG2 cells, the cytotoxicity generated by silica particles strongly depended on the particle size, and smaller silica particle possessed higher toxic effect. In order to further elucidate the possible mechanisms of cell injuries, intracellular reactive oxygen species (ROS) was measured. Increased ROS level was also observed in a size dependent way. However, the result showed the fine particle did not promote intracellular ROS level significantly, while cell injuries were detected in this treated group. Thus, our data demonstrated that exposure to different sizes of silica particles resulted in a size dependent cytotoxicity in cultured HepG2 cells, and ROS generation should be one possible damage pathway but might not be completely responsible for the toxic effect produced by silica particles.


Assuntos
Nanopartículas/química , Nanopartículas/toxicidade , Dióxido de Silício/química , Apoptose/efeitos dos fármacos , Ciclo Celular/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Dano ao DNA , Células Hep G2 , Humanos , Tamanho da Partícula , Espécies Reativas de Oxigênio/metabolismo
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