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1.
In Vitro Cell Dev Biol Anim ; 57(7): 685-694, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34518994

RESUMO

The destruction of biological activity such as senescence and apoptosis caused by oxidative stress could play a pivotal role in the poor therapeutic efficiency of bone marrow mesenchymal stem cells (BMSCs) transplantation. Mitoquinone (MitoQ) has a highly effective mitochondrial antioxidant effect, and has been widely used in many oxidative damage models. This study aimed to investigate the protective effect of MitoQ on the oxidative stress-mediated senescence of canine BMSCs and the underlying mechanism. The senescence of BMSCs was determined by senescence-associated ß-galactosidase staining and quantitative real-time PCR. The expression of p-Nrf2 protein was detected by Western blotting. The results demonstrated that, as BMSCs were expanded in vitro, the senescent phenotype appeared. And the senescence of BMSCs may be caused by oxidative stress, manifested by increasing the level of ROS and decreasing the activity of antioxidant enzymes. Treatment of MitoQ down-regulated the mRNA levels of senescence-related and apoptosis-related genes, but up-regulated the mRNA levels of proliferation-related genes. Meanwhile, ROS generation and senescent activity were reduced in MitoQ-treated BMSCs. Further mechanism studies showed that MitoQ obviously promoted Nrf2 phosphorylation, and also facilitated the translocation of Nrf2 into the nucleus. Moreover, treatment of MitoQ increased the mRNA levels of downstream antioxidant genes and enhanced the activities of superoxide dismutase, catalase, and glutathione peroxidase. Thus, our study revealed that MitoQ, via the Nrf2/ARE signaling pathway, exerts an antioxidant effect as well as potentially delays OS-mediated senescence during BMSCs that were expanded in vitro, which may serve as a novel strategy to optimize the clinical application of BMSCs.

2.
Ecotoxicol Environ Saf ; 225: 112718, 2021 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-34478984

RESUMO

As a common environmental pollutant, nickel chloride (NiCl2) poses serious threat to human and animals health. NiCl2 has adverse effects on reproductive function in male, however, the underlying mechanisms are not fully illuminated. In this study, 64 male ICR mice were divided into four groups (8 mice per each period/ group), in which mice orally administrated with 0, 7.5, 15 or 30 mg/kg body weight for 14 or 28 consecutive days, respectively. The results showed that the sperm concentration (12.95%, 29.78% and 37.63% -) and sperm motility (19.79%, 34.88% and 43.10%) were dose-dependent significantly reduced, and the total sperm malformation rates (110.15%, 206.84% and 292.27%) were dose-dependent significantly elevated in the 7.5, 15 and 30 mg/kg NiCl2 treatment groups (vs control at 28 days), respectively (P < 0.05). Meanwhile, NiCl2 also decreased the relative weights of testis and epididymis and caused histopathological lesions of testis and epididymis. Furthermore, serum testosterone levels were significantly decreased after NiCl2 treatment. And the findings showed that NiCl2 down-regulated the expression of LH-R, StAR, P450scc, 3ß-HSD, 17ß-HSD, ABP and INHßB in the testis, however, the relative genes in the hypothalamus (Kiss-1, GPR54 and GnRH) and pituitary (GnRH-R, LHß and FSHß) did not exhibit noticeable change. In summary, NiCl2 induced spermatogenesis disorder by testicular damage and hypothalamic-pituitary-testis axis disruption in mice, and only impaired the genes on the testis of HPT axis.


Assuntos
Motilidade Espermática , Testículo , Animais , Masculino , Camundongos , Camundongos Endogâmicos ICR , Níquel , Espermatogênese , Testosterona
3.
Ecotoxicol Environ Saf ; 225: 112760, 2021 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-34509165

RESUMO

Obesity is a risk factor of many diseases, but could be beneficial to the individuals with bacterial infection. The present study was conducted to investigate the relationship between obesity and heart during nonfatal bacterial infection. Male normal (lean) and diet-induced obesity mice (DIO, fed with high-fat diet) were chosen to perform nasal instillation with E. coli to establish a nonfatal acute mouse model. The cardiac histopathology, inflammation and oxidative damage, as well as apoptosis were detected post-infection. The results revealed that the Escherichia coli (E.coli)-infected mice exhibited increased cardiac index, contents of IL-1ß, IL-6, IL-8, TNF-α, leptin and resistin, levels of apoptotic proteins (caspase-3 and caspase-9, and bax/bcl-2 ratio), cardiac pathological changes and oxidative stress. Furthermore, these parameters were more serious in the lean mice than those in the DIO mice. In summary, our findings gave a new sight that E.coli infection impaired heart via histopathological lesions, inflammation and oxidative stress and excessive apoptosis of cardiomyocytes. Interestingly, obesity exerted attenuated effects on the heart of mice with non-fatal infection of E.coli through decreased inflammation, oxidative stress and apoptosis of cardiac tissue.


Assuntos
Escherichia coli , Estresse Oxidativo , Animais , Apoptose , Inflamação , Masculino , Camundongos , Camundongos Obesos
4.
J Hazard Mater ; 416: 125903, 2021 08 15.
Artigo em Inglês | MEDLINE | ID: mdl-34492839

RESUMO

Copper is considered as an indispensable trace element for living organisms. However, over-exposure to Cu can lead to adverse health effects on human. In this study, CuSO4 decreased sperm concentration and motility, increased sperm malformation rate. Concurrently, testicular damage including testicular histopathological aberrations and reduction of testis relative weight were observed. Then, the mechanism underlying Cu-induced testicular toxicity was explored. According to the results, CuSO4 elevated ROS production while reducing antioxidant function. Additionally, CuSO4 induced apoptosis which was featured by MMP depolarization and up-regulated levels of cleaved-caspase-3, cleaved-caspase-8, cleaved-caspase-9, caspase-12, cleaved-PARP and Bax, whereas down-regulated Bcl-2 expression. Meanwhile, CuSO4 caused testis DNA damage (up-regulation of γ-H2AX protein expression) and suppressed DNA repair pathways including BER, NER, HR, MMR, together with the NHEJ repair pathways, yet did not affect MGMT. To investigate the role of oxidative stress in CuSO4-induced apoptosis and DNA damage, the antioxidant NAC was co-treated with CuSO4. NAC attenuated CuSO4-induced ROS production, inhibited apoptosis and DNA damage. Furthermore, the spermatogenesis disorder was also abolished in the co-treatment with CuSO4 and NAC group. Altogether, abovementioned results indicated that CuSO4-induced spermatogenesis disorder is related to oxidative stress-mediated DNA damage and germ cell apoptosis, impairing male reproductive function.


Assuntos
Estresse Oxidativo , Espermatogênese , Apoptose , Dano ao DNA , Humanos , Masculino , Espermatozoides , Testículo/metabolismo
5.
Int J Mol Sci ; 22(18)2021 Sep 17.
Artigo em Inglês | MEDLINE | ID: mdl-34576206

RESUMO

Actinobacillus pleuropneumoniae is a pathogen that infects pigs and poses a serious threat to the pig industry. The emergence of quinolone-resistant strains of A.pleuropneumoniae further limits the choice of treatment. However, the mechanisms behind quinolone resistance in A.pleuropneumoniae remain unclear. The genomes of a ciprofloxacin-resistant strain, A. pleuropneumoniae SC1810 and its isogenic drug-sensitive counterpart were sequenced and analyzed using various bioinformatics tools, revealing 559 differentially expressed genes. The biological membrane, plasmid-mediated quinolone resistance genes and quinolone resistance-determining region were detected. Upregulated expression of efflux pump genes led to ciprofloxacin resistance. The expression of two porins, OmpP2B and LamB, was significantly downregulated in the mutant. Three nonsynonymous mutations in the mutant strain disrupted the water-metal ion bridge, subsequently reducing the affinity of the quinolone-enzyme complex for metal ions and leading to cross-resistance to multiple quinolones. The mechanism of quinolone resistance in A. pleuropneumoniae may involve inhibition of expression of the outer membrane protein genes ompP2B and lamB to decrease drug influx, overexpression of AcrB in the efflux pump to enhance its drug-pumping ability, and mutation in the quinolone resistance-determining region to weaken the binding of the remaining drugs. These findings will provide new potential targets for treatment.

6.
Ecotoxicol Environ Saf ; 223: 112583, 2021 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-34352574

RESUMO

Nickel (Ni), a widely distributed metal, is an important pollutant in the environment. Although kidney is a crucial target of Ni toxicity, information on autophagy and the potential mechanisms of Ni-induced renal toxicity are still poorly described. As we discovered, NiCl2 could induce renal damage including decrease in renal weight, renal histological alterations, and renal function injury. According to the obtained results, NiCl2 could obviously increase autophagy, which was characterized by increase of LC3 expression and decrease of p62 expression. Meanwhile, the result of ultrastructure observation showed increased autolysosomes numbers in the kidney of NiCl2-treated mice. In addition, NiCl2 increased mRNA and protein levels of autophagy flux proteins including Beclin1, Atg5, Atg12, Atg16L1, Atg7, and Atg3. Furthermore, NiCl2 induced autophagy through AMPK and PI3K/AKT/mTOR pathways which featured down-regulated expression levels of p-PI3K, p-AKT and p-mTOR and up-regulated expression levels of p-AMPK and p-ULK1. In summary, the above results indicate involvement of autophagy in renal injury induced by NiCl2, and NiCl2 induced autophagy via PI3K/AKT/mTOR and AMPK pathways in mouse kidney.


Assuntos
Fosfatidilinositol 3-Quinases , Proteínas Proto-Oncogênicas c-akt , Proteínas Quinases Ativadas por AMP/genética , Proteínas Quinases Ativadas por AMP/metabolismo , Animais , Autofagia , Rim/metabolismo , Camundongos , Níquel , Fosfatidilinositol 3-Quinases/genética , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Serina-Treonina Quinases TOR/genética , Serina-Treonina Quinases TOR/metabolismo
7.
Ecotoxicol Environ Saf ; 222: 112518, 2021 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-34271501

RESUMO

Copper (Cu), as a common chemical contaminant in environment, is known to be toxic at high concentrations. The current research demonstrates the effects of copper upon hepatocyte cell-cycle progression (CCP) in mice. Institute of cancer research (ICR) mice (n = 240) at an age of four weeks were divided randomly into groups treated with different doses of Cu (0, 4, 8, and 16 mg/kg) for 21 and 42 days. Results showed that high Cu exposure caused hepatocellular G0/G1 cell-cycle arrest (CCA) and reduced cell proportion in the G2/M phase. G0/G1 CCA occurred with down-regulation (p < 0.05) of Ras, p-PI3K (Tyr458), p-Akt (Thr308), p-forkhead box O3 (FOXO3A) (Ser253), p-glycogen synthase kinase 3-ß (GSK3-ß) (Ser9), murine double minute 2 (MDM2) protein, and mRNA expression levels, and up-regulation (p < 0.05) of PTEN, p-p53 (Ser15), p27, p21 protein, and mRNA expression levels, which subsequently suppressed (p < 0.05) the protein and mRNA expression levels of CDK2/4 and cyclin E/D. These results indicate that Cu exposure suppresses the Ras/PI3K/Akt signaling pathway to reduce the level of CDK2/4 and cyclin E/D, which are essential for the G1-S transition, and finally causes hepatocytes G0/G1 CCA.


Assuntos
Fosfatidilinositol 3-Quinases , Proteínas Proto-Oncogênicas c-akt , Animais , Linhagem Celular Tumoral , Proliferação de Células , Cobre/toxicidade , Pontos de Checagem da Fase G1 do Ciclo Celular , Quinase 3 da Glicogênio Sintase , Camundongos , Fosfatidilinositol 3-Quinases/genética , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais
8.
Sci Rep ; 11(1): 13725, 2021 07 02.
Artigo em Inglês | MEDLINE | ID: mdl-34215807

RESUMO

Enterobacteria that produce extended-spectrum ß-lactamase (ESBL) such as Escherichia coli (E. coli) are common in our environment and known to cause serious health implications in humans and animals. ß-lactam antibiotics such as penicillins, cephalosporins and monobactams are the most commonly used anti-bacterials in both humans and animals, however, Gram negative bacteria (such as E. coli) that produces extended-spectrum ß-lactamases (ESBLs) have the ability to hydrolyze most ß-lactams therefore making them resistant to ß-lactam antibiotics. Recent extensive researches on the epidemiology and genetic characteristics of extended-spectrum ß-lactamase (ESBL)-producing E. coli reported the existence of ESBL-producing E. coli in humans, companion animals and poultry. Therefore, this experiment was performed to investigate the prevalence and genetic characteristics of ß-lactamase producing E. coli isolated from beef cattle farms in the Sichuan-Chongqing circle of China. Phenotypic confirmation of ESBL-producing E. coli was performed using the double disk synergy test. Polymerase Chain Reaction (PCR) was used to detect blaCTX-M, blaSHV and blaTEM gene codes, then after, isolates were divided into different phylogenetic groups and multi-locus sequence typing (MLST). The results showed that out of the 222 E. coli strains isolated from the beef cattle, 102 strains showed ESBL phenotypes. The PCR results showed that blaCTX-M was the predominant ESBL gene identified among the E. coli strains with 21 (9.5%) isolates having this gene, followed by blaSHV which was found in 18 (8.1%) isolates. The majority of these ESBL positive isolates were assigned to phylogroup A (19.8%) followed by phylogroup B1 (13.5%). In addition, from the MLST results on ESBL positive isolates (n = 30) we identified 19 STs, ST398 (ST398cplx) and ST7130 which were the prevalent population (20%). In conclusion, the high prevalence of CTX-M, and SHV in the study confirmed its association with E. coli infection; therefore, this calls for health concerns on ESBL-producing E. coli. As far as we know, this is the first comprehensive research report relating to ESBL-producing E. coli incidence in Chinese beef cattle.

9.
Artigo em Inglês | MEDLINE | ID: mdl-34291412

RESUMO

Sichuan, located in the upper reaches of the Yangtze River, is the gathering place of many rivers and plays an important role in sturgeon aquaculture and wild sturgeon protection in China, where it suffered the severe influence of Streptococcus iniae infection in sturgeon. However, the annual thousands of tons of antibiotic usage in Sichuan may accumulate in water and cause obstacles to the prevention of S. iniae infection. In contrast, the regional antibiotic resistance characteristics have been rarely unknown. Seventeen S. iniae strains were collected from the major sturgeon culture areas in Sichuan, and the genotyping and the distribution of antibiotic resistance profiles (ARPs) and genes (ARGs) of S. iniae were established in this study. The results showed that the isolates could be divided into four subtypes by pulsed-field gel electrophoresis analysis. Besides, most isolates showed multiple resistance to the antibiotic such as amikacin, neomycin, enrofloxacin, lincomycin, and sulfamethoxazole. Also, sturgeon-derived S. iniae has a relatively low similarity with other fish-derived S. iniae in the world but high similarity with three animal-derived pathogens from Sichuan in previous studies. Moreover, a total of 37 ARGs were detected positively based on 95 ARGs detection, in which aac(6')-Ib(aka aacA4)-01, aac(6')-Ib(aka aacA4)-02, aadA1, floR, blaTEM, sulA/folP-03, and tetA-02 were most prevalent. Our study indicated that the ARGs of sturgeon-derived S. iniae were significantly enhanced compared with the ATCC29178 strains and have a risk of accessing more ARGs from other bacteria in water in Sichuan. This study claimed that sturgeon has a potential risk in the prevention and control of Streptococcosis in Sichuan, the upper reaches of Yangtze River, based on the antibiotic resistance analysis of S. iniae, and it may also increase the risk of highly resistant S. iniae transmission into the middle and lower reaches.

10.
Front Immunol ; 12: 699807, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34220862

RESUMO

Resistin, a cysteine-rich protein, expressed in adipocytes, was initially proposed as a link between obesity and diabetes in mice. In humans, resistin is considered to be a pro-inflammatory molecule expressed in immune cells, which plays a regulatory role in many chronic inflammatory diseases, metabolic diseases, infectious diseases, and cancers. However, increasing evidence shows that resistin functions as a host defense peptide of innate immunity, in terms of its wide-spectrum anti-microbial activity, modulation of immunity, and limitation of microbial product-induced inflammation. To date, the understanding of resistin participating in host defense mechanism is still limited. The review aims to summarize current knowledge about the biological properties, functions, and related mechanisms of resistin in host defense, which provides new insights into the pleiotropic biological function of resistin and yields promising strategies for developing new antimicrobial therapeutic agents.

11.
Biol Trace Elem Res ; 2021 Jun 25.
Artigo em Inglês | MEDLINE | ID: mdl-34173155

RESUMO

Cadmium (Cd), a heavy metal element, cumulates in the testis and can cause male reproductive toxicity. Although vitamin E (VE) as one of potential antioxidants protects the testis against toxicity of Cd, the underlying mechanism remained uncompleted clear. The aim of this study was to investigate whether the Nrf-2 pathway is involved with the protective effect of VE on testicular damages caused by sub-chronic Cd exposure. Thirty-two SD rats were divided into four groups and orally administrated with VE and/or Cd for 28 consecutive days: control group, VE group (100 mg VE/kg), Cd group (5 mg CdCl2/kg), and VE + Cd group (100 mg VE/kg + 5 mg CdCl2/kg). The results showed that 28-day exposure of Cd caused accumulation of Cd, histopathological lesions, and alternations of sperm parameters (elevated rate of abnormal sperm, decreased count of sperm, declined motility, and viability of sperm). Moreover, the rats exposed to Cd showed significant oxidative stress (increased contents of MDA and decreased levels or activities of T-AOC, GSH, CAT, SOD and GSH-Px) and inhibition of Nrf-2 signaling pathway (downregulation of Nrf-2, HO-1, NQO-1, GCLC, GCLM and GST) of the testes. In contrast, VE treatment significantly reduced the Cd accumulation, alleviated histopathological lesions and dysfunctions, activated Nrf-2 pathway, and attenuated the oxidative stress caused by Cd in the testes of rats. In conclusion, VE, through upregulating Nrf-2 pathway, could protect testis against oxidative damages induced by sub-chronic Cd exposure.

12.
Toxicol Appl Pharmacol ; 418: 115500, 2021 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-33744278

RESUMO

Copper (Cu) is considered as an essential trace element for living organisms. However, over-exposure to Cu can lead to adverse health effects on human and animals. There are limited researches on pulmonary toxicity induced by Cu. Here, we found that copper sulfate (CuSO4)-treatment could induce pulmonary fibrosis with Masson staining and up-regulated protein and mRNA expression of Collagen I and α-Smooth Muscle Actin (α-SMA) in mice. Next, the mechanism underlying Cu-induced pulmonary fibrosis was explored, including transforming growth factor-ß1 (TGF-ß1)-mediated Smad pathway, mitogen-activated protein kinases (MAPKs) pathway and epithelial-mesenchymal transition (EMT). CuSO4 triggered pulmonary fibrosis by activation of the TGF-ß1/Smad pathway, which was accomplished by increasing TGF-ß1, p-Smad2 and p-Smad3 protein and mRNA expression levels. Also, up-regulated protein and mRNA expression of p-JNK, p-ERK, and p-p38 demonstrated that CuSO4 activated MAPKs pathways. Concurrently, EMT was activated by increasing vimentin and N-cadherin while decreasing E-cadherin protein and mRNA expression levels. Altogether, the abovementioned findings indicate that CuSO4 treatment may induce pulmonary fibrosis through the activation of EMT induced by TGF-ß1/Smad pathway and MAPKs pathways, revealing the mechanism Cu-caused pulmonary toxicity.


Assuntos
Sulfato de Cobre , Transição Epitelial-Mesenquimal , Pulmão/metabolismo , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Fibrose Pulmonar/metabolismo , Proteínas Smad/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Animais , Modelos Animais de Doenças , Feminino , Regulação da Expressão Gênica , Pulmão/patologia , Masculino , Camundongos Endogâmicos ICR , Proteínas Quinases Ativadas por Mitógeno/genética , Fosforilação , Fibrose Pulmonar/induzido quimicamente , Fibrose Pulmonar/genética , Fibrose Pulmonar/patologia , Transdução de Sinais , Proteínas Smad/genética , Fator de Crescimento Transformador beta1/genética
13.
Biol Trace Elem Res ; 199(12): 4675-4687, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-33565019

RESUMO

Cadmium (Cd), a widely distributed heavy metal, is extremely toxic to the kidney. Vitamin E (VE) is an important antioxidant in the body. It is known that VE exerts a protective effect on renal oxidative damage caused by Cd, but the effect and mechanism of VE on apoptosis are not fully understood. Thus, we conducted this study to explore the protective effect of VE on Cd-induced renal apoptosis and to elucidate its potential mechanism. Thirty-two 9-week-old male Sprague-Dawley rats were randomly divided into four groups, namely control, VE (100 mg/kg VE), Cd (5 mg/kg CdCl2), and VE + Cd (100 mg/kg VE + 5 mg/kg CdCl2), and received intragastric administration of Cd and/or VE for 4 weeks. The results showed that Cd exposure significantly reduced the weight of the body and kidney, elevated the accumulation of Cd in the kidney as well as the levels of BUN and Scr in serum, caused renal histological alterations, decreased the GSH and T-AOC contents and antioxidant enzyme (SOD, CAT, GSH-PX) activities, and increased renal MDA content. And the increased number of TUNEL-positive cells by Cd was accompanied by upregulated mRNA and protein expressions of apoptotic regulatory molecules (Bax, Caspase-3, GRP94, GRP78, Caspase-8) and downregulated Bcl-2 expressions. However, the combined treatment of Cd and VE could restore the above parameters to be close to those in the control rats. In conclusion, VE supplement could alleviate Cd-induced rat renal damage and oxidative stress through enhancing the antioxidant defense system and inhibiting apoptosis of renal cells.

14.
Biol Trace Elem Res ; 2021 Feb 16.
Artigo em Inglês | MEDLINE | ID: mdl-33594525

RESUMO

The aim of this study was to investigate the effects of different doses of selenium (Se) on oxidative damage and neurotransmitter-related parameters in arsenic (As)-induced broiler brain tissue damage. Two hundred 1-day-old avian broilers were randomly divided into five groups and fed the following diets: control group (As 0.1 mg/kg + Se 0.2 mg/kg), As group (As 3 mg/kg + Se 0.2 mg/kg), low-Se group (As 3 mg/kg + Se 5 mg/kg), medium-Se group (As 3 mg/kg + Se 10 mg/kg), and high-Se group (As 3 mg/kg + Se 15 mg/kg). Glutathione (GSH), glutathione peroxidase (GSH-PX), nitric oxide (NO), nitric oxide synthase (NOS) activity, glutamate (Glu) concentration, glutamine synthetase (GS) activity, acetylcholinesterase (TchE) activity, and the apoptosis rate of brain cells were measured. The results showed that 3 mg/kg dietary As could induce oxidative damage and neurotransmitter disorder of brain tissue, increase the apoptosis rate of brain cells and cause damage to brain tissue, decrease activities of GSH and GSH-PX, decrease the contents of NO, decrease the activities of iNOS and tNOS, increase contents of Glu, and decrease activities of Gs and TchE. Compared with the As group, the Se addition of the low-Se and medium-Se groups protected against As-induced oxidative damage, neurotransmitter disorders, and the apoptosis rate of brain cells, with the addition of 10 mg/kg Se having the best effect. However, 15 mg/kg Se not only did not produce a protective effect against As damage but actually caused similar or severe damage.

15.
Arch Virol ; 166(4): 1259-1262, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33582856

RESUMO

In 2019, diarrhea cases occurred on cattle farms in Qionglai and Guang'an, Sichuan Province. Two out of 20 (10%) serum and nasal swab samples were positive when tested using a bovine viral diarrhea virus (BVDV) antigen-capture ELISA kit. Two non-cytopathic strains of BVDV were isolated and named QL1903 and GA190608, respectively. The nucleotide sequences of the genomes of the two isolates were 89.52% identical. Phylogenetic analysis based on the 5'-UTR sequence revealed that the BVDV isolate QL1903 belonged to BVDV subtype 1b, whereas isolate GA190608 clustered with strains HN1814, EN-19, and BJ09_26 in a separate branch, which has tentatively been classified as a new genetic subtype, "1v".


Assuntos
Doença das Mucosas por Vírus da Diarreia Viral Bovina/virologia , Vírus da Diarreia Viral Bovina Tipo 1/classificação , Vírus da Diarreia Viral Bovina Tipo 1/genética , Regiões 5' não Traduzidas/genética , Animais , Doença das Mucosas por Vírus da Diarreia Viral Bovina/diagnóstico , Bovinos , Linhagem Celular , Vírus da Diarreia Viral Bovina Tipo 1/imunologia , Vírus da Diarreia Viral Bovina Tipo 1/isolamento & purificação , Variação Genética , Genoma Viral/genética , Genótipo , Filogenia , RNA Viral/genética , Proteínas Virais/imunologia
16.
Sci Rep ; 11(1): 909, 2021 01 13.
Artigo em Inglês | MEDLINE | ID: mdl-33441700

RESUMO

Cladosporium cladosporioides causes asthma and superficial and deep infections, mostly in immunodeficient individuals and animals. This study aimed to investigate whether C. cladosporioides spores can enter the lungs through pulmonary circulation and influence pulmonary immune response. We intravenously injected mice with C. cladosporioides spore suspension and conducted several assays on the lungs. Pulmonary hemorrhage symptoms and congestion were most severe on days 1, 2, and 3 post-inoculation (PI). Extensive inflammatory cell infiltration occurred throughout the period of infection. More spores and hyphae colonizing the lungs were detected on days 1, 2, and 3 PI, and fewer spores and hyphae were observed within 21 d of infection. Numerous macrophages, dendritic cells, and neutrophils were observed on day 5 PI, along with upregulation of CD54, an intercellular adhesion molecule. Th1 and Th2 cells increased after infection; specifically, Th2 cells increased considerably on day 5 PI. These results suggest that days 2 and 5 PI represent the inflammatory peak in the lungs and that the Th2 and Th1 signaling pathways are potentially involved in pulmonary immune responses. In conclusion, the further adaptive immune responses played important roles in establishing effective pulmonary immunity against C. cladosporioides systemic infections based on innate immune responses.


Assuntos
Imunidade Adaptativa/imunologia , Cladosporium/imunologia , Pneumopatias Fúngicas/imunologia , Animais , Asma/imunologia , Cladosporium/metabolismo , Cladosporium/patogenicidade , Modelos Animais de Doenças , Feminino , Imunidade Inata/imunologia , Pulmão/patologia , Camundongos , Camundongos Endogâmicos C57BL , Neutrófilos/imunologia , Pneumonia/imunologia , Esporos Fúngicos/imunologia , Esporos Fúngicos/patogenicidade , Células Th2/imunologia
17.
Ecotoxicol Environ Saf ; 208: 111656, 2021 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-33396170

RESUMO

Although copper is among the indispensable trace elements in animal physiological processes, it exerts toxicity upon over-exposure. The present study aimed to investigate hepatocyte autophagy induced by CuSO4 and its potential mechanism. A total of 240 ICR mice (four-week-old, 120 males and 120 females) were randomly divided into four groups, in which mice separately received 0, 4, 8, and 16 mg/kg of Cu (Cu2+-CuSO4) for 42 d. The results of increased autophagosomes and autophagy marker LC3B brown cell staining showed that excessive intake of Cu enhanced hepatocyte autophagy. Simultaneously, Cu inhibited the activity of mTOR through suppressing mRNA and protein expressions in mTOR, which in turn up-regulated expression levels of ULK1 and initiated autophagy. Also, over-exposure to Cu increased mRNA and protein expressions of Beclin1, Atg12, Atg5, Atg16L1, Atg7, Atg3, and LC3 and decreased mRNA and protein expressions of p62. These results indicate that excess Cu can enhance hepatocyte autophagy via inhibiting the mTOR signaling pathway and regulating mRNA and protein expressions of factors implicated to autophagy in mice.


Assuntos
Autofagia/efeitos dos fármacos , Cobre/toxicidade , Hepatócitos/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Serina-Treonina Quinases TOR/metabolismo , Animais , Autofagossomos/efeitos dos fármacos , Autofagossomos/metabolismo , Autofagia/genética , Feminino , Regulação da Expressão Gênica/efeitos dos fármacos , Hepatócitos/metabolismo , Hepatócitos/patologia , Masculino , Camundongos , Camundongos Endogâmicos ICR , Serina-Treonina Quinases TOR/genética
18.
Ecotoxicol Environ Saf ; 208: 111610, 2021 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-33396130

RESUMO

Hepatic oxidative stress, as one important mechanism of cadmium (Cd)-induced hepatic toxicity, could, as known, be ameliorated by vitamin E (VE). However, the underlying mechanism remains to be elucidated. To investigate whether the antioxidant vitamin E can protect against Cd-induced sub-chronic liver injury associated with oxidative stress and nuclear factor erythrocyte 2-related factor 2 (Nrf2) pathway, male Sprague-Dawley rats (nine-week-old) were randomly divided into four groups (eight rats/group), namely, control, VE (100 mg/kg VE), Cd (5 mg/kg CdCl2) and VE+Cd (100 mg/kg VE+5 mg/kg CdCl2), and received intragastric administration of Cd and/or VE for four weeks. Cd-exposure alone resulted in reduced liver weight, liver histological alteration and oxidative stress, accumulation of Cd in the liver, elevated ALT and AST concentrations in serum together with decreased mRNA and protein expressions of Nrf2 pathway related molecules (Nrf2, HO-1, NQO-1, GCLC, GCLM and GST). However, the co-treatment of Cd and VE significantly ameliorated the changes mentioned above, and promoted the expression of genes and proteins of Nrf2 pathway related molecules in comparison to the Cd-exposure alone. Our results indicate that the protective effect of VE against Cd-induced sub-chronic hepatic damage in rats is associated with the inhibition of oxidative stress and activation of Nrf2 pathway.


Assuntos
Antioxidantes/farmacologia , Cádmio/toxicidade , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Poluentes Ambientais/toxicidade , Fator 2 Relacionado a NF-E2/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Vitamina E/farmacologia , Animais , Antioxidantes/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/patologia , Fígado/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Testes de Função Hepática , Masculino , Tamanho do Órgão/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Transdução de Sinais
19.
Environ Sci Pollut Res Int ; 28(5): 4893-4901, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-33230792

RESUMO

Nickel (Ni) is a widely distributed metal in the environment and an important pollutant due to its widespread industrial applications. Ni has various toxicity in humans and experimental animals, including carcinogenicity. However, the carcinogenic effects of Ni remain troublesome. Cell cycle dysregulation may be an important carcinogenic mechanism and is also a potential molecular mechanism for Ni complexes anti-cancerous effects. Therefore, we conducted a literature review to summarize the effects of Ni on cell cycle. Up to now, there were three different reports on Ni-induced cell cycle arrest: (i) Ni can induce cell cycle arrest in G0/G1 phase, phosphorylation and degradation of IkappaB kinase-alpha (IKKα)-dependent cyclin D1 and phosphoinositide-3-kinase (PI3K)/serine-threonine kinase (Akt) pathway-mediated down-regulation of expressions of cyclin-dependent kinases 4 (CDK4) play important role in it; (ii) Ni can induce cell cycle arrest in S phase, but the molecular mechanism is not known; (iii) G2/M phase is the target of Ni toxicity, and Ni compounds cause G2/M cell cycle phase arrest by reducing cyclinB1/Cdc2 interaction through the activation of the ataxia telangiectasia mutated (ATM)-p53-p21 and ATM-checkpoint kinase inhibitor 1 (Chk1)/Chk2-cell division cycle 25 (Cdc25) pathways. Revealing the mechanisms of cell cycle dysregulation associated with Ni exposure may help in the prevention and treatment of Ni-related carcinogenicity and toxicology.


Assuntos
Proteínas de Ciclo Celular , Níquel , Animais , Proteínas Mutadas de Ataxia Telangiectasia , Carcinogênese , Ciclo Celular , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Divisão Celular , Humanos , Níquel/toxicidade , Transdução de Sinais , Proteína Supressora de Tumor p53/metabolismo
20.
Biol Trace Elem Res ; 199(3): 1080-1089, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32476085

RESUMO

The aim of the present study was to investigate the abilities of selenium to counteract the toxic damage of arsenic (As). Two hundred 1-day-old healthy male broilers were randomly divided into five groups and fed the following diets: control group (0.1 mg/kg As + 0.2 mg/kg Se), As group (3 mg/kg As + 0.2 mg/kg Se), As + Se group I (3 mg/kg As + 5 mg/kg Se), As + Se group II (3 mg/kg As + 10 mg/kg Se), and As + Se group III (3 mg/kg As + 15 mg/kg Se), respectively. The relative weight of the liver, hepatic protein content, GSH-Px levels, SOD activities, NO contents, iNOS and tNOS activities, and increased malondialdehyde contents, ALT and AST activities, and the apoptotic hepatocytes were analyzed. Adding 3 mg/kg arsenic to the diet caused the growth and development of chicken liver to be blocked, resulting in decrease of protein contents in liver tissue, decrease of SOD and GSH-Px activities, increase of MDA contents, decrease of NO contents, decrease of iNOS and TNOs activities, increase of ALT and AST activities, increase of apoptosis rates of liver cells. Compared to the 3-mg/kg arsenic group, adding 5 mg/kg and 10 mg/kg selenium, respectively, could repair the liver growth retardation and steatosis caused by arsenic, increase the protein contents in liver tissue, increase the activities of SOD and GSH-Px, reduce the contents of MDA, increase the contents of NO, enhance the activities of iNOS and TNOs, reduce the activities of ALT and AST, and reduce the rates of apoptosis of liver cells, in which the best effects are to add 10 mg/kg selenium. While 15 mg/kg of sodium selenite may induce progression of As-induced hepatic lesions, the results indicated that 5 and 10 mg/kg of sodium selenite supplied in the diet, through mechanisms of oxidative stress and apoptosis regulation, may ameliorate As-induced hepatic lesions in a dose-dependent manner.


Assuntos
Arsênio , Neoplasias Hepáticas , Selênio , Animais , Arsênio/toxicidade , Galinhas , Fígado , Masculino , Selênio/farmacologia
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