RESUMO
Objective: The aim of this study is to explore the potential modulatory role of quercetin against Endotoxin or lipopolysaccharide (LPS) induced septic cardiac dysfunction. Methods: Specific pathogen-free chicken embryos ( n = 120) were allocated untreated control, phosphate buffer solution (PBS) vehicle, PBS with ethanol vehicle, LPS (500 ng/egg), LPS with quercetin treatment (10, 20, or 40 nmol/egg, respectively), Quercetin groups (10, 20, or 40 nmol/egg). Fifteen-day-old embryonated eggs were inoculated with abovementioned solutions via the allantoic cavity. At embryonic day 19, the hearts of the embryos were collected for histopathological examination, RNA extraction, real-time polymerase chain reaction, immunohistochemical investigations, and Western blotting. Results: They demonstrated that the heart presented inflammatory responses after LPS induction. The LPS-induced higher mRNA expressions of inflammation-related factors (TLR4, TNFα, MYD88, NF-κB1, IFNγ, IL-1ß, IL-8, IL-6, IL-10, p38, MMP3, and MMP9) were blocked by quercetin with three dosages. Quercetin significantly decreased immunopositivity to TLR4 and MMP9 in the treatment group when compared with the LPS group. Quercetin significantly decreased protein expressions of TLR4, IFNγ, MMP3, and MMP9 when compared with the LPS group. Quercetin treatment prevented LPS-induced increase in the mRNA expression of Claudin 1 and ZO-1, and significantly decreased protein expression of claudin 1 when compared with the LPS group. Quercetin significantly downregulated autophagy-related gene expressions (PPARα, SGLT1, APOA4, AMPKα1, AMPKα2, ATG5, ATG7, Beclin-1, and LC3B) and programmed cell death (Fas, Bcl-2, CASP1, CASP12, CASP3, and RIPK1) after LPS induction. Quercetin significantly decreased immunopositivity to APOA4, AMPKα2, and LC3-II/LC3-I in the treatment group when compared with the LPS group. Quercetin significantly decreased protein expressions of AMPKα1, LC3-I, and LC3-II. Quercetin significantly decreased the protein expression to CASP1 and CASP3 by immunohistochemical investigation or Western blotting in treatment group when compared with LPS group. Conclusion: Quercetin alleviates cardiac inflammation induced by LPS through modulating autophagy, programmed cell death, and myocardiocytes permeability.
Assuntos
Lipopolissacarídeos , Quercetina , Embrião de Galinha , Animais , Quercetina/farmacologia , Quercetina/uso terapêutico , Lipopolissacarídeos/toxicidade , Metaloproteinase 9 da Matriz , Caspase 3 , Metaloproteinase 3 da Matriz , Receptor 4 Toll-Like , Claudina-1 , Inflamação/induzido quimicamente , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Apoptose , RNA Mensageiro , Autofagia , NF-kappa BRESUMO
This study was performed to investigate the effects of stocking density on performance, meat quality and tibia development in Pekin ducks reared on a plastic wire floor. A total of 372 healthy, 21-day-old, male ducks with similar body weight (BW) were randomly allotted to stocking densities of five (low), eight (medium) and 11 (high) birds/m2 . Each group had six replicates. Results showed that compared with the low density group, medium and high stocking density caused a decrease in final BW at 42 days old, and in average daily gain, European performance index (p < .01) and meat pH at 45 min postmortem (p < .001), and an increase of meat drip loss (p < .01). High stocking density resulted in an increase of feed/gain ratio (p < .001), but a decrease of tibia calcium (p < .01) and phosphorus content (p < .05). Meat color, shear force values, tibia size (weight, length, and width) and breaking strength were not significantly influenced by stocking density. In conclusion, stocking density over eight birds/m2 negatively affects growth performance, but meat quality and tibia development are not dramatically influenced. Based on this study, the stocking density of male Pekin ducks should be adjusted between five and eight birds/m2 .
Assuntos
Criação de Animais Domésticos , Patos/crescimento & desenvolvimento , Qualidade dos Alimentos , Abrigo para Animais , Carne , Tíbia/crescimento & desenvolvimento , Animais , Cálcio/metabolismo , Cor , Pisos e Cobertura de Pisos , Concentração de Íons de Hidrogênio , Masculino , Fósforo/metabolismo , Densidade Demográfica , Resistência ao Cisalhamento , Tíbia/metabolismoRESUMO
Cardiomyocyte apoptosis is closely associated with the pathogenesis of heart failure. Jujuboside A (JUA) is a type of saponin isolated from the seeds of Zizyphus jujuba. In traditional Chinese medicine, it is believed that JUA possesses multiple biological effects, including antianxiety, antioxidant and antiinflammatory activities. The present study aimed to evaluate the effects of JUA on norepinephrine (NE)induced apoptosis of H9c2 cells and to investigate its underlying mechanisms. Rat H9c2 cardiomyocytes were pretreated with JUA and were then exposed to NE as an in vitro model of myocardial apoptosis. A cell viability assay, scanning electron microscopy, transmission electron microscopy, flow cytometry assay, acridine orange/ethidium bromide staining, reverse transcriptionquantitative polymerase chain reaction and western blotting, all revealed that NE induced H9c2 cell apoptosis. The results demonstrated that NE inhibited cell viability, and enhanced cell damage and apoptosis of H9c2 cells. Conversely, pretreatment with JUA was able to reverse NEinduced decreased cell viability and increased apoptosis. Furthermore, JUA suppressed upregulation of the Bcell lymphoma 2 (Bcl2)associated X protein/Bcl2 ratio, and inhibited the increased protein expression levels of cleaved caspase3 and cleaved caspase9 following NE exposure. However, the protein expression levels of cleaved caspase12 and cleaved caspase8 were not significantly altered following exposure to NE or JUA pretreatment. In addition, in JUApretreated cells, the protein expression levels of phosphorylated (p)p38 and pcJun Nterminal kinase were downregulated compared with in NEtreated cells. Furthermore, JUA regulated the activation of extracellular signalregulated kinase (ERK) in NEtreated cells and significantly increased the expression levels of pAKT. Taken together, these data suggested that JUA may protect against NEinduced apoptosis of cardiomyocytes via modulation of the mitogenactivated protein kinase and AKT signaling pathways. Therefore, JUA may be considered a potential therapeutic strategy for the treatment of heart disease.
Assuntos
Apoptose/efeitos dos fármacos , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Norepinefrina/farmacologia , Proteínas Proto-Oncogênicas c-akt/metabolismo , Saponinas/farmacologia , Transdução de Sinais/efeitos dos fármacos , Animais , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Ratos , Proteína X Associada a bcl-2/metabolismoRESUMO
One pregnant captive Irrawaddy dolphin (Orcaella brevirostris), with a body length of 225 cm, was found dead on 8 June 2009. The dolphin was anorexic and circling at the bottom of the pool before death. Laboratory tests revealed an increased leukocyte count and decreased platelet count; increased erythrocyte sedimentation rate; and slightly decreased red blood cell count, hemoglobin, and hematocrit. Alkaline phosphatase, creatinine, and glucose were significantly decreased. Moreover, uric acid and alanine aminotransferase and aspartate aminotransferase levels were elevated. A 57-cm fetus was recovered. The respiratory system, intestinal mucosa, mesentery and mesenteric lymph nodes, and spleen were congested and hemorrhagic. The heart, liver, and kidney appeared normal. Klebsiella spp. and Staphylococcus aureus were identified in the amniotic fluid. This is the first case report of bacterial infection in an Irrawaddy dolphin.