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1.
Poult Sci ; 100(4): 100990, 2021 Jan 19.
Artigo em Inglês | MEDLINE | ID: mdl-33647718

RESUMO

Goose nephritic astrovirus (GNAstV) was first isolated in 2018, causing great economic losses to the goose industry. However, little is known about host immune response to GNAstV infection. In this study, forty 2-day-old goslings were randomly divided into 2 groups: infection and negative control groups. Each gosling in the infection group was challenged with 0.5 mL GNAstV-JSHA intramuscularly, whereas the gosling in the negative control group was inoculated with the same amount of PBS. Histopathological changes and virus location in the spleen and kidney were examined, and the expression of immune-related genes was determined by qPCR at 7 and 14 d after infection. Our results showed that GNAstV infection induced degeneration and necrosis of splenic lymphocytes and renal epithelial cells, and these cells were positive for the virus. In addition, GNAstV infection induced the activation of pattern recognition receptors (RIG-I, MDA-5, and TLR3) and key adaptor molecules (MyD88, MAVS, and IRF7) in the spleen and kidney, and upregulated the gene expression of interferon-α in the spleen and antiviral proteins (MX1, OASL, and IFITM3) in the spleen and kidney. Moreover, high expression levels of interleukin (IL)-1ß and IL-8 in the spleen and iNOS in the spleen and kidney were found. These results indicated that GNAstV infection activated host innate immune response. Furthermore, GNAstV infection increased the expression levels of CD8+, MHCI, and MHCII, indicating that adaptive immune response was activated. Besides, TGF-ß was highly expressed in the spleen and kidney, which may be an immune evasion strategy of GNAstV to cause infection. Interestingly, both IL-1ß and IL-6 mRNA levels were decreased in the kidney, which may help reduce kidney lesions. This is the first study to report changes in immune-related gene expression in response to GNAstV infection, and our results provide insights into viral pathogenesis.

2.
Virus Res ; 291: 198220, 2021 Jan 02.
Artigo em Inglês | MEDLINE | ID: mdl-33152381

RESUMO

Cyclic GMP-AMP synthase (cGAS) is a main sensor used to detect microbial DNA in the cytoplasm, which subsequently induces the production of interferon (IFN) via the cGAS/STING/IRF3 signaling pathway, leading to an antiviral response. However, some viruses have evolved multiple strategies to escape this process. Pseudorabies virus (PRV) is a double-stranded DNA virus belonging to the Alphaherpesvirinae subfamily, which can cause serious damage to the porcine industry. Many herpesvirus components have been reported to counteract IFN production, whereas little is known of PRV. In the present study, we found that PRV glycoprotein E (gE) was involved in counteracting cGAS/STING-mediated IFN production. Ectopic expression of gE decreased cGAS/STING-mediated IFN-ß promoter activity and the level of mRNA expression. Moreover, gE targeted at or downstream of IRF3 was found to inhibit IFN-ß production. However, gE did not affect the phosphorylation, dimerization and nuclear translocation of IRF3. Furthermore, gE is located on the nuclear membrane and could subsequently degrade CREB-binding protein (CBP). MG132, a proteasome inhibitor, decreased CBP degradation and restored the IFN-ß production induced by gE. Finally, gE-deleted PRV induced a higher level of IFN-ß production and reduced CBP degradation compared to wild-type PRV. Together, these results demonstrate that PRV gE can inhibit cGAS/STING-mediated IFN-ß production by degrading CBP to interrupt the enhanced assembly of IRF3 and CBP.

3.
Poult Sci ; 99(12): 6355-6370, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-33248551

RESUMO

Tilmicosin is widely used to treat respiratory infections in animals and has been reported to induce cardiac damage and even sudden death. However, its exact mechanisms, especially in chickens, remain unclear. This study confirmed the dose-dependent damaging effect of tilmicosin on primary chicken myocardial cells. Primary chicken myocardial cells treated with tilmicosin (0.5 µg/mL) for 0 h, 12 h, and 48 h were subjected to RNA sequencing and bioinformatics analysis. Transcriptomic analysis revealed that cytokine-cytokine receptor interactions, calcium signaling pathway, peroxisomes, phagosomes, mitogen-activated protein kinase (MAPK) signaling pathway, and oxidative phosphorylation were significantly and differentially affected after 12 h or 48 h of tilmicosin treatment. Further evidence demonstrated consistently increased proinflammatory factors, peroxidation, and ferroptosis, and intracellular ion imbalance was caused by tilmicosin for 12 h, but this imbalance had recovered at 48 h. Meanwhile, intracellular resistance to tilmicosin-induced toxicity involved the active regulation of cyclooxygenase-1 and ATPase H+/K+-transporting beta subunit at 48 h, sustained activation of MAPK12, and downregulation of dual specificity phosphatase 10 at 12 h. In summary, this study suggests that tilmicosin exerts its cardiotoxicity in primary chicken myocardial cells through multiple mechanisms and finds several intracellular molecular targets to resist the toxicity.

4.
Res Vet Sci ; 133: 124-130, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32977120

RESUMO

In order to explore the function of vitamin C (VC) and VC-Na in the relief of heat stress injury in chicken cardiomyocytes, 150 30-day-old specific-pathogen-free chickens were randomly divided into a control group (fed normal drinking water), a VC group (50 µg/mL VC in drinking water), and a VC-Na group (50 µg/mL VC-Na in drinking water). After 7 days of adaptation feeding, the chickens were subjected to heat stress at 40 ± 2 °C and 60%-70% humidity for 0, 1, 3, 5, and 10 h, respectively, and the sera and heart tissues of the chickens were collected immediately at the corresponding heat stress time points. The effects of VC and VC-Na supplementation on the relief of chicken myocardial cell injury following heat stress was studied by detecting the levels of LDH, CK, CK-MB, and total antioxidant capacity (T-AOC) in the sera, and through histopathological analysis and the expression of CRYAB, Hsp27, and Hsp70 in the myocardial cells. The results showed that supplementing with 50 µg/mL VC or VC-Na significantly reduced the levels of LDH, and CK-MB in serum as well as heat-stress-induced granular and vacuolar degeneration, myocardial fiber breakage, and cell necrosis, indicating effective resistance to heat-stress damage. Additionally, the levels of T-AOC in serum were increased in the VC and VC-Na groups, suggesting enhancing of antioxidant capacity. Furthermore, the expression of CRYAB were induced at 0, 3, 5, and 10 h (P < 0.01) in both VC and VC-Na group, and that of Hsp70 were induced at 0 h (P < 0.05) in VC group and at 0, 3, 5, 10 h (P < 0.01) in VC-Na group. Thus, supplementing chicken diets with VC or VC-Na presented heat-stress damage resistance by enhancing antioxidant capacity and inducing expression of CRYAB and Hsp70.

5.
Int J Mol Med ; 45(6): 1888-1908, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32236591

RESUMO

Heat shock protein 90 (Hsp90) is associated with resisting heat­stress injury to the heart, particularly in myocardial mitochondria. However, the mechanism underlying this effect remains unclear. The present study was based on the high expression of Hsp90 during heat stress (HS) and involved inducing higher expression of Hsp90 using aspirin in mouse hearts. Higher Hsp90 levels inhibited HS­induced myocardial damage and apoptosis, and mitochondrial dysfunction, by stimulating Akt (protein kinase B) activation and PKM2 (pyruvate kinase M2) signaling, and subsequently increasing mitochondrial Bcl­2 (B­cell lymphoma 2) levels and its phosphorylation. Functional inhibition of Hsp90 using geldanamycin verified that reducing the association of Hsp90 with Akt and PKM2 caused the functional decline of phosphorylated (p)­Akt and PKM2 that initiate Bcl­2 to move into mitochondria, where it is phosphorylated. Protection by Hsp90 was weakened by blocking Akt activation using Triciribine, which could not be recovered by normal initiation of the PKM2 pathway. Furthermore, increased Hsp70 levels induced by Akt activation in myocardial cells may flow into the blood to resist heat stress. The results provided in vivo mechanistic evidence that in myocardial cells, Hsp90 resists heat stress via separate activation of the Akt­Bcl­2 and PKM2­Bcl­2 signaling pathways, which contribute toward preserving cardiac function and mitochondrial homeostasis.

6.
Poult Sci ; 99(4): 1967-1974, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32241477

RESUMO

In 2018, a new goose astrovirus (GAstrV) was reported in China, which causes 2 to 20% deaths in 4- to 16-day-old goslings causing great damages to the livestock industry. Gout is the typical feature of GAstrV infection in goslings. However, the mechanism of gout formation remains unclear. In the present study, 2-day-old goslings were infected intramuscularly with GAstrV for 14 D. One quarter of the infected goslings died, and typical gout pathological changes were found in the dead infected goslings. Pathological changes were observed in the morphology of the kidney and liver, such as degeneration, necrosis, and inflammatory cell infiltration. Accordingly, a high virus load was found in both organs. The serum level of uric acid in the inoculated goslings was higher, whereas no differences were found in levels of creatinine, calcium, and phosphorus. Moreover, the xanthine dehydrogenase (XOD) and adenosine deaminase (ADA) activities and the mRNA levels of xanthine dehydrogenase, adenosine deaminase, phosphoribosyl pyrophosphate amidotransferase, and phosphoribosyl pyrophosphate synthetase 1 in livers increased, wheres the multidrug resistance-associated protein 4 mRNA level and Na-K-ATPase activity in the kidneys decreased. These results showed that GAstrV infection could cause lesions on the liver and kidney and then increase the expression or activity of enzymes related to uric acid production in the liver and decrease renal excretion function, which contribute to hyperuricemia and gout formation.


Assuntos
Infecções por Astroviridae/veterinária , Proteínas Aviárias/genética , Proteínas de Transporte/genética , Gansos , Gota/veterinária , Doenças das Aves Domésticas/metabolismo , Ácido Úrico/metabolismo , Animais , Infecções por Astroviridae/complicações , Infecções por Astroviridae/metabolismo , Infecções por Astroviridae/virologia , Avastrovirus/fisiologia , Proteínas Aviárias/metabolismo , Proteínas de Transporte/metabolismo , Modelos Animais de Doenças , Fezes/química , Gota/metabolismo , Gota/virologia , Rim/metabolismo , Fígado/química , Doenças das Aves Domésticas/virologia , Purinas/metabolismo
7.
Mol Biol Rep ; 47(5): 4087-4091, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32246248

RESUMO

Hormones have become a useful therapeutic aspect of clinical endocrinology but how to use them to optimize the health benefits and avoid adverse effects is a major challenge. Estrogen is an indispensable hormone for proper biological functioning but is also implicated with the pathology of both the reproductive and non-reproductive tissues. Abnormal estrogen receptor signaling may increase the risk of development of a variety of diseases including colorectal cancer (CRC). Estrogen receptor beta (ERß) is the predominant subtype in the colonic epithelium and confers the anti-tumor effect through various mechanisms. Many investigators have embarked on the search for the biological mechanisms by which estrogen and estrogen-like compounds may influence the pathogenesis of CRC. This review explores the recent findings on the therapeutic role of ERß in the colonic epithelium as a prospective candidate for targeted endocrine therapy in CRC.

8.
Int J Mol Sci ; 21(5)2020 Feb 28.
Artigo em Inglês | MEDLINE | ID: mdl-32121259

RESUMO

Heat stress can particularly affect the kidney because of its high rate of adenosine triphosphate consumption. Competition between apoptosis and autophagy-mediated survival always exists in damaged tissue. And Hsp90 can enhance cellular protection to resist heat stress. However, the relationship between Hsp90 and the above competition and its underlying mechanism in the kidney are unclear. The present study found that heat stress induced obvious histopathological and oxidative injury, which was connected with cellular apoptosis and autophagy in the kidney and was associated with the levels of Hsp90 expression or function. The data showed that during heat stress, Hsp90 activated the PKM2-Akt signaling pathway to exert antiapoptotic effects and induce Hsp70 expression regulated by HSF-1, stimulated autophagy-mediated survival through the HIF-1α-BNIP3/BNIP3L pathway, and finally protected the kidney from heat-stress injury. Moreover, the nuclear translocation of PKM2, (p-) Akt, HSF-1, and HIF-1α was enhanced by heat stress, but only intranuclear p-Akt and HSF-1 were specifically influenced by Hsp90, contributing to regulate the cellular ability of resisting heat-stress damage. Our study provided new insights regarding the molecular mechanism of Hsp90 in the kidney in response to heat-stress injury, possibly contributing to finding new targets for the pharmacological regulation of human or animal acute kidney injury from heat stress in future research.


Assuntos
Apoptose , Autofagia , Proteínas de Choque Térmico HSP90/metabolismo , Resposta ao Choque Térmico , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Rim/patologia , Proteínas Proto-Oncogênicas c-akt/metabolismo , Piruvato Quinase/metabolismo , Animais , Antioxidantes/metabolismo , Sobrevivência Celular , Proteínas de Choque Térmico HSP70/metabolismo , Rim/metabolismo , Masculino , Proteínas de Membrana/metabolismo , Camundongos Endogâmicos C57BL , Proteínas Mitocondriais/metabolismo , Modelos Biológicos , Oxirredução , Fosforilação , Transdução de Sinais
9.
Cell Stress Chaperones ; 25(2): 379, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32002806

RESUMO

Due to an unfortunate mistake, an incorrect image appeared in Fig. 3 (Aspirin 24 h) of the original publication.

10.
Cells ; 9(1)2020 01 18.
Artigo em Inglês | MEDLINE | ID: mdl-31963688

RESUMO

Heat stress (HS) often causes sudden death of humans and animals due to heart failure, mainly resulting from the contraction of cardiac microvasculature followed by myocardial ischemia. Cardiac microvascular endothelial cells (CMVECs) play an important role in maintaining vasodilatation. Aspirin (ASA) is well known for its protective abilities of febrile animals. However, there is little knowledge about molecular resistance mechanisms of CMVECs and which role ASA may play in this context. Therefore, we used a heat stress model of rat cardiac microvascular endothelial cell cultures in vitro and investigated the cell injuries and molecular resistance mechanism of CMVECs caused by heat stress, and the effect of aspirin (ASA) on it. HS induced severe pathological damage of CMVECs and cellular oxidative stress and dysfunction of NO release. Hsp90 was proven to be indispensable for resisting HS-injury of CMVECs through PI3K-Akt and PKM2 signaling pathways. Meanwhile, PKM2 functioned in reducing Akt phosphorylation. ASA treatment of CMVECs induced a significant expression of Hsp90, which promoted both Akt and PKM2 signals, which are beneficial for relieving HS damage and maintaining the function of CMVECs. Akt activation also promoted HSF-1 that regulates the expression of Hsp70, which is known to assist Hsp90's molecular chaperone function and when released to the extracellular liquid to protect myocardial cells from HS damage. To the best of our knowledge, this is the first study to show that HS damages CMVECs and the protection mechanism of Hsp90 on it, and that ASA provides a new potential strategy for regulating cardiac microcirculation preventing HS-induced heart failure.

11.
Mol Cell Biochem ; 461(1-2): 213-214, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31562574

RESUMO

In the original publication of the article, one of the images was selected by mistake in Fig. 3 (HS + ASA, 5 h). The correct version of Fig. 3 is given in this correction.

12.
Cell Stress Chaperones ; 24(6): 1067-1078, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31401771

RESUMO

In this study, we investigated the function of co-enzyme Q10 (Q10) in autophagy of primary chicken myocardial cells during heat stress. Cells were treated with Q10 (1 µΜ, 10 µΜ, and 20 µM) before exposure to heat stress. Pretreatment of chicken myocardial cells with Q10 suppressed the decline in cell viability during heat stress and suppressed the increase in apoptosis during heat stress. Treatment with 20 µM Q10 upregulated autophagy-associated genes during heat stress. The expression of LC3-II was highest in cells treated with 20 µM Q10. Pretreatment with Q10 decreased reactive oxygen species (ROS) levels during heat stress. The number of autophagosomes was significantly increased by 20 µM Q10 treatment, as demonstrated by electron microscopy or monodansylcadaverine (MDC) fluorescence. SQSTM1 accumulation was diminished by Q10 treatment during heat stress, and the number of LC3II puncta was increased. Treatment with 20 µM Q10 also decreased the activation of the PI3K/Akt/mTOR pathway. Our results showed that co-enzyme Q10 can protect primary chicken myocardial cells by upregulating autophagy and suppressing the PI3K/Akt/mTOR pathway during heat stress.


Assuntos
Apoptose/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Resposta ao Choque Térmico/efeitos dos fármacos , Miócitos Cardíacos/efeitos dos fármacos , Ubiquinona/análogos & derivados , Animais , Apoptose/fisiologia , Sobrevivência Celular/fisiologia , Células Cultivadas , Galinhas , Miocárdio/citologia , Miócitos Cardíacos/citologia , Fosfatidilinositol 3-Quinases/metabolismo , Serina-Treonina Quinases TOR/metabolismo , Ubiquinona/farmacologia
13.
Poult Sci ; 98(11): 5321-5329, 2019 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-31222278

RESUMO

In recent years, emerging avian reovirus (ARV) strains causing viral arthritis have become a challenge to the worldwide chicken industry, and were responsible for significant economic losses. In this study, we characterized emerging variant ARV strains and examined their genetic relationship and pathogenicity variation with reference strains. A total of 18 emerging variant ARV strains were isolated from tendon and capsular synovial fluid of broiler chickens with clinical cases of arthritis/tenosynovitis at commercial farms in China. Comparative analysis based on σC sequence showed that 4/18 isolates were in the same cluster (Cluster 1) as vaccine strains (S1133), whereas 14 of 18 isolates were in Clusters 2, 3, and 6. The field isolates shared a rather low identity (38.1 to 81.9%) with S1133 in Cluster 1, especially for those from Cluster 6 (38.1 to 67.2%). A higher ARV isolation rate was observed in chicken embryos (47/61) compared to cell culture (37/61) through PCR with a detection primer. A total of 3 isolates were selected to infect specific-pathogen-free (SPF) chickens, showing that the tested isolates, especially that from Cluster 6, displayed greater pathogenicity than S1133 strain, characterized by higher incidence. These findings suggest that the virulence of Chinese ARVs has been increasing rapidly in recent years, and the vaccine need to be updated correspondingly.


Assuntos
Galinhas , Orthoreovirus Aviário/genética , Orthoreovirus Aviário/patogenicidade , Doenças das Aves Domésticas/epidemiologia , Infecções por Reoviridae/veterinária , Animais , Artrite/epidemiologia , Artrite/veterinária , Artrite/virologia , China/epidemiologia , Incidência , Filogenia , Doenças das Aves Domésticas/virologia , Prevalência , Infecções por Reoviridae/epidemiologia , Infecções por Reoviridae/virologia , Organismos Livres de Patógenos Específicos , Virulência
14.
Mol Reprod Dev ; 86(6): 673-685, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-30989754

RESUMO

Heat stress is a major stressor that can lead to male reproductive dysfunction. Sertoli cells play a crucial role in spermatogenesis by providing germ cells with structural and nutritional support, and contributing to blood-testis barrier formation. Vitamin C (Vc) is an antioxidant capable of neutralizing reactive oxygen species and preventing lipid peroxidation widely used because it is inexpensive and highly accessible. In the present study, we investigated the protective effect of Vc on TM4 cells following heat stress. Pretreatment with Vc could effectively inhibit apoptosis (p < 0.01), lipid peroxidation, and lactate dehydrogenase (LDH) activity. However, a significant increase in the malondialdehyde (MDA) level and LDH activity (p < 0.01) was observed in TM4 cells without Vc-pretreatment, in conjunction with vacuole degeneration and karyopyknosis. In addition, both the messenger RNA and protein levels of CryAB, Hsp27, Hsp70, and Hsp110 substantially increased in the 3 and 12 hr recovery groups (p < 0.01). Vc also prevented microtubule aggregation following heat stress. These results suggest that pretreatment with Vc-protected TM4 cells against heat stress by reducing the level of oxidative stress and inducing heat shock protein expression.


Assuntos
Ácido Ascórbico/farmacologia , Regulação da Expressão Gênica/efeitos dos fármacos , Proteínas de Choque Térmico/biossíntese , Resposta ao Choque Térmico/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Células de Sertoli/metabolismo , Linhagem Celular , Humanos , Masculino , Células de Sertoli/citologia
15.
Poult Sci ; 98(2): 1002-1011, 2019 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-30339219

RESUMO

In this report, we investigated the protective function of co-enzyme Q10 on chicken hearts during in vivo heat stress (HS) and the relationship with Hsp70 expression. The concentration of co-enzyme Q10 (Q10) in the serum indicated that Q10 exogenously added prior HS was fully absorbed by chickens and is maintained at high levels during HS. The level of heart and oxidative damage-associated enzymes in the serum revealed that treatment with Q10 decreased the activity of CK-MB, CK, and LDH compared with the HS group; moreover, oxidative injury was also alleviated by Q10 according to the level of SOD, MDA, and T-AOC in the serum compared with HS group during heat stress. A pathological examination indicated that the chicken hearts suffered serious damage during HS, including hemorrhage, granular changes, karyopyknosis, and cardiac muscle fiber disorder; however, the extent of heart damage was reduced in HS + Q10 group. Our results indicated that the addition of Q10 could upregulate the expression of Hsp70 during HS compared with the HS group. Compared with the HS group, the addition of Q10 significantly increased the gene expression of hsf1 during HS and hsf3 at 5 h of HS. The expression of hsf2 and hsf4 was not influenced by HS. Q10 could only accelerate the trimerization of HSF1 as well binding activities to Hsp70 HSE according to native page and ChIP assays. These findings suggest that co-enzyme Q10 can protect chicken hearts from in vivo HS by inducing HSF1 binding activity and Hsp70 expression.


Assuntos
Proteínas Aviárias/genética , Galinhas/fisiologia , Proteínas de Choque Térmico HSP70/genética , Coração/fisiologia , Fatores de Transcrição de Choque Térmico/genética , Temperatura Alta/efeitos adversos , Ubiquinona/análogos & derivados , Animais , Proteínas Aviárias/metabolismo , Proteínas de Choque Térmico HSP70/metabolismo , Fatores de Transcrição de Choque Térmico/metabolismo , Ubiquinona/farmacologia , Vitaminas/farmacologia
16.
Cell Stress Chaperones ; 24(1): 59-68, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30246229

RESUMO

CRYAB is a small heat shock protein (sHSP) that has previously been shown to protect the heart against various cellular stresses; however, its precise function in myocardial cell injury caused by heat stress remains unclear. This study aimed to investigate the molecular mechanism by which CRYAB protects cardiomyocytes against heat stress. We constructed two H9C2 cell lines that stably express CRYAB protein to differing degrees: CRYAB-5 and CRYAB-7. Both CRYAB-5 and CRYAB-7 showed significantly reduced granular degeneration and vacuolar degeneration following heat stress compared to control cells. In addition, CRYAB overexpression in H9C2 cells relieved cell cycle proportion at the G0/G1 phase following heat stress compared to control cells. These protective effects were associated with the level of CRYAB protein expression. Our immunofluorescence analysis showed CRYAB could translocate from the cytoplasm to the nucleus under heat stress conditions, but that CRYAB co-localized with F-actin (which accumulates under stress conditions). Indeed, overexpression of CRYAB significantly reduced the aggregation of F-actin in H9C2 cells caused by heat stress. Furthermore, overexpressing CRYAB protein significantly reduced the apoptosis of cardiomyocytes induced by heat stress, likely by reducing the expression of cleaved-caspase 3. Collectively, our results show overexpression of CRYAB significantly increases the heat resistance of H9C2 cardiomyocytes, likely by reducing F-actin aggregation (thus stabilizing the cytoskeleton), regulating the cell cycle, and preventing caspase-mediated apoptosis.


Assuntos
Actinas/metabolismo , Apoptose , Caspases/metabolismo , Cristalinas/metabolismo , Resposta ao Choque Térmico , Proteínas Associadas aos Microtúbulos/metabolismo , Miócitos Cardíacos/patologia , Agregados Proteicos , Animais , Ciclo Celular , Linhagem Celular , Cristalinas/genética , Citoproteção , Resposta ao Choque Térmico/genética , Proteínas Associadas aos Microtúbulos/genética , Ratos , Recombinação Genética/genética , Transcrição Genética
17.
Oxid Med Cell Longev ; 2018: 7014126, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30425783

RESUMO

Heat stress negatively affects poultry production and animal health. In response, animals invoke a heat stress response by inducing heat shock proteins (HSPs). Scientists are actively seeking natural products that can enhance the heat shock response. The present study aimed at assessing the effects of a purified rosemary extract comprising antioxidant compounds on the heat shock response and HSP expression profile in broiler chickens. The response of broilers to HS in the presence of purified rosemary extract was assessed using an in vivo myocardial cell model. Pathological lesions of heart tissue were examined microscopically. The levels and activities of enzymes associated with heart damage and oxidative damage were detected. Immunohistochemical staining was performed for HSPs in myocardial cells. The results showed that lactate dehydrogenase (LDH), creatine kinase (CK), and myocardial CK (CKMB) levels were reduced by the purified rosemary extract before and during heat stress. Heat stress alone increased CK and CKMB levels. The levels of oxidative damage-associated enzymes were compared between the rosemary + heat stress and heat stress-alone groups. The results indicated that in terms of these enzymes, the purified rosemary extract induced a more antioxidative state. Pathological examinations showed that heat stress caused myocardial fiber fracture, karyopyknosis, and degeneration. The addition of purified rosemary extract ameliorated these lesions to some degree, preserving more of the basic structure. Heat stress decreased the cellular levels of crystallin alpha B (CRYAB) and HSP70. The addition of the purified rosemary extract significantly increased the levels of CRYAB and HSP70 during heat stress (p < 0.0001). Immunohistochemistry showed that after rosemary treatment, CRYAB and HSP70 showed more intense staining compared with the no heat stress control group. In the rosemary + heat group, after 10 hours of heat stress, the staining intensity of these two proteins remained higher than in the heat stress group. Thus, purified rosemary extract could induce high levels of HSP70 and CRYAB in chicken hearts before and during heat stress. Purified rosemary extract could be used to alleviate heat stress in broiler chickens.


Assuntos
Galinhas/metabolismo , Proteínas de Choque Térmico HSP70/metabolismo , Resposta ao Choque Térmico/efeitos dos fármacos , Extratos Vegetais/farmacologia , Rosmarinus/química , Cadeia B de alfa-Cristalina/metabolismo , Animais , Cromatografia Líquida de Alta Pressão , Emulsões/química , Miocárdio/enzimologia , Miocárdio/patologia , Nanopartículas/química , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/isolamento & purificação
18.
Cell Stress Chaperones ; 23(5): 1033-1040, 2018 09.
Artigo em Inglês | MEDLINE | ID: mdl-29779133

RESUMO

The present study investigates the effects of heat stress on the kidney in broilers, based on previous findings which showed that heat stress caused cardiac damage in broilers. Further, the possible renoprotective role of aspirin and the heat shock proteins HSP60 and HSP47 was also investigated. The enzyme levels of urea and uric acid, which are indicators of renal damage, and lactate dehydrogenase, an indicator of oxidative damage, were measured in chickens that were only exposed to heat stress, chickens that were pretreated with aspirin before heat stress, and chickens that were only treated with aspirin. Further, histological examination of renal tissue from the three groups was also performed. Finally, expression of HSP60 and HSP47 was also examined. In the heat stress group, the enzyme measurements were indicative of renal dysfunction and oxidative damage, and the histological findings were indicative of renal ischemia and damage. Aspirin seemed to have a protective effect against the renal damage caused by the stress, based on the enzyme measurements and histopathological findings in the aspirin-treated group. The findings also indicate that aspirin may induce HSP60 and HSP47 expression in renal cells. Finally, the expression patterns of HSP60 and HSP47 indicated that they may play a renoprotective role, as their expression was higher in the aspirin-treated groups. In conclusion, the present findings show that heat stress causes renal damage in poultry and that aspirin may play a protective role against this damage via pathways that involve HSP60 and HSP47.


Assuntos
Proteínas Aviárias/metabolismo , Chaperonina 60/metabolismo , Galinhas/metabolismo , Proteínas de Choque Térmico HSP47/metabolismo , Resposta ao Choque Térmico , Rim/patologia , Animais , Aspirina/farmacologia , Galinhas/anatomia & histologia , Galinhas/sangue , Rim/efeitos dos fármacos , Rim/metabolismo , L-Lactato Desidrogenase/sangue , Ureia/sangue , Ácido Úrico/sangue
19.
Mol Cell Biochem ; 449(1-2): 195-206, 2018 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-29671254

RESUMO

In this report, we investigate the protective mechanism of co-enzyme Q10 on chicken primary myocardial cells during heat stress. Morphological observations indicate that addition of co-enzyme Q10 protects myocardial cells from heat stress, reduces the damage of mitochondria and nucleus, and decreases the mean number of vacuolated mitochondria. We have previously shown that co-enzyme Q10 can protect myocardial cells by upregulating the expression of Hsp70. Therefore, signaling pathways involved in this process were explored. No changes of total MAPK protein (P38MAPK, JNK, ERK) expression in the experimental groups were detected, with the exception of total JNK1. Co-enzyme Q10 failed to increase the expression of JNK1 compared to the HS group which was treated with heat stress only. Addition of Q10 upregulated the expression of p-P38MAPK, p-JNK, and p-ERK1. Inhibitors of P38MAPK and JNK, SB203580 and SP600125, respectively, weakened the upregulation of Hsp70 by co-enzyme Q10, indicating that MAPK pathways participate in the Hsp70 upregulation by co-enzyme Q10. Co-enzyme Q10 upregulates the expression of p-MEK3/6 and p-MEK4, but not p-MEK7 during heat stress. Expression of p-PKCα and p-PKCß1 was also elevated following the addition of co-enzyme Q10 during heat stress, and addition of PKC inhibitors decreased the expression of Hsp70 induced by co-enzyme Q10. This confirms that PKC is also associated with the upregulation of Hsp70. In HS+Q10 group, addition of SP600125 or SB203580 could increase cell apoptosis under heat stress. Our results suggest that co-enzyme Q10 upregulates the expression of Hsp70 during heat stress to protect chicken primary myocardial cells via the PKC-MEK3/4/6-P38MAPK/JNK pathways.


Assuntos
Proteínas Aviárias/metabolismo , Galinhas/metabolismo , Proteínas de Choque Térmico HSP70/biossíntese , Resposta ao Choque Térmico/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo , Miócitos Cardíacos/metabolismo , Proteína Quinase C/metabolismo , Ubiquinona/análogos & derivados , Regulação para Cima/efeitos dos fármacos , Animais , Embrião de Galinha , Ubiquinona/farmacologia
20.
Cell Stress Chaperones ; 23(4): 735-748, 2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-29442224

RESUMO

Heat stress is exacerbated by global warming and affects human and animal health, leading to heart damage caused by imbalances in reactive oxygen species (ROS) and the antioxidant system, acid-base chemistry, electrolytes and respiratory alkalosis. Vitamin C scavenges excess ROS, and sodium bicarbonate maintains acid-base and electrolyte balance, and alleviates respiratory alkalosis. Herein, we explored the ability of vitamin C alone and in combination with equimolar sodium bicarbonate (Vitamin C-Na) to stimulate endogenous antioxidants and heat shock proteins (HSPs) to relieve heat stress in H9C2 cells. Control, vitamin C (20 µg/ml vitamin C for 16 h) and vitamin C-Na (20 µg/ml vitamin C-Na for 16 h) groups were heat-stressed for 1, 3 or 5 h. Granular and vacuolar degeneration, karyopyknosis and damage to nuclei and mitochondria were clearly reduced in treatment groups, as were apoptosis, lactate dehydrogenase activity and ROS and malondialdehyde levels, while superoxide dismutase activity was increased. Additionally, CRYAB, Hsp27, Hsp60 and Hsp70 mRNA levels were upregulated at 3 h (p < 0.01), and protein levels were increased for CRYAB at 0 h (p < 0.05) and 1 h (p < 0.01), and for Hsp70 at 3 and 5 h (p < 0.01). Thus, pre-treatment with vitamin C or vitamin C-Na might protect H9C2 cells against heat damage by enhancing the antioxidant ability and upregulating CRYAB and Hsp70.


Assuntos
Antioxidantes/farmacologia , Ácido Ascórbico/farmacologia , Proteínas de Choque Térmico/metabolismo , Resposta ao Choque Térmico/efeitos dos fármacos , Bicarbonato de Sódio/farmacologia , Animais , Apoptose/efeitos dos fármacos , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , L-Lactato Desidrogenase/metabolismo , Malondialdeído , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/patologia , Miócitos Cardíacos/ultraestrutura , Ratos , Espécies Reativas de Oxigênio/metabolismo , Superóxido Dismutase/metabolismo , Transcrição Genética/efeitos dos fármacos
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