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BACKGROUND: Placental exosomes are a kind of intercellular communication media secreted by placental cells during pregnancy, exosomogenesis and release are regulated by many secretory glycoproteins. CREG1 is a kind of secreted glycoprotein widely expressed in various organs and tissues of the body, which inhibits cell proliferation and enhances cell differentiation. The aim of this study was to explore the role of CREG1 in regulating exosomogenesis during the proliferation and differentiation of placental trophoblast cells in early pregnant dairy cows by targeting IGF2R and participating in regulating organoid differentiation via exosomes transport. METHODS: Molecular biological methods were firstly used to investigate the expression patterns of CREG1, IGF2R and exosomal marker proteins in early placental development of pregnant dairy cows. Subsequently, the effects of CREG1 on the formation and release of bovine placental trophoblast (BTCs) derived exosomes by targeting IGF2R were investigated. Further, the effects of CREG1 on the change of gene expression patterns along with the transport of exosomes to recipient cells and participate in regulating the differentiation of organoids were explored. RESULTS: The expression of CREG1, IGF2R and exosomal marker proteins increased with the increase of pregnancy months during the early evolution of placental trophoblast cells in dairy cows. Overexpression of Creg1 enhanced the genesis and release of exosomes derived from BTCs, while knocking down the expression of Igf2r gene not only inhibited the genesis of exosomes, but also inhibited the genesis and release of exosomes induced by overexpression of CREG1 protein. Interestingly, IGF2R can regulate the expression of CREG1 through reverse secretion. What's more, the occurrence and release of trophoblast-derived exosomes are regulated by CREG1 binding to IGF2R, which subsequently binds to Rab11. CREG1 can not only promote the formation and release of exosomes in donor cells, but also regulate the change of gene expression patterns along with the transport of exosomes to recipient cells and participate in regulating the early development of placenta. CONCLUSIONS: Our study confirmed that CREG1 is involved in the exosomogenesis and release of exosomes during the proliferation and differentiation of placental trophoblast cells in early pregnant dairy cows by targeting IGF2R, and is involved in the regulation of organoid differentiation through exosome transport.
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Diferenciación Celular , Exosomas , Placenta , Receptor IGF Tipo 2 , Trofoblastos , Animales , Exosomas/metabolismo , Bovinos , Trofoblastos/metabolismo , Trofoblastos/citología , Femenino , Embarazo , Receptor IGF Tipo 2/metabolismo , Receptor IGF Tipo 2/genética , Placenta/metabolismo , Placenta/citología , Organoides/metabolismo , Organoides/citología , Proliferación CelularRESUMEN
Bovine viral diarrhoea virus (BVDV) can infect cows on days 30-110 of gestation and crossing the placental barrier, resulting in persistently infected (PI) and causing significant economic losses to dairy farming. Bovine placental trophoblast cells (BTCs) are the major cells in the early chorionic tissue of the placenta and play important roles in placental resistance to viral transmission. In this study, we have confirmed that BTCs is among a groups of cell types those could be infected by BVDV in vivo, and BVDV infection stimulates the autophagic responses in BTCs and promotes the release of exosomes. Meanwhile, the exosomes derived from BTCs can be used by BVDV to spread between placental trophoblast cells, and this mode of transmission cannot be blocked by antibodies against the BVDV E2 protein, whereas the replication and spread of BVDV in BTCs can be blocked by inhibiting autophagy and exosomogenesis. Our study provides a theoretical and practical basis for scientific prediction and intervention of reproductive disorders caused by BVDV infection in cows of different gestation periods from a novel perspective.
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Autofagia , Diarrea Mucosa Bovina Viral , Virus de la Diarrea Viral Bovina , Exosomas , Trofoblastos , Animales , Bovinos , Femenino , Trofoblastos/virología , Trofoblastos/inmunología , Exosomas/metabolismo , Exosomas/virología , Diarrea Mucosa Bovina Viral/transmisión , Diarrea Mucosa Bovina Viral/virología , Diarrea Mucosa Bovina Viral/inmunología , Embarazo , Virus de la Diarrea Viral Bovina/fisiología , Virus de la Diarrea Viral Bovina/inmunología , Placenta/virología , Placenta/inmunología , Células Cultivadas , Replicación ViralRESUMEN
AIMS: The study aimed to evaluate the effects of dietary folic acid (FA) on the production performance of laying hens, egg quality, and the nutritional differences between eggs fortified with FA and ordinary eggs. METHODS: A total of 288 26-week-old Hy-Line Brown laying hens (initial body weights 1.65 ± 0.10 kg) with a similar weight and genetic background were used. A completely randomized design divided the birds into a control group and three treatment groups. Each group consisted of six replicates, with twelve chickens per replicate. Initially, all birds were fed a basal diet for 1 week. Subsequently, they were fed a basal diet supplemented with 0, 5, 10, or 15 mg/kg FA in a premix for a duration of 6 weeks. RESULTS: Supplementation of FA could significantly (p < 0.05) enhance the FA content in egg yolks, particularly when 10 mg/kg was used, as it had the most effective enrichment effect. Compared to the control group, the Glu content in the 10 and 15 mg/kg FA groups showed a significant (p < 0.05) decrease. Additionally, the contents of Asp, Ile, Tyr, Phe, Cys, and Met in the 15 mg/kg FA group were significantly (p < 0.05) lower compared to the other groups. Adding FA did not have significant effects on the levels of vitamin A and vitamin E in egg yolk, but the vitamin D content in the 5 and 10 mg/kg FA groups showed a significant (p < 0.05) increase. Furthermore, the addition of FA did not have a significant effect on the levels of Cu, Fe, Mn, Se, and Zn in egg yolk. The dietary FA did not have a significant effect on the total saturated fatty acids (SFA) and polyunsaturated fatty acid (PUFA) content in egg yolk. However, the total monounsaturated fatty acid (MUFA) content in the 5 and 10 mg/kg groups significantly (p < 0.05) increased. These changes in nutritional content might be attributed to the increased very low-density lipoprotein (VLDL) protein content. The significant decrease in solute carrier family 1 Member 1 (SLC1A1), solute carrier family 1 Member 2 (SLC1A2), and solute carrier family 1 Member 3 (SLC1A3) gene expression compared to the control group appeared to be the reason for the decrease in amino acid content in egg yolk within the dietary FA group. CONCLUSION: The findings suggest that the appropriate addition of FA can enhance the levels of MUFA and vitamin D in egg yolks, thereby improving their nutritional value. Excessive intake of FA can decrease the effectiveness of enriching FA in egg yolk and impact the enrichment of certain amino acids. The yolk of eggs produced by adding 10 mg/kg of FA to the feed contains the optimal amount of nutrients. This study informs consumers purchasing FA-fortified eggs.
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As a pivotal player in spermatogenesis, the blood-testis barrier (BTB) made from junction apparatus coexisting in Sertoli cells (SCs) is impaired with an increase in age and ultimately induces spermatogenic dysfunction or even infertility. It has been corroborated that bone marrow mesenchymal stem cell (BMSC) transplantation can efficiently repair and regenerate the testicular function. As vital mediators of cell-to-cell communication, MSC-derived exosomes (Exos) can directly serve as therapeutic agents for tissue repair and regeneration. However, the therapeutic value of BMSC-Exos in aging-induced BTB damage remains to be confirmed. In this study, we explored that the old porcine testes had defective autophagy, which aggravated BTB disruption in SCs. BMSC-Exos could decrease ROS production and NLRP3 inflammasome activation but enhanced autophagy and tight junction (TJ) function in D-gal-triggered aging porcine SCs and mouse model testes, according to in vitro and in vivo experiments. Furthermore, rapamycin, NAC, MCC950, and IL-1Ra restored the TJ function in D-gal-stimulated aging porcine SCs, while BMSC-Exos' stimulatory effect on TJ function was inhibited by chloroquine. Moreover, the treatment with BMSC-Exos enhanced autophagy in D-gal-induced aging porcine SCs by means of the AMPK/mTOR signal transduction pathway. These findings uncovered through the present study that BMSC-Exos can enhance the BTB function in aging testes by improving autophagy via the AMPK/mTOR signaling pathway, thereby suppressing ROS production and NLRP3 inflammasome activation.
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Abnormal function and fibrosis of endometrium caused by cows' endometritis pose difficult implantation of embryos and uterine cavity adhesions. 17ß-Estradiol (E2) serves as the most effective aromatized estrogen, and its synthetase and receptors have been detected in the endometrium. Studies have demonstrated the positive role of estrogen in combating pathological fibrosis in diverse diseases. However, it is still unknown whether E2 regulates endometrium fibrosis in bovine endometritis. Herein, we evaluated the expression patterns of transforming growth factor-ß1 (TGF-ß1), epithelial-mesenchymal transformation (EMT)-related proteins (α-SMA, vimentin N-cadherin and E-cadherin), cytochrome P450 19A1 (CYP19A1), and G protein-coupled estrogen receptor (GPER) in bovine healthy endometrium and Inflammatory endometrium. Our data showed that the inflamed endometrium presented low CYP19A1 and GPER expression, and significantly higher EMT process versus the normal tissue. Moreover, we established a TGF-ß1-induced fibrosis model in BEND cells, and found that E2 inhibited the EMT process of BEND cells in a dose-dependent manner. The anti-fibrotic effect of E2 was blocked by the GPER inhibitor G15, but not the estrogen nuclear receptors (ERs) inhibitor ICI182780. Moreover, the GPER agonist G1 inhibited fibrosis and Smad2/3 phosphorylation but increased the expression of TGFBR3 in BEND cells. Transfection with TGFBR3 small interfering RNA blocked the effect of G1 on fibrosis of BEND cells and upregulated the expression of P-Smad2/3. Our in vivo data also showed that E2 and G1 affected uterus fibrosis in mice endometritis model caused by LPS, which was associated with the inhibition of TGFBR3/Smad2/3 signaling. In conclusion, our data implied that E2 alleviates the fibrosis of TGF-ß1-induced BEND cells, which is associated with the GPER mediation of TGFBR3/Smad2/3 signaling.
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Endometritis , Estradiol , Proteoglicanos , Receptores de Factores de Crecimiento Transformadores beta , Factor de Crecimiento Transformador beta1 , Animales , Bovinos , Femenino , Ratones , Endometritis/metabolismo , Endometrio/metabolismo , Células Epiteliales/metabolismo , Transición Epitelial-Mesenquimal , Estradiol/farmacología , Estrógenos/metabolismo , Fibrosis , Receptores Acoplados a Proteínas G/metabolismo , Factor de Crecimiento Transformador beta1/metabolismo , Proteínas Smad/metabolismoRESUMEN
Brucellosis is a notorious zoonotic disease caused by Brucella, which can lead to reproductive diseases in humans and animals, such as infertility and abortion. Lipopolysaccharides (LPS) are the main virulence factor of Brucella. LPS derived from Brucella are different and non-classical and are less toxic and less active than LPS isolated from E. coli. However, the effects and possible mechanisms of Brucella LPS-caused pregnancy loss remain to be revealed. In the present study, we investigated the effects of Brucella suis S2 LPS on early pregnancy loss in mice. The results indicated that embryo implantation failure was induced by Brucella LPS treatment in a dose-dependent manner. The injection of Brucella LPS mainly resulted in fibrinolysis in the decidual area of the uterus on the 6th day post coition (dpc), infiltration of large granular cells among the decidual cells near the embryo on the 8th dpc, a large number of gaps in the decidual area, and cell necrosis around the embryo. In addition, the expression of Cyclin D3 mRNA in the uterus on the 7th and 8th dpc and IGFBP-1 mRNA and the progesterone receptor in the uterus on the 6th and 7th dpc were also inhibited. Moreover, the expression of decidualization marker Cyclin D3 and decidualization prolactin-associated protein (dPRP) in endometrial stromal cells were also inhibited by Brucella LPS treatment in vitro. In summary, Brucella LPS affect the process of endometrial decidualization in mice by affecting the structure of the decidua and the expression of decidual marker factors in endometrial stromal cells.
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Brucella suis , Decidua , Embarazo , Humanos , Femenino , Ratones , Animales , Decidua/metabolismo , Lipopolisacáridos/farmacología , Brucella suis/metabolismo , Ciclina D3/metabolismo , Escherichia coli/metabolismo , Útero , ARN Mensajero/metabolismoRESUMEN
Sperm motility is an important index for the evaluation of semen quality. Improving sperm motility is important to improve reproductive performance, promote breeding process, and reduce production cost. However, the molecular mechanisms regulating sperm motility in chickens remain unclear. In this study, histological observation and whole-transcriptome analysis were performed on testicular tissue of chickens with high and low sperm motility. Histological observations showed that roosters with high sperm motility exhibited better semen quality than those with low sperm motility. In addition, the germinal epithelial cells of roosters with low sperm motility were loosely arranged and contained many vacuoles. RNA-seq results revealed the expression of 23,033 mRNAs, 2,893 lncRNAs, and 515 miRNAs in chicken testes. Among them, there were 417 differentially expressed mRNAs (DEmRNAs), 106 differentially expressed lncRNAs (DElncRNAs), and 15 differentially expressed miRNAs (DEmiRNAs) between high and low sperm motility testes. These differentially expressed genes were involved in the G protein-coupled receptor signaling pathway, cilia structure, Wnt signaling, MAPK signaling, GnRH signaling, and mTOR signaling. By integrating the competitive relationships between DEmRNAs, DElncRNAs, and DEmiRNAs, we identified the regulatory pathway of MSTRG.3077.3/MSTRG.9085.1-gga-miR-138-5p-CADM1 and MSTRG.2290.1-gga-miR-142-3p-GNAQ/PPP3CA as crucial in the modulation of chicken sperm motility. This study provides new insights into the function and mechanism of ceRNAs in regulating sperm motility in chicken testes.
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MicroARNs , ARN Largo no Codificante , Masculino , Animales , Pollos/fisiología , Motilidad Espermática/genética , Análisis de Semen/veterinaria , Transcriptoma , ARN Largo no Codificante/genética , MicroARNs/genéticaRESUMEN
Intramuscular fat (IMF) is an important factor affecting chicken quality. However, the age-related mechanism of IMF deposition has not yet been elucidated. In this study, the IMF, phospholipids (PL), triglycerides (TG), and fatty acid (FA) content in the breast muscle of Beijing-You chicken (BJY) at 1, 56, 98, and 120 d of age was measured, and mRNA and miRNA sequencing was integrated to explore the regulatory genes of IMF deposition. The results showed that the IMF content of BJY at 1 d of age was significantly higher than that at later stage of birth (P < 0.05). The transcriptome sequencing results showed that 7, 225 differentially expressed genes (DEGs) and 243 differentially expressed miRNAs (DE-miRNAs) were identified. The cluster analysis showed that the expression of DEGs and DE-miRNAs at 1 d of age was significantly different from that at later stages of birth. Furthermore, a potential mRNA-miRNA regulatory network related to IMF deposition was established by weighted gene co-expression network analysis (WGCNA); gga-miR-29c-3p-PIK3R1, gga-miR-6701-3p-PTEN, gga-miR-363-3p-PTEN, gga-miR-1563-WWP1, gga-miR-449c/d-5p-TRAF6, and gga-miR-6701-3p-BMPR1B were identified as key mRNA-miRNA pairs for the regulation of IMF deposition. These results will help elucidate the mechanism of IMF formation mediated by miRNAs in chickens, and provide a theoretical foundation for the genetic improvement of broiler meat quality.
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As a functional fatty acid, α-linolenic acid (ALA) is essential in promoting animal testosterone biosynthesis. This study investigated the effects of ALA on testosterone biosynthesis and the possible mechanism underlying the signaling pathway in primary Leydig cells of the rooster. METHODS: Primary rooster Leydig cells were treated with ALA (0, 20, 40, or 80 µmol/L) or pretreated with a p38 inhibitor (50 µmol/L), a c-Jun NH2-terminal kinase (JNK) inhibitor (20 µmol/L), or an extracellular signal-regulated kinase (ERK) inhibitor (20 µmol/L) before ALA treatment. Testosterone content in the conditioned culture medium was detected using an enzyme-linked immunosorbent assay (ELISA). The expression of steroidogenic enzymes and JNK-SF-1 signaling pathway factors was detected using real-time fluorescence quantitative PCR (qRT-PCR). RESULTS: Supplementation with ALA significantly increased testosterone secretion within culture media (P < 0.05), and the optimized dose was 40 µmol/L. Compared with the control group, steroidogenic acute regulatory protein (StAR), cholesterol side-chain cleavage enzyme (P450scc), and 3ß-hydroxysteroid dehydrogenase (3ß-HSD) mRNA expression significantly increased (P < 0.05) in the 40 µmol/L ALA group; 17-hydroxylase/c17-20 lyase (P450c17) and p38 mRNA expressions were not significantly different in the 40 µmol/L ALA group; ERK and JNK mRNA expressions were significantly upregulated (P < 0.05) in 40 µmol/L ALA group. In the inhibitor group, testosterone levels were significantly downregulated (P < 0.05). Compared with the 40 µmol/L ALA group, StAR, P450scc, and P450c17 mRNA expressions were significantly decreased (P < 0.05), and 3ß-HSD mRNA expression in the p38 inhibitor group did not change; StAR, P450scc, and 3ß-HSD mRNA expressions were significantly decreased (P < 0.05), and P450c17 mRNA expression in ERK inhibitor group did not change; StAR, P450scc, 3ß-HSD, and P450c17 mRNA expressions were significantly decreased (P < 0.05) in JNK inhibitor group. Additionally, the increased steroidogenic factor 1 (SF-1) gene expression levels induced by ALA were reversed when the cells were pre-incubated with JNK and ERK inhibitors. The levels in the JNK inhibitor group were significantly lower than those in the control group (P < 0.05). CONCLUSION: ALA may promote testosterone biosynthesis by activating the JNK-SF-1 signaling pathway to upregulate StAR, P450scc, 3ß-HSD, and P450c17 expression in primary rooster Leydig cells.
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Células Intersticiales del Testículo , Ácido alfa-Linolénico , Masculino , Animales , Células Intersticiales del Testículo/metabolismo , Factor Esteroidogénico 1/metabolismo , Factor Esteroidogénico 1/farmacología , Ácido alfa-Linolénico/farmacología , Pollos/genética , 3-Hidroxiesteroide Deshidrogenasas/metabolismo , ARN Mensajero/metabolismo , Testosterona/metabolismo , Transducción de Señal , Enzima de Desdoblamiento de la Cadena Lateral del Colesterol/genética , Enzima de Desdoblamiento de la Cadena Lateral del Colesterol/metabolismoRESUMEN
Dihydrotestosterone (DHT) is a potent nonaromatizable 5α-reduced androgen with both positive and negative effect on inflammation process. However, it remains unknown whether DHT can regulate Lipopolysaccharides (LPS)-induced inflammation in bovine endometrial epithelial cells (bEECs). Here, we demonstrated that the DHT biosynthesis ability and androgen receptors (AR) expression is defective in bovine endometrial with endometritis, which aggravates endometrial inflammation. In vitro study, we established a LPS-induced inflammation model in bEECs, and found that DHT inhibited the TLR4 and MyD88 protein as well as TNF-α, IL-1ß, and IL-6 mRNA of bEECs in a dose-dependent manner. Moreover, the anti-inflammation effect of DHT was blocked by AR inhibitor flutamide. Together, we demonstrated that supplementing DHT can alleviate the inflammation response of bEECs caused by LPS, which is associated with AR regulating the inhibition of TLR4/MyD88 signaling pathway.
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Enfermedades de los Bovinos , Endometritis , Femenino , Animales , Bovinos , Lipopolisacáridos/toxicidad , Dihidrotestosterona/farmacología , Dihidrotestosterona/metabolismo , Receptores Androgénicos/metabolismo , Factor 88 de Diferenciación Mieloide/genética , Factor 88 de Diferenciación Mieloide/metabolismo , Factor 88 de Diferenciación Mieloide/farmacología , Receptor Toll-Like 4/genética , Receptor Toll-Like 4/metabolismo , Inflamación/inducido químicamente , Inflamación/metabolismo , Inflamación/veterinaria , Transducción de Señal , Endometritis/inducido químicamente , Endometritis/veterinaria , Endometritis/metabolismo , Células Epiteliales , Enfermedades de los Bovinos/metabolismoRESUMEN
The flavor of chicken meat is influenced by muscle metabolites and regulatory genes and varies with age. In this study, the metabolomic and transcriptomic data of breast muscle at four developmental stages (days 1, 56, 98, and 120) of Beijing-You chickens (BJYs) were integrated and 310 significantly changed metabolites (SCMs) and 7,225 differentially expressed genes (DEGs) were identified. A Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed that SCMs and DEGs were enriched in amino acid, lipid, and inosine monophosphate (IMP) metabolism pathways. Furthermore, genes highly associated with flavor amino acids, lipids, and IMP were identified by a weighted gene co-expression network analysis (WGCNA), including cystathionine ß-synthase (CBS), glycine amidinotransferase (GATM), glutamate decarboxylase 2 (GAD2), patatin-like phospholipasedomain containing 6 (PNPLA6), low-specificity L-threonine aldolase (ItaE), and adenylate monophosphate deaminase 1 (AMPD1) genes. A regulatory network related to the accumulation of key flavor components was constructed. In conclusion, this study provides new perspectives regarding the regulatory mechanisms of flavor metabolites in chicken meat during development.
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Improving chronic wound healing remains a challenge in the clinical practice. In this study, we developed double-crosslinked angiogenic 3D-bioprinted patches for diabetic wound healing by the photocovalent crosslinking of vascular endothelial growth factor (VEGF) using ultraviolet (UV) irradiation. 3D printing technology can precisely customize the structure and composition of patches to meet different clinical requirements. The biological polysaccharide alginate and chondroitin sulfate methacryloyl were used as biomaterials to construct the biological patch, which could be crosslinked using calcium ion crosslinking and photocrosslinking, thereby improving its mechanical properties. More importantly, acrylylated VEGF could be easily and rapidly photocrosslinked under UV irradiation, which simplified the step of chemically coupling growth factors and prolonged VEGF release time. These characteristics suggest that 3D-bioprinted double-crosslinked angiogenic patches are ideal candidates for diabetic wound healing and other tissue engineering applications.
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Diabetes Mellitus , Andamios del Tejido , Andamios del Tejido/química , Sulfatos de Condroitina , Factor A de Crecimiento Endotelial Vascular , Alginatos/química , Ingeniería de Tejidos , Impresión Tridimensional , Cicatrización de Heridas , Hidrogeles/química , Diabetes Mellitus/tratamiento farmacológicoRESUMEN
Exosomes are a subtype of extracellular vesicles (EVs) with a size range between 30 and 150 ânm, which can be released by the majority of cell types and circulate in body fluid. They function as a long-distance cell-to-cell communication mechanism that modulates the gene expression profile and fate of target cells. Increasing evidence has indicated exosomes' central role in regulating various complex reproductive processes. However, to our knowledge, a review that focally and vividly describes the role of exosomes in reproductive development is still lacking. This review highlights our knowledge about the contribution of exosomes to early mammalian reproduction, such as gametogenesis, fertilization, early embryonic development, implantation, placentation and pregnancy. The discussion is primarily drawn from literature pertaining to the mammalian lineage with emphasis on the roles of exosomes in human reproduction and laboratory and livestock models.
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Chicken meat quality and flavor are determined by abundant metabolites. In this study, HPLC-QTRAP-MS-based metabolomic analysis was used to evaluate the characteristic metabolites in the breast muscle of Beijing You chickens aged 56, 98, and 120 days. A total of 544 metabolites in 32 categories were identified, among which amino acids and organic acids were the most abundant. 60 and 55 differential metabolites were identified between 56 and 98 days of age, 98 and 120 days of age, respectively. The content of l-carnitine, l-methionine and 3-hydroxybutyrate increased significantly at 98 or 120 days of age. Arginine biosynthesis, purine metabolism, alanine, aspartic acid, and glutamic acid metabolism were important metabolic pathways that affect chicken meat flavor. This study can help to elucidate the metabolic mechanism of breast muscle during Beijing You chicken development and provide a theoretical reference for the improvement of chicken meat quality and flavor.
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Blood-testis barrier (BTB) made of concomitant junction apparatus between Sertoli cells (SCs) is crucial for spermatogenesis. The tight junction (TJ) function is impaired in SCs with age, exhibiting an intimate relationship to testicular dysfunction induced by age. In this study, compared with those in young boars, TJ proteins (i.e., Occludin, ZO-1, and plus Claudin-11) were discovered to have reduced expressions in testes, and spermatogenesis ability declined in old boars. An in vitro age model for D-gal-treated porcine SCs was established, the performance of Curcumin as a natural antioxidant and anti-inflammatory compound in affecting the TJ function of SCs was appraised, and related molecular mechanisms were exploited. The results manifested that 40 g/L D-gal downregulated ZO-1, Claudin-11, and Occludin in terms of the expression in SCs, whereas Curcumin restored such expressions in D-gal-treated SCs. Using the AMPK and SIRT3 inhibiters demonstrated that activation of the AMPK/SIRT3 pathway was associated with Curcumin, which not only rescued the expression of ZO-1, Occludin, Claudin-11, and SOD2 but also inhibited the production of mtROS and ROS and the activation of NLRP3 inflammasome and release of IL-1ß in D-gal-treated SCs. Furthermore, with mtROS scavenger (mito-TEMPO), NLRP3 inhibitor (MCC950) plus IL-1Ra treatment ameliorated D-gal-caused TJ protein decline in SCs. In vivo data also showed that Curcumin alleviated TJ impairment in murine testes, improved D-gal-triggered spermatogenesis ability, and inactivated the NLRP3 inflammasome by virtue of the AMPK/SIRT3/mtROS/SOD2 signal transduction pathway. Given the above findings, a novel mechanism where Curcumin modulates BTB function to improve spermatogenesis ability in age-related male reproductive disorder is characterized.
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Curcumina , Sirtuina 3 , Animales , Masculino , Porcinos , Ratones , Células de Sertoli/metabolismo , Inflamasomas/metabolismo , Uniones Estrechas/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Ocludina/metabolismo , Sirtuina 3/metabolismo , Proteínas Quinasas Activadas por AMP/metabolismo , Curcumina/farmacología , Curcumina/metabolismo , Proteínas de Uniones Estrechas/metabolismo , Transducción de Señal , Claudinas/metabolismoRESUMEN
Aims: The study aimed to evaluate the effects of pretreated Chinese herbal medicine (PCHM) on egg quality, production performance, histopathological changes in the uterus, antiox idant capacity, and antioxidant gene expression in late-phase layers. Methods: Jinghong No.1 layers (n = 360, 68 weeks old) were assigned randomly to one of f our dietary interventions. Each treatment was replicated six times. Repeat 15 chickens per g roup. All birds were fed a diet composed of a corn-soybean meal-based diet supplemented with 0, 0.2, 0.4, or 0.8% PCHM for 6 weeks. Results: Dietary PCHM supplementation had no significant effects on laying rate, feed con sumption, yolk color, and shape index. With increasing PCHM level the Haugh unit linearly increased (P < 0.05). Supplementation of 0.8% PCHM increased egg weight, compared with the control (P < 0.05). PCHM can effectively alleviated the pathological changes caused by aging in the uterus including hemorrhage, and many inflammatory cell infiltrations. Supplementation of 0.4% PCHM increased glutathione peroxidase (GSHPx) in liver, magnum, and plasm considerably, compared with the control (P < 0.05). Supplementation of PCHM decr ease in the liver, magnum, and uterus on malondialdehyde (MDA) content, compared with the control (P < 0.05). Compared with the control group, mRNA expressions of glutathione peroxidase 1 (GPX1), peroxidase 4 (GPX4), catalase (CAT), and nuclear factor E2-related factor 2 (Nrf2) in the magnum, liver, and uterus were dramatically rose in the 0.4% PCHM supplementation group (P < 0.05). In summary, dietary supplementation after PCHM increased egg weight and quality in late-phase laying hens. Conclusion: Dietary PCHM increased the antioxidative capacity of late-phase laying hens, which could be associated with increased mRNA expression of antioxidant enzymes and Nrf2. These findings provide potential for using PCHM to increase the production performance in late-phase laying hens.
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Bovine viral diarrhea (BVD) is a worldwide infectious disease caused by bovine viral diarrhea virus (BVDV) infection, which invades the placenta, causes abortion, produces immune tolerance and continuously infects calves, and causes huge economic losses to the cattle industry. The endoplasmic reticulum (ER) is an important organelle in cells, which is prone to ER stress after being stimulated by pathogens, thus activating the ER stress-related apoptosis. Studies have confirmed that BVDV can utilize the ER of its host to complete its own proliferation and stimulate ER stress to a certain extent. However, the role of ER stress in BVDV infecting bovine placental trophoblast cells (BTCs) and inducing apoptosis is still unclear. We are using the cytopathic strain of BVDV (OregonC24Va), which can cause apoptosis of BTCs, as a model system to determine how ER stress induced by BVDV affects placental toxicity. We show that OregonC24Va can infect BTCs and proliferate in it. With the proliferation of BVDV in BTCs, ER stress-related apoptosis is triggered. The ER stress inhibitor 4-PBA was used to inhibit the ER stress of BTCs, which not only inhibited the proliferation of BVDV, but also reduced the apoptosis of BTCs. The ER stress activator Tg can activate ER stress-related apoptosis, but the proliferation of BVDV does not change in BTCs. Therefore, BVDV utilizes the UPR of activated ER stress to promote the proliferation of BVDV in the early stage of infection, and activates the ER stress-related apoptosis of BTCs in the later stage with the virus proliferation to promote the cell apoptosis and further spread of the virus. Our research provides a new theoretical basis for exploring the placental infection and vertical transmission of BVDV.
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Virus de la Diarrea Viral Bovina Tipo 1 , Virus de la Diarrea Viral Bovina , Animales , Femenino , Bovinos , Embarazo , Trofoblastos , Placenta , Apoptosis/fisiología , Virus de la Diarrea Viral Bovina/fisiología , Estrés del Retículo Endoplásmico , DiarreaRESUMEN
In recent years, the incidence of the reproductive diseases is increasing year-by-year, leading to abortion or fetal arrest, which seriously affects the reproductive health of human beings and the reproductive efficiency of animals. Exosomes are phospholipid bilayer vesicles that are widely distributed in living organisms and released by the cells of various organs and tissues. Exosomes contain proteins, RNA, lipids, and other components and are important carriers of information transfer between cells, which play a variety of physiological and pathological regulatory functions. More and more studies have found that exosomes and their connotations play an important role in the diagnosis, prognosis and treatment of diseases. A systematic review was conducted in this manuscript and then highlights our knowledge about the diagnostic and therapeutic applications of exosomes to reproductive diseases, such as polycystic ovary syndrome (PCOS), endometriosis, premature ovarian failure (POF), preeclampsia, polycystic, endometrial cancer, cervical cancer, ovarian cancer, and prostate gland cancer.
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The development of efficient electrochemical seawater splitting catalysts for large-scale hydrogen production is of great importance. In this work, we report an amorphous Co-Mo-B film on Ni foam (Co-Mo-B/NF) via a facile one-step electrodeposition process. Such amorphous Co-Mo-B/NF possesses superior activity with a small overpotential of 199 mV at 100 mA cm-2 for a hydrogen evolution reaction in alkaline seawater. Notably, Co-Mo-B/NF also maintains excellent stability for at least 24 h under alkaline seawater electrolysis.
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Spermatogenesis, sperm motility, and apoptosis are dependent on the regulation of glandular hormones and mitochondria. Natural astaxanthin (ASTA) has antioxidant, anti-inflammatory, and anti-apoptotic properties. The present study evaluates the effects of ASTA on testosterone synthesis and mitochondrial function in aging roosters. Jinghong No. 1 layer breeder roosters (n = 96, 53-week old) were fed a corn−soybean meal basal diet containing 0, 25, 50, or 100 mg/kg ASTA for 6 weeks. The levels of plasma reproductive hormones and the mRNA and protein levels of molecules related to testosterone synthesis were significantly improved (p < 0.05) in the testes of the ASTA group roosters. In addition, antioxidant activities and free radical scavenging abilities in roosters of the ASTA groups were higher than those of the control group (p < 0.05). Mitochondrial electron transport chain complexes activities and mitochondrial membrane potential in sperm increased linearly with dietary ASTA supplementation (p < 0.05). The levels of reactive oxygen species and apoptosis factors decreased in roosters of the ASTA groups (p < 0.05). Collectively, these results suggest that dietary ASTA may improve testosterone levels and reduce sperm apoptosis, which may be related to the upregulation of the testosterone synthesis pathway and the enhancement of mitochondrial function in aging roosters.