关键词：
Gansulinema gen. nov.;Komarkovaeasiopsis gen. nov.;cyanobacteria;polyphasic methods;taxonomy
摘要：
To increase the understanding of simple thin filamentous cyanobacteria in harsh environmental areas, we previously isolated and identified four strains (XN101, XN102, GS121, NX122) from desert soils and hot spring in China. As a result, two new Oculatellacean genera of these four strains, Gansulinema gen. nov. and Komarkovaeasiopsis gen. nov., are described based on a polyphasic approach. The ultrastructure of these strains showed a similar arrangement of peripheral thylakoids with three to four parallel layers, indicating that they belonged to the orders Nodosilineales, Oculatellales, or Leptolyngbyales. In the 16S rRNA gene phylogeny, two sequences of the Gansulinema strains and the two sequences of the Komarkovaeasiopsis strains formed two independent and robust clusters, within the order Oculatellales. The 16S rRNA gene sequences of strains of Komarkovaeasiopsis and Gansulinema showed low identity to each other (≤93.2%) and to other sequences of the Oculatellacean genera (≤94.5% and ≤93.3%, respectively). Furthermore, the 16S-23S internal transcribed spacer rRNA region secondary structures of strains of Komarkovaeasiopsis and Gansulinema were not consistent with all existing descriptions of Oculatellacean taxa. These data suggest that cyanobacterial communities are rich sources of new taxa in under-exploited areas, such as desert soils and hot spring in China.
摘要：
The present study was conducted to decipher the protection effects of ellagic acid (EA) on piglets infected with porcine epidemic diarrhea virus (PEDV). Thirty 7-day-old piglets were randomly assigned to three treatment groups: control, PEDV, and EA + PEDV groups. After a 3-day period of adaption, piglets in the EA + PEDV group were orally administered with 20 mg/kg·BW EA during days 4-11 of the trial. On day 8, piglets were orally administered with PEDV at a dose of 10(6) TCID(50) (50% tissue culture infectious dose) per pig. Additionally, intestinal porcine epithelial (IPEC-1) cells infected with PEDV were used to investigate the anti-PEDV effect of EA in vitro. The results showed that EA at a dose of 10-40 μmol/L increased the viability of PEDV-infected IPEC-1 cells, and EA administration mitigated intestinal edema in piglets challenged with PEDV. Further studies indicated that EA treatment significantly increased the proportion of white blood cells in blood and concentrations of IL-6, IL-1β, and IL-10 in the serum, but decreased the TNF-α content and gene expression of IL-6, IL-1β, TNF-α, and CXCL2 in the jejunum. Moreover, EA intervention considerably elevated the activity of total superoxide dismutase (T-SOD), but decreased the H(2)O(2) concentration in the ileum of piglets. Importantly, EA suppressed the increased expression of antiviral-related genes and proteins (including MXI, ISG15, HSP70, and p-IRF7) induced by PEDV challenge in the jejunum. Furthermore, PEDV infection increased the protein abundance of p-JAK2 and p-STAT3, which were further enhanced by EA supplementation. In conclusion, our results revealed that EA could promote the restoration of intestinal homeostasis by regulating the interferon pathway that was interrelated with the activation of JAK2/STAT3 signaling. These findings provide theoretical basis for the use of EA as a therapy targeting PEDV infection in piglets.
摘要：
Glaesserella parasuis, an important respiratory bacterial pathogen, causes Glässer’s disease in piglets, with potential immunosuppression. We established a piglet infection model and explored the immunosuppression mechanism to improve our understanding of the host immune response to G. parasuis. Twenty piglets were randomly divided into two groups (n = 10). The infection group was intraperitoneally challenged with 2 × 108 CFU of G. parasuis in 2 mL TSB. The control group was intraperitoneally injected with equivalent TSB. After 72 h, the piglets were sacrificed, and spleen tissue was collected. PD-1/PD-L1 expression was determined. The splenocytes were isolated to detect CD3+ T, CD3+CD4+ T, CD3+CD8+ T and CD3−CD21+cell differentiation. Via data-independent acquisition (DIA), we compared the proteomics of healthy and infected spleen tissues. Glaesserella parasuis modified CD3+ T, CD3+CD4+ T, CD3+CD8+ T and CD3−CD21+ cell differentiation and PD-1/PD-L1 expression in the spleen. The infection group had 596 proteins with significant differences in expression, of which 301 were significantly upregulated and 295 downregulated. Differentially expressed proteins (DEPs) were mainly related to immune responses. This is the first study on PD-1/PD-L1 expression in the spleen associated with immunosuppression in a piglet model to explore the protein changes related to immune responses via DIA.
摘要：
Selenium-enriched Cardamine violifolia (SEC), a cruciferous plant, exerts excellent antioxidant and anti-inflammatory capacity, but its effect on hepatic function is unclear. This study investigated the effect and potential mechanism of SEC on hepatic injury induced by lipopolysaccharide (LPS). Twenty-four weaned piglets were randomly allotted to treatment with SEC (0.3 mg/kgSe) and/or LPS (100 μg/kg). After 28 days of the trial, pigs were injected with LPS to induce hepatic injury. These results indicated that SEC supplementation attenuated LPS-induced hepatic morphological injury and reduced aspartate aminotransferase (AST) and alkaline phosphatase (ALP) activities in plasma. SEC also inhibited the expression of pro-inflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α) after the LPS challenge. In addition, SEC improved hepatic antioxidant capacity via enhancing glutathione peroxidase (GSH-Px) activity and decreasing malondialdehyde (MDA) concentration. Moreover, SEC downregulated the mRNA expression of hepatic myeloid differentiation factor 88 (MyD88) and nucleotide-binding oligomerization domain proteins 1 (NOD1) and its adaptor molecule receptor interacting protein kinase 2 (RIPK2). SEC also alleviated LPS-induced hepatic necroptosis by inhibiting RIPK1, RIPK3, and mixed-lineage kinase domain-like (MLKL) expression. These data suggest that SEC potentially mitigates LPS-induced hepatic injury via inhibiting Toll-like receptor 4 (TLR4)/NOD2 and necroptosis signaling pathways in weaned piglets.
摘要：
Molecular docking, molecular dynamics, and in vitro experiments were used in this study to verify that baicalin inhibits monosodium urate crystal‐induced renal tubular epithelial cell pyroptosis through the NLRP3/GSDMD and Panx‐1/P2X7 pathways. Abstract Pyroptosis is a programmed cell death process that frequently occurs in many diseases, including hyperuricemic nephropathy (HN). In HN, a range of stimuli mediates inflammation, leading to the activation of inflammasomes and the production of gasdermin D (GSDMD). Baicalin (BA), a natural flavonoid renowned for its antioxidant and anti‐inflammatory properties, was investigated for its role in HN in this study. Initially, HN‐like inflammation and pyroptosis were induced in HK‐2 cells with treatment of monosodium urate (MSU), followed by the BA treatment. The expression of pyroptosis‐associated genes, Panx‐1 and P2X7, at both mRNA and protein levels was assessed through real‐time polymerase chain reaction (RT‐qPCR) and Western blotting (WB) without or with BA treatment. The results showed that expression of Panx‐1 and P2X7 at mRNA and protein levels was increased in MSU‐treated HK‐2 cells, which subsequently decreased upon the BA treatment. Further experiments showed that BA could combine NLRP3 inflammasome and GSDMD, destabilizing GSDMD protein. Moreover, BA protected the cell membrane from MSU‐induced damage, as evidenced by Hoechst 33342 and PI double staining, lactate dehydrogenase (LDH) assays, and electron microscopy observations. These results suggest that BA is involved in the regulating Panx‐1/P2X7 pathways and thus inhibits pyroptosis, highlighting its potential therapeutic effect for HN.
作者机构：
[Zhang, Qi; Ge, Feng; Yang, Mingkun; Zhao, Jindong; Jia, Kun; Liu, Xin; Cao, Gaoxiang] Chinese Acad Sci, State Key Lab Freshwater Ecol & Biotechnol, Inst Hydrobiol, Wuhan 430072, Peoples R China.;[Zhang, Qi; Ge, Feng; Yang, Mingkun; Jia, Kun; Cao, Gaoxiang] Univ Chinese Acad Sci, Coll Adv Agr Sci, Beijing 100049, Peoples R China.;[Liu, Xin] Wuhan Polytech Univ, Sch Anim Sci & Nutr Engn, Wuhan 430070, Peoples R China.;[Zhao, Jindong] Peking Univ, Coll Life Sci, State Key Lab Prot & Plant Genet Engn, Beijing 100871, Peoples R China.
通讯机构：
[Ge, F; Zhao, JD ] C;[Ge, F ] U;Chinese Acad Sci, State Key Lab Freshwater Ecol & Biotechnol, Inst Hydrobiol, Wuhan 430072, Peoples R China.;Univ Chinese Acad Sci, Coll Adv Agr Sci, Beijing 100049, Peoples R China.;Peking Univ, Coll Life Sci, State Key Lab Prot & Plant Genet Engn, Beijing 100871, Peoples R China.
摘要：
Lysine acetylation is a conserved regulatory posttranslational protein modification that is performed by lysine acetyltransferases (KATs). By catalyzing the transfer of acetyl groups to substrate proteins, KATs play critical regulatory roles in all domains of life; however, no KATs have yet been identified in cyanobacteria. Here, we tested all predicted KATs in the cyanobacterium Synechococcus sp. PCC 7002 (Syn7002) and demonstrated that A1596, which we named cyanobacterial Gcn5-related N-acetyltransferase (cGNAT2), can catalyze lysine acetylation in vivo and in vitro. Eight amino acid residues were identified as the key residues in the putative active site of cGNAT2, as indicated by structural simulation and site-directed mutagenesis. The loss of cGNAT2 altered both growth and photosynthetic electron transport in Syn7002. In addition, quantitative analysis of the lysine acetylome identified 548 endogenous substrates of cGNAT2 in Syn7002. We further demonstrated that cGNAT2 can acetylate NAD(P)H dehydrogenase J (NdhJ) in vivo and in vitro, with the inability to acetylate K89 residues, thus decreasing NdhJ activity and affecting both growth and electron transport in Syn7002. In summary, this study identified a KAT in cyanobacteria and revealed that cGNAT2 regulates growth and photosynthesis in Syn7002 through an acetylation-mediated mechanism. The cyanobacterial Gcn5-related N-acetyltransferase regulates the growth and photosynthesis of Synechococcus PCC 7002 through an acetylation-mediated mechanism.
摘要：
Protein homeostasis is essential for cyanobacteria to maintain proper cellular function under adverse and fluctuating conditions. The AAA+ superfamily of proteolytic complexes in cyanobacteria plays a critical role in this process, including ClpXP, which comprises a hexameric ATPase ClpX and a tetradecameric peptidase ClpP. Despite the physiological effects of ClpX on growth and photosynthesis, its potential substrates and underlying mechanisms in cyanobacteria remain unknown. In this study, we employed a streptavidin-biotin affinity pull-down assay coupled with label-free proteome quantitation to analyze the interactome of ClpX in the model cyanobacterium Synechocystis sp. PCC 6803 (hereafter Synechocystis). We identified 503 proteins as potential ClpX-binding targets, many of which had novel interactions. These ClpX-binding targets were found to be involved in various biological processes, with particular enrichment in metabolic processes and photosynthesis. Using protein-protein docking, GST pull-down, and biolayer interferometry assays, we confirmed the direct association of ClpX with the photosynthetic proteins, ferredoxin-NADP(+) oxidoreductase (FNR) and phycocyanin subunit (CpcA). Subsequent functional investigations revealed that ClpX participates in the maintenance of FNR homeostasis and functionality in Synechocystis grown under different light conditions. Overall, our study provides a comprehensive understanding of the extensive functions regulated by ClpX in cyanobacteria to maintain protein homeostasis and adapt to environmental challenges.
作者机构：
[Wen, Defeng; Liu, Yu; Wang, Nan; Guo, Pu; Ye, Chun; Fu, Shulin; Lu, Qirong] Hubei Key Laboratory of Animal Nutrition and Feed Science, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan 430023, China;[Wu, Zhongyuan] Hubei Key Laboratory of Animal Nutrition and Feed Science, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan 430023, China. Electronic address: zhongywu@whpu.edu.cn;[Qiu, Yinsheng] Hubei Key Laboratory of Animal Nutrition and Feed Science, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan 430023, China. Electronic address: qiuyinsheng6405@whpu.edu.cn
通讯机构：
[Zhongyuan Wu; Yinsheng Qiu] H;Hubei Key Laboratory of Animal Nutrition and Feed Science, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan 430023, China
摘要：
Bacterial lipopolysaccharide (LPS) exposure is a key inducer of intestinal inflammatory injury in weaned piglets, resulting in decreased growth performance of pigs and causing severe economic losses to the swine industry; however, the mechanism of intestinal inflammatory injury is still unclear. Baicalin is one of the main active ingredients extracted from the natural plant Scutellaria baicalensis that has biological functions, including anti-inflammatory activity. The aim of this study is to investigate the effect and mechanism of baicalin intervention on intestinal inflammatory injury caused by bacterial LPS exposure. In the present study, network pharmacology, molecular docking and DARTS results identified that baicalin has the potential to target PARP1, thereby potentially regulating a series of inflammation-related pathways, including the MAPK, NF-κB and Toll-like receptor signalling pathways, which play the role of antagonizing LPS-induced intestinal inflammatory injury. Further application of the LPS-induced IPEC-J2 cell model validated the finding that baicalin could alleviate LPS-induced intestinal inflammatory injury by inhibiting the PARP1-mediated NF-κB and NLRP3 signalling pathway. These findings demonstrate that baicalin can regulate the expression of PARP1 and that PARP1 has the potential to serve as an effective therapeutic target in the LPS-induced intestinal inflammatory injury.
摘要：
Contamination with fumonisin B1 (FB1) represents a global health problem. FB1 exposure may also trigger intestinal injury by activating inflammatory responses, leading to a reduction in production performance and economic benefits. However, the mechanism of FB1-induced intestinal inflammatory injury is still unclear. At the same time, it is urgent to develop antibiotic alternatives and therapeutic targets to alleviate antibiotic resistance and to ensure effective treatment of intestinal inflammatory injury. We combined network pharmacology and in vitro experiments to explore the core therapeutic targets and potential mechanism of luteolin in FB1-induced intestinal inflammatory injury. Network pharmacology and molecular docking revealed that nuclear factor kappa B (NF-kappa B) p65, extracellular signal-regulated kinase (ERK), interleukin 6 (IL-6) and IL-1 beta are the important targets, and the NF-kappa B and ERK signalling pathways are critical in FB1-induced intestinal inflammatory injury. Besides, in vitro experiments further demonstrated that luteolin can inhibit FB1-induced intestinal inflammatory injury by inhibiting activation of the NF-kappa B and ERK signalling pathways and reducing the expression of IL-6 and IL-1 beta in IPEC-J2 cells. We have comprehensively illustrated the potential targets and molecular mechanism by which luteolin can alleviate FB1-induced intestinal inflammatory injury. Luteolin may be an effective antibiotic alternative to prevent intestinal inflammatory injury.
摘要：
The effects of monolaurin (ML) on the health of piglets infected with porcine epidemic diarrhoea virus (PEDV) have not been fully understood. This study aimed to investigate its role in blood biochemical profile, intestinal barrier function, antioxidant function and the expression of antiviral genes in piglets infected with PEDV. Thirty-two piglets were randomly divided into four groups: control group, ML group, PEDV group and ML + PEDV group. Piglets were orally administrated with ML at a dose of 100 mg/kg·BW for 7 d before PEDV infection. Results showed that PEDV infection significantly decreased D-xylose content and increased intestinal fatty acid-binding protein content, indicating that PEDV infection destroyed intestinal barrier and absorption function. While it could be repaired by ML administration. Moreover, ML administration significantly decreased plasma blood urea nitrogen and total protein content upon PEDV infection. These results suggested ML may increase protein utilisation efficiency. ML administration significantly decreased the number of large unstained cells and Hb and increased the number of leucocytes and eosinophils in the blood of PEDV-infected piglets, indicating ML could improve the immune defense function of the body. In the presence of PEDV infection, ML administration significantly increased superoxide dismutase and catalase activities in blood and colon, respectively, indicating ML could improve antioxidant capacity. Besides, ML administration reversed the expression of ISG15, IFIT3 and IL-29 throughout the small intestine and Mx1 in jejunum and ileum, indicating the body was in recovery from PEDV infection. This study suggests that ML could be used as a kind of feed additive to promote swine health upon PEDV infection.
期刊：
Science of The Total Environment,2024年922:171015 ISSN：0048-9697
通讯作者：
Yi Zhao<&wdkj&>Jin-Long Li
作者机构：
[Dai, Xue-Yan; Guo, Jian-Ying; Lin, Jia; Saleem, Muhammad Asmat Ullah; Zhao, Yi; Zhu, Shi-Yong; Li, Jin-Long; Jiang, Fu-Wei] College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China;[Lin, Jia] Hubei Key Laboratory of Animal Nutrition and Feed Science, Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan Polytechnic University, Wuhan 430023, PR China;[Zhu, Shi-Yong] College of Animal Science and Veterinary Medicine, Qingdao Agricultural University, Qingdao 266109, PR China;[Dai, Xue-Yan] Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, PR China;[Zhao, Yi; Li, Jin-Long] Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin 150030, PR China
通讯机构：
[Yi Zhao; Jin-Long Li] C;College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China<&wdkj&>Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin 150030, PR China<&wdkj&>Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, Northeast Agricultural University, Harbin 150030, PR China
摘要：
Atrazine (ATZ) is the most prevalent herbicide that has been widely used in agriculture to control broadleaf weeds and improve crop yield and quality. The heavy use of ATZ has caused serious environmental pollution and toxicity to human health. Lycopene (LYC), is a carotenoid that exhibits numerous health benefits, such as prevention of cardiovascular diseases and nephropathy. However, it remains unclear that whether ATZ causes cardiorenal injury or even cardiorenal syndrome (CRS) and the beneficial role of LYC on it. To test this hypothesis, mice were treated with LYC and/or ATZ for 21days by oral gavage. This study demonstrated that ATZ exposure caused cardiorenal morphological alterations, and several inflammatory cell infiltrations mediated by activating NF-κB signaling pathways. Interestingly, dysregulation of MAPK signaling pathways and MAPK phosphorylation caused by ATZ have been implicated in cardiorenal diseases. ATZ exposure up-regulated cardiac and renal injury associated biomarkers levels that suggested the occurrence of CRS. However, these all changes were reverted, and the phenomenon of CAR was disappeared by LYC co-treatment. Based on our findings, we postulated a novel mechanism to elucidate pesticide-induced CRS and indicated that LYC can be a preventive and therapeutic agent for treating CRS by targeting MAPK/NF-κB signaling pathways.
期刊：
Journal of Hazardous Materials,2023年459:132262 ISSN：0304-3894
通讯作者：
Wang, X;Yang, XZ
作者机构：
[Wang, Xu; Guo, Pu; Wang, Xinru; Hu, Siyi; Lu, Qirong; Yang, Yaqin] Huazhong Agr Univ, Natl Reference Lab Vet Drug Residues HZAU, Wuhan 430070, Hubei, Peoples R China.;[Wang, Xu; Guo, Pu; Wang, Xinru; Hu, Siyi; Lu, Qirong; Yang, Yaqin] Huazhong Agr Univ, MAO Key Lab Detect Vet Drug Residues, Wuhan 430070, Hubei, Peoples R China.;[Wang, Xu; Guo, Pu; Hu, Siyi; Lu, Qirong; Yang, Yaqin] Huazhong Agr Univ, MAO Lab Risk Assessment Qual & Safety Livestock &, Wuhan 430070, Hubei, Peoples R China.;[Yang, XZ; Yang, Xinzhou] South Cent Univ Nationalities, Sch Pharmaceut Sci, Wuhan 430070, Hubei, Peoples R China.;[Guo, Pu; Lu, Qirong] Wuhan Polytech Univ, Hubei Key Lab Anim Nutr & Feed Sci, Wuhan 430023, Peoples R China.
通讯机构：
[Yang, XZ ] S;[Wang, X ] H;Huazhong Agr Univ, Natl Reference Lab Vet Drug Residues HZAU, Wuhan 430070, Hubei, Peoples R China.;Huazhong Agr Univ, MAO Key Lab Detect Vet Drug Residues, Wuhan 430070, Hubei, Peoples R China.;South Cent Univ Nationalities, Sch Pharmaceut Sci, Wuhan 430070, Hubei, Peoples R China.
关键词：
Agonist;BBB;Daucosterol;PGC-1α;T-2 toxin
摘要：
T-2 toxin is a common environmental pollutant and contaminant in food and animal feed that represents a great challenge to human and animal' health throughout the world. Using natural compounds to prevent the detrimental effects of T-2 toxin represents an attractive strategy. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1 alpha) is a critical regulator in various cellular processes. Recently, PGC-1 alpha activation has been reported to confer protection against neurological injuries. We aimed to identify a potent PGC-1 alpha activator from plants as a chemopreventive compound and to demonstrate the efficacy of the compound in attenuating T-2 toxin-induced blood-brain barrier (BBB) toxicity. We identified daucosterol, which binds directly to the 71-74 (-1100 to -1000 bp) position of the second promoter of human PGC-1 alpha by hydrogen bonding. An in vitro and in vivo T-2 toxin induced BBB injury model revealed that this compound can protect against this injury by increasing transepithelial/transendothelial electrical resistance, reducing sodium fluorescein (NaF) infiltration and increasing the expression of tight junction-related proteins (zonula occludens-1 (ZO-1), occludin (OCLN), claudin-5 (CLDN5)) expression. In conclusion, we identified daucosterol as representing a novel of PGC-1 alpha activators and illustrated the mechanism of specific binding site. Furthermore, we have demonstrated the feasibility of using natural compounds targeting PGC-1 alpha as a therapeutic approach to protect humans from environmental insults that may occur daily such as lipopolysaccharide.
摘要：
Deoxynivalenol (DON) is one of the most prevalent mycotoxins in feed, which causes organ toxicity in animals. Therefore, reducing DON-induced organ toxicity can now be accomplished effectively using protective agents. This review provides an overview of multiple studies on a wide range of protective agents and their molecular mechanisms against DON organ toxicity. Protective agents include plant extracts, yeast products, bacteria, peptides, enzymes, H2, oligosaccharides, amino acids, adsorbents, vitamins and selenium. Among these, biological detoxification of DON using microorganisms to reduce the toxicity of DON without affecting the growth performance of pigs may be the most promising detoxification strategy. This paper also evaluates future developments related to DON detoxification and discusses the detoxification role and application potential of protective agents. This paper provides new perspectives for future research and development of safe and effective feed additives.
摘要：
Estrus is crucial for cow fertility in modern dairy farms, but almost 50% of cows do not show the behavioral signs of estrus due to silent estrus and lack of suitable and high-accuracy methods to detect estrus. MiRNA and exosomes play essential roles in reproductive function and may be developed as novel biomarkers in estrus detection. Thus, we analyzed the miRNA expression patterns in milk exosomes during estrus and the effect of milk exosomes on hormone secretion in cultured bovine granulosa cells in vitro. We found that the number of exosomes and the exosome protein concentration in estrous cow milk were significantly lower than in non-estrous cow milk. Moreover, 133 differentially expressed exosomal miRNAs were identified in estrous cow milk vs. non-estrous cow milk. Functional enrichment analyses indicated that exosomal miRNAs were involved in reproduction and hormone-synthesis-related pathways, such as cholesterol metabolism, FoxO signaling pathway, Hippo signaling pathway, mTOR signaling pathway, steroid hormone biosynthesis, Wnt signaling pathway and GnRH signaling pathway. Consistent with the enrichment signaling pathways, exosomes derived from estrous and non-estrous cow milk both could promote the secretion of estradiol and progesterone in cultured bovine granulosa cells. Furthermore, genes related to hormonal synthesis (CYP19A1, CYP11A1, HSD3B1 and RUNX2) were up-regulated after exosome treatment, while exosomes inhibited the expression of StAR. Moreover, estrous and non-estrous cow-milk-derived exosomes both could increase the expression of bcl2 and decrease the expression of p53, and did not influence the expression of caspase-3. To our knowledge, this is the first study to investigate exosomal miRNA expression patterns during dairy cow estrus and the role of exosomes in hormone secretion by bovine granulosa cells. Our findings provide a theoretical basis for further investigating milk-derived exosomes and exosomal miRNA effects on ovary function and reproduction. Moreover, bovine milk exosomes may have effects on the ovaries of human consumers of pasteurized cow milk. These differential miRNAs might provide candidate biomarkers for the diagnosis of dairy cow estrus and will assist in developing new therapeutic targets for cow infertility.
通讯机构：
[Hongsen Xu] H;Hubei Key Laboratory of Animal Nutrition and Feed Science, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan 430023, China
摘要：
This study investigated the effects of dietary chitosan on growth, antioxidant, immunity, intestinal morphology and resistance against Aeromonas hydrophila of hybrid sturgeon (Acipenser baerii female x Acipenser schrenckii male). Sturgeons (18.18 +/- 0.08 g) were randomly divided into four groups, fed with chitosan-supplemented diets for 8 weeks and then infected with A. hydrophila. The results showed significant differences of body weight gain, specific growth rate and feed conversion ratio in sturgeon fed chitosan and control diets. The oral administration of chitosan significantly increased the acid phosphatase, alkaline phosphatase, lysozyme, myeloperoxidase, su-peroxide dismutase, glutathione peroxidase and catalase activities, as well as the complement 3 and 4 contents and disease resistance against A. hydrophila. Moreover, enhancement of muscular thickness and goblet cells in mid intestine and increase of muscular thickness and villus height in spiral valve were observed in the chitosan supplemented groups. In addition, dietary chitosan-supplemented diets mitigated the changes of antioxidant and immune activity induced by A. hydrophila challenge, as well as prevented fish from bacterial invasion. The optimal dose was 3.00 g chitosan/kg diet for hybrid sturgeon.
摘要：
Recent research has emphasized the significance of investigating the interplay between organelles, with endoplasmic reticulum mitochondria contact sites (ERMCSs) being recognized as critical signaling hubs between organelles. The objective of the current study was to assess the impact of deoxynivalenol (DON) on jejunal mitochondria, ER, and ERMCSs. Twelve piglets (35 d, 10.22 ± 0.35 kg) were randomized into two groups: control group, basal diet; the DON group, basal diet + 1.5 mg/kg DON. The findings revealed that DON decreased growth performance, induced jejunal oxidative stress, and impaired jejunal barrier function. DON was also found to induce mitochondrial dysfunction, trigger endoplasmic reticulum stress (ERS) in the piglets' jejunum, and activate mitochondrial and ER apoptosis pathways by upregulating apoptosis-related proteins (Caspase-8, Caspase-12, Bax, and CHOP). To investigate the involvement of ERMCSs in DON-induced intestinal injury, we measured the protein levels of ERMCS proteins, such as mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), and glucose-regulated protein 75 (GRP75) and Pearson's correlation coefficient of ERMCS proteins and ERMCS ultrastructure. Our finding showed that DON upregulated the protein level of Mfn2 and GRP75 and increased the percentage of mitochondria with ERMCSs/total mitochondria, the length of ERMCSs compared to the perimeter of mitochondria, and the Pearson's correlation coefficient of voltage-dependent anion-selective channel protein 1 (VDAC1) and inositol 1,4,5-triphosphate receptors (IP3Rs) in piglets' jejunum. Furthermore, DON shortened the distance between mitochondria and ER at ERMCSs. These findings suggested that DON impaired mitochondrial function, triggered ERS, and increased ERMCSs, indicating that the increased ERMCSs could be related to mitochondrial dysfunction and ERS involved in the intestinal injury of piglets induced by DON.
摘要：
Aim: Inflammation and apoptosis are main pathological processes that lead to the development of hyperuricemic nephropathy (HN). This study aims to explore whether baicalin (BA) and baicalein (BAI) can relieve the damage through PI3K/AKT/NF-kappa B signal pathway and provide more reliable and precise evidence for the treatment of HN. Methods: HN mice were induced by yeast extract with potassium oxonate (PO), and HK-2 cells were induced by monosodium urate (MSU). Molecular docking, western blot, q-PCR, and other methods were used to explore the changes of various indicators in HN mice and HK-2 cells. Results: Molecular docking results showed that BA and BAI had good binding ability with PI3K, AKT, p65 and I kappa B alpha. BA and BAI significantly ameliorated the levels of renal function, decreased the p-PI3K, p-AKT and p-p65 expression, down-regulated the BAX/BCL2 and CASP3, and blunted the mRNA levels of tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-18 in both renal tissue of HN mice and HK-2 cells induced by MSU. BA and BAI also decreased the oxidative stress level of MSU-induced HK-2 cells. Conclusion: BA and BAI were confirmed to attenuate HN through alleviating renal inflammatory and apoptosis in cells and tissues by inhibiting PI3K/AKT/NF-kappa B pathway. BA and BAI were expected to be developed as new anti-HN drugs. Summary at a glance Baicalin and baicalein were confirmed to attenuate hyperuricemic nephropathy through alleviating renal inflammatory and apoptosis in cells and tissues by inhibiting PI3K/AKT/NF-kappa B pathway.
作者机构：
[Guo, S. S.; Liu, Z. P.; Li, L. L.; Xu, P. T.; Ding, B. Y.; Chao, J. R.; Zhang, Z. F.] Wuhan Polytech Univ, Engn Res Ctr Feed Prot Resources Agr By Prod, Hubei Key Lab Anim Nutr & Feed Sci, Minist Educ, Wuhan 430023, Peoples R China.;[Lv, H. Y.] China Agr Univ, Coll Anim Sci & Technol, State Key Lab Anim Nutr, Beijing 100193, Peoples R China.;[Lv, H. Y.] Beijing Ctr Biol Co Ltd, Beijing 102600, Peoples R China.
通讯机构：
[L.L. Li; S.S. Guo] E;Engineering Research Center of Feed Protein Resources on Agricultural By-Products, Ministry of Education, Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China
关键词：
Cnicus japonicus;Lonicera flos;antioxidant status;inflammatory cytokine;laying hen
摘要：
This study was conducted to investigate the effects of Lonicera flos and Cnicus japonicus extracts (LCE) on the laying performance, egg quality, morphology, antioxidant status, inflammatory-related cytokines, and shell matrix protein expression of oviduct in laying hens. A total of 1,728 Roman Pink laying hens aged 73-wk-old were randomly assigned into 4 groups (18 replicates/group, 24 layers/replicate) fed basal diets supplemented with 0, 300, 500, and 1,000 mg of LCE per kg of diet, respectively. The trial lasted for 11 wk, including 2-wk adjustment period and 9-wk testing period. The results indicated that laying hens fed diets supplemented with LCE linearly increased egg weight, yolk color and shell thickness at wk 78 and albumen height, Haugh unit and shell thickness at wk 83 (P < 0.05). At wk 78, LCE groups linearly affected the hydrogen peroxide content in magnum (P < 0.05) and 300 mg/kg LCE groups had the highest catalase activity in isthmus (P < 0.05). At wk 83, LCE groups linearly reduced (P < 0.05) hydrogen peroxide content in the magnum and isthmus and malondialdehyde content in the uterus whereas increased catalase activity in isthmus (P < 0.05). Furthermore, LCE levels quadratically affected glutathione peroxidase activity in isthmus at wk 83 (P < 0.05). At wk 78, the mRNA expressions of inducible nitric oxide synthase and interferon-γ in isthmus and ovalbumin and ovocleidin-116 in uterus had linear effects in response to LCE levels (P < 0.05) and 1,000 mg/kg LCE group had the lowest mRNA expression of interleukin-6 in magnum (P < 0.05). At wk 83, LCE supplementation linearly decreased the mRNA expression of interleukin-1β, interferon-γ and tumor necrosis factor-α in magnum and tumor necrosis factor-α and inducible nitric oxide synthase in uterus (P < 0.05). It is concluded that LCE improved egg quality partly by modulating antioxidant status, inflammatory-related cytokines and shell matrix protein expression of oviduct in laying hens.
摘要：
Sepsis is a life-threatening organ dysfunction caused by the dysregulated response of the host to an infection, and treatments are limited. Recently, a novel selenium source, selenium-enriched Cardamine violifolia (SEC) has attracted much attention due to its anti-inflammatory and antioxidant properties, but little is known about its role in the treatment of sepsis. Here, we found that SEC alleviated LPS-induced intestinal damage, as indicated by improved intestinal morphology, and increased disaccharidase activity and tight junction protein expression. Moreover, SEC ameliorated the LPS-induced release of pro-inflammatory cytokines, as indicated by decreased IL-6 level in the plasma and jejunum. Moreover, SEC improved intestinal antioxidant functions by regulating oxidative stress indicators and selenoproteins. In vitro, TNF-α-challenged IPEC-1 cells were examined and showed that selenium-enriched peptides, which are the main functional components extracted from Cardamine violifolia (CSP), increased cell viability, decreased lactate dehydrogenase activity and improved cell barrier function. Mechanistically, SEC ameliorated LPS/TNF-α-induced perturbations in mitochondrial dynamics in the jejunum and IPEC-1 cells. Moreover, CSP-mediated cell barrier function is primarily dependent on the mitochondrial fusion protein MFN2 but not MFN1. Taken together, these results indicate that SEC mitigates sepsis-induced intestinal injury, which is associated with modulating mitochondrial fusion.
