链球菌是引起奶牛乳房炎的重要病原菌,其中无乳链球菌(S.agalactiae)、停乳链球菌(S.dysgalac-tiae)和乳房链球菌(S.uberis)是奶牛乳房炎主要的致病性链球菌.为同时、快速地检测牛奶样品中这3种重要链球菌,本研究根据无乳链球菌Sip基因、停乳链球菌Mig基因及乳房链球菌pauA基因设计特异性引物,同时以细菌16SrRNA基因为内参,建立了多重PCR检测方法,并进行条件优化.结果显示,该方法最佳退火温度为58℃,最佳扩增循环数为25个循环,本方法同时检测无乳链球菌、停乳链球菌及乳房链球菌时,检测限分别为1×103 CFU/mL、1×103 CFU/mL及1×104 CFU/mL,灵敏性高.该方法对大肠杆菌、金黄色葡萄球菌、肺炎克雷伯氏菌、单核细胞增生李斯特菌等10种菌均无交叉反应,特异性好.模拟样品结果显示,当奶样中3种菌的初始浓度均为1 CFU/mL时,37℃增菌6 h即可检出乳房链球菌,增菌8 h以上3种菌可全部检出.结果表明,该多重PCR检测方法具有较好的特异性和灵敏性,对同时快速检测牛奶中无乳链球菌、停乳链球菌及乳房链球菌具有重要意义,也为奶牛乳房炎的监管、诊治提供了技术支持.

Ochratoxin A (OTA) is universally known to induce nephrotoxicity via inducing oxidative stress and apoptosis, inhibiting protein synthesis and activating autophagy. Our previous studies have proved that OTA induces nephrotoxicity in vitro and in vivo by adjusting the NOD-like receptor protein 3 (NLRP3) inflammasome activation and caspase-1-dependent pyroptosis. Based on these findings, we further investigated the protective role of selenomethionine (SeMet) on OTA-caused nephrotoxicity using the Madin-Darby canine kidney (MDCK) epithelial cells as an in vitro model, proposing to offer a new way for remedying OTA-induced nephrotoxicity by nutritional manipulation. We measured the cell vitality, lactate dehydrogenase (LDH) activity and the expression of renal fibrotic genes, NLRP3 inflammasome and pyroptosis related genes. MTT and LDH results indicated that SeMet supplementation significantly mitigated 2.0 mu g/ml OTA-induced cytotoxicity in MDCK cells (p < 0.05). Meanwhile, SeMet alleviated OTA induced increase of reactive oxygen species in MDCK cells. Then, the expressions of alpha-SMA, Vimentin, and TGF-beta were detected both in mRNA and protein levels. The results indicated 8 mu M SeMet supplementation could significantly downregulate the expression of OTA-induced renal fibrosis-related genes (p < 0.05). In addition, the upregulation of OTA-induced NLRP3 inflammasome and pyroptosis downstream genes was also significantly inhibited by 8 mu M of SeMet (p < 0.05). In summary, SeMet could alleviate OTA-induced renal fibrotic genes expression and reduce NLRP3-caspase-1-dependent pyroptosis. Therefore, SeMet supplementation may become an effective approach for preserving animals from renal injury exposed to OTA.

Ochratoxin A (OTA), a prevalent nephrotoxic mycotoxin contaminant in food and feedstuff, has been reported to induce renal injury. To disclose the nephrotoxicity of continuous administration of OTA and to investigate potential mechanisms related to pyroptosis, male C57BL/6 mice were intraperitoneally injected with 1.0 and 2.0 mg/kg B.W. OTA every other day for 14 days. At 2.0 mg/kg B.W. OTA administration significantly increased histological injury and renal fibrosis molecules (α-SMA, Vimentin, TGF-β) and activated the NOD-like receptor protein 3 (NLRP3) inflammasome and induced pyroptosis compared with control. In the in vitro tests, Madin–Darby canine kidney (MDCK) epithelial cells were exposed to 0–4.0 μg/ml OTA for 24 h in serum-free medium. Data showed that OTA dose-dependently affected cell viability and significantly up-regulated renal fibrosis genes (α-SMA, Vimentin, TGF-β). 2.0 μg/ml OTA significantly induced NLRP3 inflammasome activation and caspase-1-dependent pyroptosis, increasing the expression and secretion of pro-inflammatory cytokines (IL-6, TNF-α) and pyroptosis-related genes (GSDMD, IL-1β, IL-18) in MDCK cells. These outcomes were significantly abrogated after inhibiting NLRP3 activation with inhibitor MCC950 and silencing NLRP3 with small interfering RNA (siRNA). Furthermore, knockdown of caspase-1 also ameliorated OTA-induced renal fibrosis via the inhibition of pyroptosis. Collectively, the chosen doses of OTA-triggered nephrotoxicity through NLRP3 inflammasome activation and caspase-1-dependent pyroptosis both in vitro and in vivo.

Ochratoxin A (OTA), one of the major food contaminating mycotoxins, has been reported to cause renal fibrosis through pyroptosis, but the detailed mechanism of its nephrotoxicity remains to be further investigated. Autophagy can be seen in the physiological and pathological processes of the body, and whether its role is positive or negative has not been fully elucidated. The aim of this paper was to explore the role of autophagic-inflammasomal pathway on pyroptosis caused by low levels of OTA in vitro. The results showed that OTA dose-dependently decreased cell viability in PK-15 cells and the half-maximal inhibitory concentration (IC50) was 5.9 µM. OTA could significantly increase pro-inflammatory cytokines (TNF-α, IL-1β, IL-18, IL-6) expression, induced pyroptosis and NLRP3 inflammasome formation at 1.0-4.0 µM for 48 h according to the results of qPCR, Western blotting, Immunofluorescence staining and morphologic observation. But MCC950 (an inhibitor of NLRP3) treatment or caspase-1 (sicaspase-1) knockdown could restore these changes. Additionally, we further found that reactive oxygen species (ROS) contributed to OTA-induced NLRP3 inflammasome and pyroptosis in PK-15 cells as indicated by Western blotting and immunofluorescence. Besides, we indicated that OTA induced autophagy via AKT/mTOR signaling pathway. And 3-MA (an inhibitor of autophagy) treatment or ATG5 (siATG5) knockdown enhanced ROS levels and NLRP3 inflammasome formation exposed to OTA. Taken together, our results elaborated that ROS/NLRP3-inlflammasome-mediated pyroptosis could be involved in the low levels of OTA-induced nephrotoxicity, which was negatively regulated by autophagy.

Ochratoxin A (OTA), one of the most deleterious mycotoxins, could cause a variety of toxicological effects especially nephrotoxicity in animals and humans. Taurine, a wide-distributed cytoprotective amino acid, plays an important role as a basic factor for maintaining cellular integrity homeostasis. However, the potential effect of taurine in OTA-induced nephrotoxicity remains unknown. In the present study, we demonstrated that OTA treatment at 4.0-8.0 μM increased apoptosis in PK-15 cells as shown by increased the ratio of apoptosis and protein expression of Bax and cleaved-caspase-3, decreased protein expression of Bcl-2. Meantime, OTA treatment triggered autophagy, as indicated by markedly increased the protein expression of LC3-II and fluorescence intensity of GFP-LC3 dots. Taurine supplementation decreased OTA-induced cytotoxicity and attenuated apoptosis as shown by the decreased Annexin V/PI staining and the decreased expression of apoptosis-related proteins including Bax and caspase-3. Meanwhile, taurine attenuated OTA-induced autophagy by decreased the protein expression of LC3-II and fluorescence intensity of GFP-LC3 dots to maintain cellular homeostasis. In conclusion, taurine treatment could alleviate OTA-induced apoptosis and inhibit the triggered autophagy in PK-15 cells. Our study provides supportive data for the potential roles of taurine in reducing OTA-induced renal toxicity.

Selenium deficiency and T-2 toxin exposure may contribute to the development of Keshan disease characterized by congestive cardiomyopathy. The aim of this study was to explore the role of autophagy in the aggravation of selenium deficiency on T-2 toxin-induced damages on primary cardiomyocyte. Our present study demonstrated that 0.25-1 mu M T-2 toxin damaged primary cardiomyocytes and selenium deficiency exacerbated T-2 toxin-induced damages by measuring the levels of MTT, lactate dehydrogenase and cleaved-caspase 3. T-2 toxin triggered autophagy in primary cardiomyocytes, as indicated by markedly increased expressions of LC3-II and Beclin-1 mRNA levels. Rapamycin (autophagy agonist) treatment increased autophagy levels and decreased the cytotoxicity caused by T-2 toxin while 3-methyladenine (autophagy inhibitor) treatment reduced autophagy levels and enhanced the cytotoxicity of T-2 toxin, suggesting that autophagy protect primary cardiomyocytes from the cytotoxicity of T-2 toxin. Selenium deficiency lowered cytoprotective autophagy in the primary cardiomyocytes treated by T-2 toxin. It can be concluded that autophagy induced by T-2 toxin plays a role in protecting primary cardiomyocyte, but selenium deficiency decreases the protective autophagy and then exacerbate T-2 toxin-induced damages. Our finding may partly interpret the combination effects of selenium deficiency and T-2 toxin on the development of Keshan disease.

Ochratoxin A (OTA) is reported to induce nephrotoxicity and immunotoxicity in animals and humans. However, the underlying mechanism and the effects of OTA on DNA damage have not been reported until now. The present study aims to investigate OTA-induced cytotoxicity and DNA damage and the underlying mechanism in PK15 cells and PAMs. The results showed that OTA at 2.0–8.0 µg/mL for 24 h induced cytotoxicity and DNA damage in PK15 cells and PAMs as demonstrated by decreasing cell viabilities and mRNA levels of DNA repair genes (OGG1, NEIL1 and NEIL3), increasing LDH release, Annexin V staining cells, apoptotic nuclei and the accumulation of γ-H2AX foci. OTA at 2.0–8.0 µg/mL increased DNMT1 and SOCS3 mRNA expressions about 2–4 fold in PK15 cells or 1.3–2 fold in PAMs. OTA at 2.0–8.0 µg/mL increased DNMT1, SOCS3, JAK2 and STAT3 protein expressions in PK15 cells or PAMs. DNMT inhibitor (5-Aza-2-dc), promoted SOCS3 expression, inhibited JAK2 and STAT3 expression, alleviated cytotoxicity, apoptosis and DNA damage induced by OTA at 4.0 µg/mL in PK15 cells. While, in PAMs, 5-Aza-2-dc had no effects on SOCS3 expression induced by OTA at 4.0 µg/mL, but inhibited JAK2 and STAT3 expression, and alleviated cytotoxicity, apoptosis and DNA damage induced by OTA. JAK inhibitor (AG490) or STAT3-siRNA alleviated OTA-induced cytotoxicity and DNA damage in PK15 cells or PAMs. Taken together, nephrotoxicity instead of immunotoxicity of OTA is induced by targeting SOCS3 through DNMT1-mediated JAK2/STAT3 signaling pathway. These results provide a scientific and new explanation of the underlying mechanism of OTA-induced nephrotoxicity and immunotoxicity.

犬巴贝斯虫病是通过中间媒介蜱传播的一种血液原虫病,该病在春、夏和秋季均可发生,严重地危害到了各类犬只的健康.感染犬在临床上主要表现为精神不振、食欲减退、持续不定期高热、贫血、黄疸、血红蛋白尿等现象.本文就2018年8月26日接诊的一例贵宾犬巴贝斯虫病的诊断、治疗以及护理和预后等进行简要分析,旨在为宠物饲养者和临床宠物医院从业人员提供借鉴或参考.

Porcine circovirus type 2 (PCV2) is an economically important swine pathogen but some extra trigger factors are required for the development of PCV2-associated diseases. By evaluating cap protein expression, viral DNA copies and the number of infected cells, the present study further confirmed that oxidative stress can promote PCV2 replication. The results showed that oxidative stress induced autophagy in PCV2-infected PK15 cells. Blocking autophagy with inhibitor 3-methyladenine or ATG5-specific siRNA significantly inhibited oxidative stress-promoted PCV2 replication. Importantly, autophagy inhibition significantly increased apoptosis in oxidative stress-treated PK15 cells. Suppression of apoptosis by benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone in conditions of autophagy inhibition restored PCV2 replication. Taken together, autophagy protected host cells against potential apoptosis and then contributed to PCV2 replication promotion caused by oxidative stress. Our findings can partly explain the pathogenic mechanism of PCV2 related to the oxidative stress-induced autophagy.

AIMS:The present study was to investigate the protective effects of Zn supplementation in OTA-induced apoptosis of Madin-Darby canine kidney (MDCK) epithelial cells and explore the potential mechanisms. Aiming to provides a new insight into the treatment strategy of OTA-induced nephrotoxicity by nutritional regulation.MAIN METHODS:Initially, through MTT and LDH assay revealed that Zn supplementation significantly suppressed OTA-induced cytotoxicity in MDCK cells. Then, the production of reactive oxygen species (ROS) was detected by using a DCFH-DA assay. Annexin V-FITC/PI, Hoechst 33258 staining and Flow cytometry were used to detect the apoptosis. The expressions of apoptosis-related molecules were determined by RT-PCR, Western blotting. Interestingly, OTA treatment slightly increased the levels of Metallothionein-1 (MT-1) and Metallothionein-2 (MT-2) by using RT-PCR, Western blotting assay; while Zn supplementation further improved the increase of MT-1 and MT-2 induced by OTA. However, the inhibitive effects of Zn supplementation were significantly blocked after double knockdown of MT-1 and MT-2 by using Small Interfering RNA (siRNA) Transfection method.KEY FINDINGS:Our study provides supportive data for the potential roles of Zn in reducing OTA-induced oxidative stress and apoptosis in MDCK cells.SIGNIFICANCE:Zn is one of the key structural components of many proteins, which plays an important role in several physiological processes such as cell survival and apoptosis. This metal is expected to contribute to the conservative and adjuvant treatment of kidney disease and should therefore be investigated further.

Deoxynivalenol (DON) is well-known enteropathogenic mycotoxin which can alter intestinal barrier functions. Consistently, Ochratoxin A (OTA) ingestion has been found to induce intestinal injuries, including inflammation and diarrhea. However, little is known whether OTA aggravates DON-induced toxicity. This study is designed to explore the effects of OTA on DON-induced intestinal barrier function and involved mechanism. Our results showed either DON or OTA could disrupt intestinal barrier function in a time-and dose-dependent manner, as demonstrated by decreased transepithelial electrical resistance (TEER) and increased paracellular permeability to 4 kDa dextran. However, to eliminate the involvement of cell death, nonlethal concentrations of DON and OTA were used in following experiments. The nontoxic concentration of OTA was observed to aggravate DON-induced intestinal barrier dysfunction, accompanied with tight junction disruption (Claudin-3 and Claudin-4). Moreover, nontoxic concentrations of OTA aggravated DON-induced up-regulation of pro-inflammatory cytokines expression and activated nuclear factor-kappa B (NF-kappa B) in IPEC-J2 cells. Adding NF-kappa B inhibitor (PDTC) alleviated the aggravating effects of nontoxic concentrations of OTA on DON-induced intestinal barrier dysfunction and inflammation. These findings indicate that nontoxic concentrations of OTA promoted DON-induced barrier dysfunction via NF-kappa B signaling pathway. Our experiment suggests that exposure to nontoxic concentrations of toxins also poses potentially harmful effects.

We investigated the effects of selenium-enriched probiotics (SP) on broiler meat quality under high ambient temperature and explore their underlying mechanisms. A total of 200 1-day-old male broiler chicks (Ross 308) were randomly allotted to four treatment groups, each with five replicates, in groups of ten birds. These birds were fed a corn-soybean basal diet (C), a basal diet plus probiotics supplementation (P), a basal diet plus Se supplementation in the form of sodium selenite (SS, 0.30 mg Se/kg), and a basal diet with the addition of selenium-enriched probiotics (SP, 0.30 mg Se/kg). The experiment lasted for 42 days. The birds were sacrificed by cervical dislocation, and the breast muscles were removed for further process. Our results showed that SP diet significantly increased (p < 0.05) the physical (pH, colors, water holding capacity, drip loss, shear force) and sensory characteristics of breast meat. All P, SS, and SP supplementation enhanced the antioxidant system by increasing (p < 0.05) the Se concentrations, glutathione (GSH) levels, activities of glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) whereas decreasing (p < 0.05) malondialdehyde (MDA) levels, with SP being higher than P and SS. Moreover, SP diet significantly upregulated (p < 0.05) the mRNA levels of glutathione peroxidase genes (GPx1, GPx4) while it downregulated heat stress biomarkers such as heat shock protein (HSP) 70 as compared to C, P, and SS diets. In conclusion, our findings suggest that SP may function as beneficial nutritive supplement that is capable of improving meat quality during the summer season.

The aim of this study was to evaluate the effects of bush sophora root polysaccharide (BSRPS) on the aflatoxin B1 (AFB1)-induced hepatotoxicity and to explore the underlying mechanisms. The primary chicken hepatocytes were used as the model in the present experiment. The results showed that AFB1 induced hepatotoxicity of chicken hepatocytes in a dose dependent manner as demonstrated by decreasing cell viability and increasing LDH activity, ALT and AST levels. AFB1 at 0.16 μM significantly increased the levels of hepatic cytochrome P450 1A5 (CYP450 1A5) mRNA and malondialdehyde (MDA) and decreased the activity and mRNA level of manganese superoxide dismutase(SOD2) and the glutathione peroxidases (GSH-Px) activity in the hepatocytes compared with the blank control. BSRPS at 8.93 μM, 17.86 μM, and 35.72 μM supplementation could significantly reverse the above-mentioned changes induced by AFB1, and 17.86 μM of BSRPS has the largest effects on protecting the AFB1-induced hepatocytes damage. Knock-down of SOD2 by SOD2-specific siRNA significantly eliminated the protective effects of BSRPS on AFB1-induced the increase of CYP450 1A5 mRNA levels and hepatotoxicity. These results suggested that the BSRPS has protective effects on AFB1-induced hepatotoxicity by down-regulating CYP450 1A5 mRNA level via up-regulating SOD2 expression in the primary chicken hepatocytes.

In this study,a TaqMan-based duplex real-time PCR assay was established for the detection of Vibrio parahaemolyticus (VP) and Vibrio cholera (VC).The specific primers and probes were designed based on the toxR gene of V.Parahaemolyticus and the ompW gene of V.cholera.The 5'-ends of probes for toxR and ompW were labeled with FAM and CY5 respectively,and their 3'-ends were all labeled with quencher BHQ1.The results showed that this PCR assay could unambiguously detect V.parahaemolyticus and V.cholera with a minimum detection limit of 10 CFU/mL indicating high sensitivity.The specificity of the assay showed that the two bacteria had no cross reaction with other pathogens (Such as Escherichia coli O157,Salmonella,Vibrio mimicus and Vibrio vulnificus).In addition,it had good repeatability between the batch and within the group,and the coefficient of variation was less than 1.5％.When the developed method was applied to assaying food samples artificially contaminated by VP or VC,the detection limit was found to be 100 CFU/mL (VP) and 50 CFU/mL (VC) in shrimp samples or 50 CFU/mL (VP) and 50 CFU/mL (VC) in shellfish samples per reaction without an enrichment step.The minimum detection limit of the method was 1 CFU/mL in shrimps contaminated by VP or VC enriching for 2 hours.A conclusion could be drawn that the duplex real-time PCR assay established here was characteristic of high sensitivity,strong specificity,and good repeatability;and the entire detection procedure including DNAextracted by this method could be completed within 1 to 3 hours.This duplex real-time PCR assay was effective in rapid detection of V.parahaemolyticus and V.cholera.

兽医临床诊断学是高等农业院校动物医学专业的一门基础核心课,是衔接兽医基础与兽医临床各课程的桥梁.传统的"以教师为主体"教学形式,其教学重点仍停留在查症、认症、辩症等相关理论的讲解上,往往是老师一人在台上讲,学生在台下不吭声地被动学习,教学效果欠佳.在现代网络信息技术的支持下,我们实施了"课前学习微视频化、课堂教学微课化、课后巩固延伸微信化"教学新模式,激发了学生的学习兴趣和热情,学生课堂的参与度增强,师生合作互动,让学生真正做到学到、学会、学懂.

Lycium barbarum polysaccharides (LBPs) have multiple biological and pharmacological functions, including antioxidant, anti-inflammatory and anticancer activities. This research was conducted to evaluate whether LBPs could alleviate carbon tetrachloride (CCl4)-induced liver fibrosis and the underlying signaling pathway mechanism. Fifty male wistar rats were randomly allocated to five groups (n=10): control, CCl4 and CCl4 with 400, 800 or 1600mg/kg LBPs, respectively. Each wistar rat from each group was used for blood and tissue collections at the end of experiment. The results showed that CCl4 induced liver fibrosis as demonstrated by increasing histopathological damage, α-smooth muscle actin expression, aspartate transaminase activities, alkaline phosphatase activities and alanine aminotransferase activities. LBPs supplementation alleviated CCl4-induced liver fibrosis as demonstrated by reversing the above parameters. In addition, CCl4 treatment induced the oxidative injury, increased the mRNA levels of tumor necrosis factor-α, monocyte chemoattractant protein-1 and interleukin-1β, and up-regulated the protein expressions of toll-like receptor 4 (TLR4), TLR2, myeloid differentiation factor 88, nuclear factor-kappa B (NF-kB) and p-p65. LBPs supplementation alleviated CCl4-induced oxidative injury, inflammatory response and TLRs/NF-kB signaling pathway expression by reversing the above some parameters. These results suggest that the alleviating effects of LBPs on CCl4-induced liver fibrosis in wistar rats may be through inhibiting the TLRs/NF-kB signaling pathway expression.

To investigate the effect of selenium on hair follicle development and expression of GPx4 protein in rabbit hair,60 New Zealand rabbits which initial weight was (690.0±7.0) g were divided into two groups(C and SS),30 rabbits in each group (male and female).The C group was fed on basal diet,the determination of dietary selenium level was 0.20 mg/kg,SS group of dietary sodium selenite,the determination of dietary selenium level was 0.36 mg/kg.Feeding 30 d.Rabbit hair follicle group structure of C group arranged neatly,a primary hair follicle was surrounded by a number of secondary follicles,hair follicles and oval cross section was normal.New Zealand rabbit hair follicle group structure of SS group was disordered,transverse section of primary follicles and part of secondary follicles were not normal.The number of secondary follicles in SS group was decreased by 36.64％ than that in C group (P＜0.05).The antioxidant properties of the skin,compared with the C group,the GPx4 activity of SS group in skin tissue significantly decreased by 58.09％ (P＜0.01),SOD activity significantly decreased by 34.39％ (P＜0.05),T-AOC activity significantly decreased by 59.25％ (P＜0.01),the content of MDA significantly increased by 242.66％ (P＜0.05).The expression of GPx4 and EGFR proteins of New Zealand rabbit skin hair follicles in SS group were significantly decreased by the 131.70％ (P＜0.01)and 128.60％ (P＜0.01) than that in C group.

In order to ensure the prophylactic effects of Se-enriched Lactobacillus on canine urolithiasis caused by too much oxalic acid from daily ration,20 local dogs were randomly divided into 5 groups,including the control group,0.5％ oxalic acid positive group,0.5％ oxalic acid and organic selenium group,0.5％oxalic acid and lactic acid bacteria group,0.5％oxalic acid and Se-enriched Lactobacillus group.The corresponding components were added to the diets,respectively.At the time of 15 d and 30 d,the blood biochemical indexes and blood selenium contents were measured both in blood and urine.The results showed that the addition of Se-enriched Lactobacillus in diet could significantly enhance the decomposition of oxalate and improve the body's antioxidant capacity,so as to prevent the formation of calcium oxalate stones.

This study was conducted to investigate the effects of arginine or N-carbamylglutamate (NCG) on production performance of lactation doe and growth performance,antioxidant ability of weaning rabbit.A total of 45 lactation does with similar weights were randomly divided into 5 groups.The control group was fed with basal diet,experiment group Ⅰ to Ⅳ were fed basal diet with 0.3％,0.6％ Arg and 0.03％,0.06％ NCG,respectively.The experiment lasted for 35 d.While,the 35 d weaned rabbits,with similar weights were randomly divided into 5 groups.The experiment diets were the same with the doe treatments.The experiment lasted for 21 d.The results showed that does' weights were significantly increased in group Ⅱ and Ⅳ.The rate of pregnancy again in group Ⅱ was the best.On 21d and 35d,the body weight of lactating rabbits in group Ⅱ and Ⅳ was significantly higher than that in control group (P＜0.05).In weaned young rabbit experiment,the finial weight and the average daily gain (ADG) of young rabbit in each treatment group were significantly higher than that in control group (P＜0.05).The average daily feed intake (ADFI) in the group Ⅱ and Ⅲ was significantly higher than that in the control group (P＜0.05),but there was no significant difference in the ratio of feed to gain (F/G).And ADFI and F/G in group Ⅰ and Ⅳ were significantly low when compared with control group (P＜0.05).However,no significant differences were observed in serum antioxidant ability of 35 d lactation rabbit between treatment and control group.After weaning 21 days,compared with control group,SOD activities of young rabbit serum in group Ⅲ and Ⅳ were significantly increased (P＜0.05).In conclusions,adding arginine or NCG can maintain does body weights,improve lactation rabbit body weights.At the same time,it can also improve weaning rabbit ADG and body weight at 56 d and decrease F/G.Even more,NCG can increase anti-oxidant capacity of weaned rabbits.

This study aims to evaluate the protective effects of selenomethionine (SeMet) on aflatoxin B1 (AFB1)-induced hepatotoxicity in primary chicken hepatocytes. Cell viability and lactic dehydrogenase activity assays revealed the dose dependence of AFB1 toxicity to chicken hepatocytes. AFB1 concentrations of >0.05 μg/mL significantly reduced glutathione and total superoxide dismutase levels and increased the malondialdehyde concentration and cytochrome P450 enzyme 1A5 (CYP450 1A5) mRNA levels (P < 0.05). AFB1, however, did not affect CYP450 3A37 mRNA levels. Supplementation with 2 μM SeMet protected against AFB1-induced changes and significantly increased selenoprotein W (SelW) mRNA levels (P < 0.05). Additionally, SelW knockdown attenuated the protective effect of SeMet on AFB1-induced damage and significantly increased the level of CYP450 1A5 expression (P < 0.05). Therefore, SeMet alleviates AFB1-induced damage in primary chicken hepatocytes by improving SelW expression, thus inhibiting CYP450 1A5 expression.