To investigate the regulatory mechanisms and pathways of visfatin under immune stress injury in weaned piglets, we established a lipopolysaccharide-induced immune stress model in weaned piglets to study how visfatin affects peripheral immune organs and intestinal function. The results revealed that visfatin improved the inflammatory response in immune-stressed weaned piglets by reducing the levels of pro-inflammatory cytokines interleukin-1β, interleukin-6 and monocyte chemoattractant protein-1, as well as decreasing the neutrophil/lymphocyte ratio. Visfatin ameliorated oxidative stress in piglets by promoting the expression of superoxide dismutase and glutathione peroxidase. It also enhanced cell proliferation in peripheral immune organs (spleen and mesenteric lymph nodes) and suppressed cell apoptosis in these organs through the death receptor apoptosis pathway, thereby improving the immune function of weaned piglets under immune stress. Moreover, it alleviated intestinal villi damage, increased the abundance of beneficial bacteria, and elevated the levels of short-chain fatty acids, thus preserving the intestinal barrier's integrity and the balance of intestinal microbiota. Hence, these data indicate that visfatin can ameliorate immune stress injury in weaned piglets by exerting anti-inflammatory and antioxidant effects, enhancing immune organ and intestinal function.

Bacillus subtilis, as a probiotic feed additive, has been increasingly applied in livestock and poultry farming. In the present study, the environmental tolerance of a strain of Bacillus subtilis, isolated from a goat farm, was investigated. This article conducts a series of experiments on the obtained strains. The results demonstrated that the isolated strain exhibits strong tolerance to high temperatures, acidic and alkaline conditions, and high concentrations of bile salts. Furthermore, its self-aggregation rate exceeded 60% after 24 h. Whole-genome sequencing revealed that the genomes of the isolated strains were functionally annotated, identifying genes associated with amino acid metabolism, vitamin biosynthesis, and other metabolic pathways. Based on this genomic analysis, the present study further evaluated the anti-inflammatory effects of a Bacillus subtilis strain isolated in a murine model of colitis induced by dextran sulfate sodium (DSS). The analyses revealed that the DSS-treated group exhibited significantly reduced expression of intestinal tight junction proteins ZO-1 and Occludin, along with elevated expression of pro-inflammatory cytokines, compared to the PBS control group. Following oral administration of 1 × 108 CFU/mL Bacillus subtilis isolated strain suspension, the DSS-treated mice showed increased expression of ZO-1 and Occludin and decreased levels of pro-inflammatory cytokines. These results indicate that the isolated strain of Bacillus subtilis has a protective effect against colitis and demonstrates probiotic potential.

Porcine Circovirus type 2 (PCV2) is recognized as the smallest animal virus known to cause reproductive failure in sows and can be vertically transmitted through the placenta to infect piglets, leading to Postweaning Multisystemic Wasting Syndrome (PMWS). Long non-coding RNAs (lncRNAs) are involved in numerous physiological and pathological processes, closely related to trophoblast cell invasion, placental development, and fetal growth restriction. To investigate whether PCV2 can infect porcine placental trophoblast cells and to characterize the lncRNA-mRNA expression profiles following infection, this study infected porcine placental trophoblast cells with PCV2 and conducted comparative transcriptome analysis between infected and uninfected cells, followed by qPCR validation of sequencing results. The study confirmed that PCV2 successfully infects porcine placental trophoblast cells, identifying 1714 differentially expressed mRNAs and 254 differentially expressed lncRNAs post-infection. Functional enrichment analysis demonstrated that PCV2 infection modulates the growth and immune responses of porcine placental trophoblast cells. Furthermore, target genes of the differentially expressed lncRNAs were identified through colocalization and coexpression analyses. GO enrichment analysis based on the target genes of the differentially expressed lncRNAs showed abundant transcription in biological processes such as metabolism and regulation of ER-to-Golgi transport, and pathway analysis indicated that PCV2 infection impacts cell cycle, TNF, and IL-17 signaling pathways. This study reveals PCV2's infectivity in porcine placental trophoblast cells, provides the lncRNA-mRNA expression profiles post-infection, and offers critical insights for understanding PCV2's impacts and advancing lncRNA research.

Glutamine cyclase, an enzyme involved in posttranslational modifications, is encoded by the glutaminyl-peptide cyclotransferase (QPCT) gene. Gene microarray analysis revealed that the QPCT gene was highly expressed in HepG2.2.15 cells compared with that in HepG2 cells. The serum expression level of the QPCT gene was detected by ELISA and was significantly greater in HBV-infected patients than in healthy controls. The mRNA and protein expression levels of the QPCT gene were markedly greater in the HBV-expressing cell lines (HepG2.2.15, and HepG2 and Huh7 cells transfected with the pBlu-HBV plasmid) than in the HepG2 and Huh7 cells. The levels of HBV pgRNA and HBV-DNA copy number, as well as the levels of HBeAg and HBsAg, also increased in the HepG2 and Huh7 cell lines cotransfected with the QPCT gene expression plasmid and the HBV 1.3-fold plasmid. Our study indicated that HBV can promote the expression of the QPCT gene, which in turn promotes the expression and replication of HBV.

The purpose of this study was to investigate the effect of porcine reproductive and respiratory syndrome virus infection on the flora in the lungs and intestines of piglets and the histological changes in the lungs and intestines. Fourteen weaned healthy piglets of 35 day old were randomly divided into infection group（n=7） and control group（n=7） after 7 days of adaptive feeding. The piglets in the infection group were inoculated with 2 mL 1×10~5 TCID 50 ·mL -1 PRRSV JTS virus solution, and the piglets in the control group were inoculated with 2 mL DMEM. Three piglets in the infection group died on 10, 12, and 19 days, respectively. The surviving piglets in the experimental group and the control group were euthanized on 21 days, and lung, intestinal tissue samples and intestinal contents were collected. Immunohistochemical staining and HE staining were used to observe the histopathological changes of lung and intestine, and high-throughput sequencing based on 16S rRNA Gene was used to analyze the flora structure of piglet lung and intestine. The results showed that the virus was distributed in the lungs and intestines of piglets in the infection group; Compared with the control group, there were significant inflammatory reactions in the lungs and intestines of the infected group. The analysis of microbial composition, structure and diversity showed that the indexes of Chao1 and ACE of piglets in the infection group increased in the lung and decreased in the intestine, while the indexes of Shannon and Simpon increased in the lung and decreased in most intestines. At the phylum level, the proportion of harmful microorganisms such as Proteus increased, while the proportion of beneficial microorganisms such as Firmicutes decreased; In the infection group, the relative proportion of pasteurebacteriaceae, duodenal lactobacilliaceae, ileal Enterobacteriaceae, cecum, colon and rectum decreased significantly, and the proportion of Pseudomonas in lung and duodenum increased significantly; In terms of genus level, the level of beneficial bacteria and lactic acid bacteria in the infection group decreased significantly, the β diversity proves that the clustering effect of small intestine and large intestine is consistent. It can be seen that PRRSV can cause lung lesions and intestinal inflammation in piglets, and affect the composition, abundance and function of lung and intestinal flora.

临床实习是动物医学专业学生培养极为重要的一环.华中农业大学动物医院近几年在双一流学科建设经费的助力下,软硬件方面都有了质的提升,对本科生在动物医院实习管理方面狠下功夫,并取得一定成效.本文主要分析华中农业教学动物医院在提升实习管理质量方面所采用的具体方案、施行措施及出现的问题,以期为增强临床生产实习的效果提供理论指导.

Streptococcus suis (S. suis) is an important zoonotic pathogen threatening the global pig farming industry. It causes respiratory and digestive tract infections simultaneously in pigs. The balanced gut microbiota not only affects the local mucosal immune response but also involves the regulation of the immune status of the distant lung tissues that is termed as "gut-lung " axis. Whether S. suis affects the gut during lung infection and how does the intestinal microbial disturbance play role in the development of lung infection during S. suis exposure is not clear yet. Therefore, in the current study, we constructed the animal model using six-week-old mice (N = 48) divided into four groups with S. suis serotype 2 (SS2)-induced lung infection and the antibiotic treated gut microbiota dysbiosis. By means of various techniques (like HE staining, RT-qPCR, Western Blot and ELISA and viability detection) we explored that S. suis can concurrently cause intestinal tissue damage and inflammation after lung infection. Moreover, gut microbiota dysbiosis changes the balance of Th1/Th2 cells that aggravates lung injury during the infection. Thus, "gut-lung " axis of the communication between the gut microbiota and lung infection was established through the spleen and blood. In addition, intestinal dysbacteriosis can affect alveolar macrophage activity for a long time and the balance of gut microbiota plays an important role in lung infection caused by S. suis. Hence, this study clarified the pulmonary infection caused by SS2 from the perspective of the intestinal microbiota providing novel theoretical basis for the treatment of related lung diseases.

Porcine reproductive and respiratory syndrome (PRRS) is a highly contagious disease caused by PRRS virus (PRRSV), characterized by sow reproductive failure and respiratory symptoms in pigs of all ages. PRRSV mainly causes severe lung damage by invading alveolar macrophages. Visfatin is closely related to acute lung injury, immune response and inflammation along with virus invasion to the host. Therefore, the current study was performed to clarify the relationship between visfatin and PRRSV infection. We used ternary piglets to construct a piglet model to explore the expression of visfatin and tight junction protein in lung injury induced by PRRSV infection, and then further studied the inhibition effect of visfatin on PRRSV replication by PRRSV infection of Marc-145 cells. Our results indicated that both PRRSV attenuated and virulent infections could damage the lung tissues, which could not only lead to severe inflammatory reaction (such as increased expression of TNF-α, TGF-β, IL-8 and IL-10) in lung tissues of piglets, but also brought about the sharp decrease of ZO-1 and Tricellulin expressions resulting in impaired alveolar epithelial barrier. Meanwhile, we found significantly up-regulated expression of visfatin in lungs and serum of pigs after PRRSV infection that were related to both the degree of lung injury and the virulence of PRRSV strain. Moreover, visfatin might inhibit the PRRSV infection to Marc-145 cells in time dependent fashion. Hence, the current investigation provides the novel information about the effect of visfatin and PRRSV co-culture on Marc-145 cells and the effect of visfatin on PRRSV proliferation at different time points.

猪的繁殖力是决定其生产效率的重要因素,而病毒感染导致的猪流产问题严重影响猪的繁殖效率.了解猪流产相关病毒的致病机制有助于提高猪的繁殖效率,然而大量的研究主要集中在病毒与宿主的蛋白质或基因组DNA上,近年来,长链非编码RNA(long noncoding RNA,lncRNA)从新的视角揭示了病毒与宿主的相互作用,为研究二者之间的互作关系提供了新的途径.lncRNA是一组长度＞200 nt的转录本,主要通过与DNA、RNA、染色质和蛋白质互作发挥功能,在某些发育阶段、组织和疾病状态中发生特异性表达,参与机体的多种调控.lncRNA是调控病毒与宿主相互作用的关键因子,在病毒感染宿主后lncRNA发生差异性表达,对应的靶基因富集到炎症和免疫相关的信号通路,参与机体的炎症、免疫和抗病毒反应.深入了解lncRNA在猪流产相关病毒与宿主之间的调控作用,对预防和治疗病毒感染导致的猪流产具有重要意义.作者对lncRNA及其与猪流产相关病毒的关系、宿主lncRNA与病毒的互作及调控通路展开了综述,并对其存在的问题及应用前景进行了展望,以期为猪的抗病育种、猪流产药物的开发和设计及流产类相关疾病的靶点治疗等提供理论依据.

Visfatin, a multifunctional adipocytokine, is particularly important in the regulation of apoptosis and inflammation through an unidentified mechanism. Clarifying the control mechanisms of visfatin on inflammation and apoptosis in RAW264.7 cells and mice immunological organs was the goal of the current investigation. In order to create a pathophysiological model, the RAW264.7 cells were stimulated with 200 ng/mL visfatin and 20 μg/mL lipopolysaccharide (LPS), either separately or combined. The effects of exogenous visfatin on inflammation and apoptosis in RAW264.7 cells were investigated by flow cytometry assay, RNA-seq analysis and fluorescence quantitative PCR. According to the findings, exogenous visfatin exhibits dual effects on inflammation by modulating the expression of IL-1α, TNFRSF1B, and LIF as well as taking part in various signaling pathways, including the MAPK and Rap1 signaling pathways. By controlling the expression levels of Bcl2l1, Bcl2a1a, and Fas and primarily participating in the PI3K/AKT signaling pathway and Hippo signaling pathway, exogenous visfatin can inhibit apoptosis in RAW264.7 cells. The visfatin inhibitor FK866 was used to further confirm the effects of visfatin on inflammation and apoptosis in mice immune organs. Subsequently, mice spleen and thymus were collected. It is interesting to note that in LPS-treated mice, suppression of endogenous visfatin might worsen the immune system's inflammatory response and even result in rapid mortality. Additionally, endogenous visfatin promotes the apoptosis in mice immune organs by regulating the expression levels of Bcl2l1, Fas, Caspase 3, Bcl2a1a, and Bax. Together, these results imply that visfatin is a multifaceted molecule that regulates inflammation and apoptosis in RAW264.7 cells and mice immunological organs by taking part in a variety of biological processes and regulating the amounts of associated cytokines expression. Our findings offer additional understandings of how visfatin affects apoptosis and inflammation.

我国在高校人才培养中存在专业基础知识不扎实、实践动手能力不强、国际化意识淡薄的短板.依托"动物组织胚胎学"国家精品课程、国家精品资源共享课程、国家精品在线开放课程,建设和完善"精品课程+精品教材+教学文件"教育教学质量保障体系,构建"综合设计型实验+创新探索型实验+本科毕业论文设计"实践动手能力培养体系,着力培养理想信念坚定、专业基础知识扎实、实践动手能力强、国际化视野开阔的新时代大学生.

Visfatin is a multifunctional protein involved in inflammatory immune stress. The aim of current study was to explore the role of visfatin in lipopolysaccharide (LPS)-induced intestinal mucosal inflammation and to confirm its cellular effect in inflammatory immune response through silencing of Toll-like receptors (TLRs). We divided Kunming mice into three groups: Saline group, LPS group, and LPS + visfatin group and performed hematoxylin and eosin staining, immunohistochemistry, quantitative polymerase chain reaction, Western blot, enzyme linked immunosorbent assay and RNA-seq analysis. Pretreatment of visfatin improves LPS-stimulated reduction of tight junction protein 1 (ZO-1) and secretory immunoglobulin A, inhibits overexpression of Claudin-1 and vascular endothelial growth factor, and reduces intestinal mucosal damage and inflammation. RNA-seq analysis of cellular transcriptomes indicated that visfatin is involved in down-regulation of mRNA level of TLR4 as well as attenuation of protein levels of TLR8 and nucleotide-binding oligomerization domain-containing protein 2, revealing that visfatin could reduce intestinal mucosal inflammation through TLR signaling pathway in mice ileum. In RAW264.7 cells, the genes silencing of Toll/IL-1R family, such as TLR4, TLR2, and IL-1R1, was accompanied by decreased expressions of inflammatory factors (TNF-α, IL-1β, IL-6 and MCP-1) along with lower cellular visfatin levels. Hence, visfatin maintains the intestinal mucosal barrier structure and attenuates the intestinal mucosal inflammation through the TLR signaling pathway. Likewise, the Toll/IL-1R family regulates the release of visfatin, which can participate in the inflammatory reaction through the regulation of inflammatory factors.

In order to obtain the porcine recombinant visfatin protein with high expression and low endotoxin content, the current study aims to express and verify the biological activity of the purified porcine recombinant visfatin protein. Firstly, four different expression strains were successfully constructed. Then they were simultaneously induced at 37 °C for 4 h and 16 °C for 16 h. The results showed that Visfatin-pET28a-Transetta was the best strain with high protein expression and purity at 16 °C induction for 16 h. After that, endotoxin was reduced from the recombinant visfatin until the residual endotoxin was less than one endotoxin units per milliliter (EU/mL). Finally, the purified porcine recombinant visfatin protein was incubated with RAW264.7 cells. The results of cell counting kit-8 (CCK-8) showed the survival rate of the cells first increased and then decreased with the increase in visfatin concentration. When the concentration of visfatin was 700 ng/mL, the survival rate of the cells was the highest. Thereafter, control (PBS), Visfatin and Visfatin + PolymyxinB (Ploy.B) groups were incubated with the RAW264.7 cells for 6 h. Real-time quantitative polymerase chain reaction (RT-qPCR) and Enzyme Linked Immuno-Sorbent Assay (ELISA) results showed that, as compared to the control group, the expressions of interleukin (IL)-1β, tumor necrosis factor (TNF)-α and monocyte chemoattractant protein (MCP)-1 in Visfatin group were significantly increased (P < 0.05). However, there was no significant difference between the Visfatin and Visfatin + Poly.B groups, indicating that porcine recombinant visfatin protein promoted the inflammatory activity of RAW264.7 cells while the residual endotoxin did not play a role, suggesting biological activity of porcine recombinant visfatin protein.

The present study aimed to explore the effects of supplemental boron on osteogenesis of tibia and to investigate the possible relationship between additional boron and the expression of bone morphogenetic protein-2 (BMP-2) in tibia of ostrich chicks. Therefore, forty-eight African ostrich chicks (15 days old) were supplemented with 0 mg/L, 40 mg/L, 80 mg/L, 160 mg/L, 320 mg/L, and 640 mg/L of boron in drinking water for 75 days. The paraffin sections of tibia used to measure histomorphometric parameters by hematoxylin and eosin (HE) staining, Masson’s staining, and immunohistochemistry (IHC). Enzyme-linked immunosorbent assay was performed to assess the level of BMP-2, osteocalcin (BGP), glucocorticoids (GCs), osteoprotegerin (OPG), and receptor activator of nuclear factor kappa-B ligand (RANKL) in serum. TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) technique was performed to detect the cell apoptosis. The results indicated that low dose of supplemental boron (40 mg/L–160 mg/L) in drinking water promotes bone development by increasing the mature ossein. The expression of BMP2 on 45 days was higher than 90 days. Serum level of BMP-2, BGP, and GCs changed significantly in groups with low dosage of boron, and OPG/RANKL ratio was upregulated from 0 to 160 mg/L. Cell apoptosis was least in 40 mg/L and 160 mg/L groups. Taken together, low dose of boron supplemented in drinking water could promote osteogenesis and growth and development of tibia by regulating the expression and secretion of BMP-2 and providing a dynamically balanced environment for tibia growth, development, and reconstruction by regulating the concentrations of BGP, GCs, and OPG/RANKL ratio in serum.

Visfatin acts as a significant regulator of inflammatory cytokines. However, the immunological response and therapeutic effects of visfatin under bacterial stress in murine lung tissue are still not clear. To investigate the role of visfatin on lipopolysaccharide (LPS)-induced acute lung injury (ALI), thirty Kunming mice were divided into Saline, LPS, and LPS + visfatin groups. After routine blood examination, the effects of visfatin on inflammatory cytokines, lung tissue structure, and expression of inflammatory mediators were explored through hematoxylin-eosin (H&E), Masson and immunohistochemical staining, quantitative polymerase chain reaction (Q-PCR), and Western blotting. Compared with the Saline group, neutrophil percentage, peripheral blood neutrophil count, and the ratio of lymphocyte count (NLR) were upregulated in LPS group. Moreover, Masson staining showed alterations in lung tissue structure; the mRNA level of different cytokines (IL-6, IL-1β, TNF-α, IL-10, TLR4, IFN-γ) was upregulated; and the protein expression of interleukin (IL)-6, myeloperoxidase (MPO), and transforming growth factor-β1 (TGF-β) was significantly (p < 0.05) different in LPS group. Compared with LPS group, neutrophil percentage significantly decreased (p < 0.01), the numbers of lymphocytes significantly (p < 0.05) increased, NLR decreased, Masson staining of the lung was extremely different (p < 0.01), the structure of the lung was slightly damaged, and the myeloperoxidase values of lung showed no differences in LPS + visfatin. Hence, visfatin inhibits the lung inflammation induced by ALI. During the ALI, visfatin acts by decreasing NLR, downregulated the expression of MPO, enhanced antioxidant capacity, and regulated the inflammatory factors IL-1β, IL-6, IL-10, and TNF-α to reduce the lung injury.

本试验旨在探索4 ℃条件下蛋白的上样体积、流速和蛋白浓度对猪内脂素重组蛋白溶液中内毒素的去除效果和蛋白损失量的影响.该研究采用商品化、修饰过的多黏菌素B为介质,特异性地去除蛋白溶液中的内毒素.在4 C条件下,选用不同的上样体积(6、8、10、12 mL)、流速(0.125～0.75 mL/min)和蛋白浓度(0.9、1.2、1.3、1.7 mg/mL)进行内毒素的去除,使用内毒素检测试剂盒定量测定内毒素含量,使用BCA蛋白浓度测定试剂盒进行蛋白浓度的测定.试验结果表明:在4 ℃条件下,蛋白上样体积12 mL、流速0.125～0.25 mL/min时,内毒素的去除效果最佳,去除率高达99.5％,内毒素的残余量(1 EU/mL)在生物安全范围以内,并且蛋白的回收率高达90～95％.试验结果证明成功去除猪内脂素重组蛋白溶液中的内毒素,为该蛋白的相关功能研究和临床应用提供参考.

Visfatin is involved in the body’s inflammation and immune response. Inflammation could promote, while visfatin may directly or indirectly mitigate the effects of apoptosis and autophagy. Whether visfatin lessens the detrimental effects of lipopolysaccharide (LPS)-induced mouse acute lung injury (ALI) is poorly understood yet. Therefore, in the current study, the regulation mechanism of visfatin on apoptosis and autophagy was explored in Kunming mice by replicating LPS-induced inflammatory ALI model. Based on the mouse model of ALI, HE staining, TUNEL, transmission electron microscopy, immunohistochemical staining, real-time fluorescence quantitative PCR and western blot were used and the results showed that the alveolar septum was thinner than that of the LPS group, slight lung interstitial and alveolar exudation appeared, and a small number of inflammatory cell infiltration was found in the visfatin intervention group, indicating reduced tissue damage in lungs. After visfatin treatment, the expression of pro-apoptotic genes Bax, Bik, and p53 decreased and the expression of anti-apoptotic genes Bcl-2 and Bcl-xl increased, and expression of autophagy factors LC3 and Beclin1 decreased, indicating that visfatin inhibits apoptosis and reduces autophagy. The expression of PI3K and p-AKT was upregulated in the visfatin intervention group, the expression of AKT was downregulated, and the PI3K/AKT signaling pathway was activated. Hence, visfatin could activate the PI3K/AKT signaling pathway, reduce the apoptotic rate in alveolar epithelial cells and the level of autophagy in ALI by regulating the expression of autophagy factors, ultimately causing a protective effect on lung tissue.

为了研究硼对小鼠脾淋巴细胞增殖及细胞因子的影响,分别采用CCK-8、ELISA及qPCR技术检测不同浓度硼协同刀豆凝集素(concanavalin A,ConA)或脂多糖(lipopolysaccharide,LPS)对小鼠脾淋巴细胞增殖、细胞因子分泌及其mRNA表达的影响.结果 显示,当硼协同ConA作用于脾淋巴细胞时,随着硼浓度的增加,细胞存活率呈先上升后下降的趋势;IL-2的分泌量逐渐下降,IL-6的分泌量没有显著变化;IL-2、IFN-γ及IL-6 mRNA的相对表达量有所增加,IL-10则表现为逐渐下降的趋势.当硼协同LPS作用于脾淋巴细胞时,随着硼浓度的增加,细胞存活率也呈先上升后下降的趋势;显著促进了IL-2、IL-6的分泌(P＜0.05);硼浓度为1,10,50 mmol/L时,IL-2及IL-10 mRNA的相对表达量均显著低于LPS单独刺激组(P＜0.05),IL-6 mRNA的相对表达量先下降后上升,IFN-γ则表现为逐渐下降.结果 说明低浓度的硼对脾淋巴细胞的增殖及细胞因子的分泌起促进作用,高浓度的硼则对细胞产生毒性作用且在一定程度上抑制相关细胞因子的分泌,且硼对脾淋巴细胞的细胞因子表达也起到了一定的调控作用.

The nuclear-related factor 2 (Nrf2) pathway is the most important mechanism in antioxidant capacity, which regulates the cell’s redox homeostasis. In addition, Nrf2 pathway also can inhibit cell apoptosis. The mechanism of boron actions on various organs is well documented. But, it is not known whether boron can also regulate the Nrf2 pathway in the kidneys. Therefore, in this research, the actions of boron on the kidneys of ostrich chicks, especially the antioxidant effects, have been studied. The ostrich chicks were divided into six groups and supplemented with boric acid (BA) (source of boron) in the drinking water (0, 40, 80, 160, 320, 640 mg respectively) to examine apoptotic, antioxidant, biochemical, and histochemical alterations induced by boron administration in the ostrich chick’s kidney. The cellular apoptosis was assessed by terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) assay. The relative antioxidant enzymes (T-AOC, MDA, GSH-Px, SOD, GR, CAT) and biochemical indices (ALT, AST, ALP, CK, LDH, BUN, CREA, UA) in the kidney were determined by spectrophotometric method. The expression of three important genes in the antioxidant pathway (Nrf2, HO-1, GCLc) was measured by quantitative real-time PCR (qPCR), and the localization of key regulator Nrf2 was examined by immunohistochemistry (IHC) method. Western blotting was also performed to further validate our results. Our results revealed that low doses of boron (up to 160 mg) had positive effect, while high doses (especially 640 mg) caused negative effect on the development of the kidney. The cellular apoptosis was in a biphasic manner by altering the boron quantities. The low doses regulate the oxidative and enzyme activity in the kidney. The IHC and western blot showed maximum localization of Nrf2 in 80 mg/L BA dose group. Furthermore, supplementation of boron at low doses upregulated the expression of genes involved in the antioxidant pathway. Taken together, the study demonstrated that low levels of boron (up to 160 mg) inhibited the cell apoptosis, regulate the enzyme activity, and improved the antioxidant system, thus may encourage the development of the ostrich chick’s kidney, while a high amount of boron especially 640 mg/L promoted cell apoptosis and reduced the antioxidant capacity, thus caused negative effect to the ostrich chick’s kidney.

为了探讨犀牛心脏的组织学结构,取非洲白犀牛心壁,采用石蜡包埋切片方法,HE染色,明视野显微镜观察,显微摄影,对非洲白犀牛心脏的组织学结构特点进行观察,并用图像分析系统进行分析.结果显示:非洲白犀牛的心壁由内到外分为心内膜、心肌膜、心外膜3层.心内膜平均厚度约为260.48 μm;心肌膜很厚,左心室最厚,平均厚度可达32.52 mm;心外膜的平均厚度为225.13 μm.心内膜下的浦肯野纤维成群排列为2～3行,在房室交界处则形成一个特殊的结节.浦肯野纤维直径约51.98 μm,多为不规则四边形,或呈长条状,最大长径可达286 μm.细胞核多为圆形,位于细胞的边缘.心室肌纤维直径约10.19 μm,心肌横纹不明显,闰盘不明显.肌纤维排列较为紧密,心肌纤维间血管丰富.本研究为犀牛生理学和兽医临床等相关学科提供了可靠的形态学依据.