BACKGROUND:Dietary aflatoxin B1 (AFB1) contamination poses a significant threat to livestock health and food safety by causing severe liver injury. l-Aspartic acid (l-Asp) is known for its antioxidant and anti-inflammatory properties but its potential to mitigate AFB1-induced hepatotoxicity and associated intestinal dysbiosis in rabbits remains unexplored. To address this, 35-day-old rabbits (n = 50) were assigned randomly to five groups: a control group, an AFB1 (0.3 mg kg-1 bodyweight) group, and three groups receiving dietary l-Asp supplementation (0.5%, 1.0%, or 1.5%) for 21 days, with AFB1 administered during the final 5 days. RESULT:The results demonstrated that l-Asp pretreatment significantly alleviated AFB1-induced impairments in growth performance and serum biochemical parameters. It also reduced hepatic collagen fiber deposition, ameliorated ileal barrier damage, and restored the gut microbiota composition and normalized bile acid metabolism, which correlated with the regulation of key metabolic receptors. CONCLUSION:This study established 1.0% l-asp as an effective, gut-liver axis-targeted intervention against AFB1 toxicity in rabbits. This work emphasizes its nutritional potential and provides a clear rationale for future studies to elucidate its molecular mechanisms. © 2026 Society of Chemical Industry.

Previous studies conducted in our laboratory have demonstrated that dietary supplementation with Bacillus coagulans BC66 (BC66) can mitigate intestinal, renal, and hepatic injuries induced by Klebsiella pneumoniae in rabbits. However, the potential of Bacillus coagulans BC66 in protecting against Klebsiella pneumoniae- induced acute lung injury remains unexplored. Therefore, the present study aimed to investigate the protective mechanism of Bacillus coagulans BC66 against acute lung injury induced by Klebsiella pneumoniae in rabbits using histological examination (hematoxylin and eosin staining, HE staining), immunofluorescence, immunohistochemistry and Western blotting. Dietary supplementation with Bacillus coagulans BC66 alleviated acute lung injury in rabbits by reducing inflammatory cell infiltration, alleviating alveolar wall thickening, and minimizing alveolar lumen narrowing. Additionally, BC66 enhanced the pulmonary barrier by upregulating proliferating cell nuclear antigen (PCNA) expression and modulating the levels of tight junction proteins, including Occludin, Claudin-1, and ZO-1. Importantly, BC66 restored T helper 17/regulatory T cell (Th17/Treg) immune balance, which was identified as the central mechanism underlying its protective effects. This immune modulation was associated with reduced production of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), and contributed to the improvement of pulmonary barrier integrity. Furthermore, the regulation of Th17/Treg balance was accompanied by downstream attenuation of oxidative stress and ferroptosis, as evidenced by increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), decreased malondialdehyde (MDA) levels, and modulation of ferroptosis-related proteins, including solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), partly through activation of the Keap1/Nrf2/HO-1 pathway.In conclusion, this study demonstrates that Bacillus coagulans BC66 protects against Klebsiella pneumoniae-induced acute lung injury primarily through restoring Th17/Treg immune balance, with subsequent downstream effects on inflammation, epithelial barrier function, oxidative stress, and ferroptosis. Notably, pretreatment with 1 × 10⁶ colony-forming units per gram (CFU/g) was the most effective. These findings provide a theoretical basis for using Bacillus coagulans BC66 as a preventive agent against acute lung injury induced by Klebsiella pneumoniae in rabbits.

This study aimed to explore the protective effects of selenomethionine (SeMet) against deoxynivalenol (DON)-induced intestinal injury in young rabbits. Forty 35-day-old rabbits were randomly assigned to four groups: control, DON, SeMet, and DON + SeMet. Rabbits in SeMet and DON + SeMet groups received oral 0.2 mg/kg SeMet daily for 21 days. From day 15, DON and DON + SeMet rabbits were treated with 0.5 mg/kg BW DON daily for 7 days. Jejunal samples were collected to evaluate villus-crypt morphology and goblet cell number via HE and PAS staining. Quantitative real-time PCR, ELISA, immunohistochemistry and Western blotting were used to detect intestinal gene and protein expression. The results demonstrated that DON activated the jejunal NF-κB pathway while suppressing mTORC1 signaling. DON triggered oxidative stress and inflammation, disrupted jejunal structure, inhibited tight junction protein expression, and induced epithelial apoptosis. SeMet supplementation efficiently alleviated DON-induced histological damage, oxidative stress and inflammation, reduced apoptosis, and restored tight junction protein levels. Collectively, SeMet ameliorates DON-caused jejunal mucosal injury via modulating mTORC1 and NF-κB signaling pathways.

Klebsiella pneumoniae (KP) infection often causes diarrhoea and intestinal barrier damage in young rabbits. The objective of this study was to explore whether selenomethionine (SeMet) can attenuate the jejunal injury caused by KP in rabbits. Therefore, we investigated the protective effect of SeMet by performing haematoxylin-eosin (HE), alcian blue periodic acid Schiff (AB-PAS), proliferating nuclear antigen (PCNA), TUNEL and immunofluorescence staining. In addition, the concentrations of Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Tumor necrosisfactor-α (TNF-α) and Interleukin-10 (IL-10) in the jejunal tissue were detected by enzyme-linked immunosorbent assay (ELISA). The results showed that after KP infection, the productivity of rabbits decreased, and the mucosal barrier of the jejunum was damaged. Moreover, KP induced jejunal inflammation, activated the TLR4/NF-κB signalling pathway, and promoted the expression of the IL-1β, IL-6, and TNF-α. In addition, KP increased the apoptotic response of intestinal cells and upregulated the expression of caspase-3 and caspase-9. SeMet pretreatment significantly decreased the degree of intestinal epithelial cell apoptosis. Therefore, we showed that SeMet can reduce inflammation and enhance intestinal barrier function to improve the production performance of rabbits infected with KP.

The chemotherapeutic drug cyclophosphamide (CTX) may damage the ovarian tissue of females and induce premature ovarian insufficiency (POI). This study aimed to investigate the therapeutic effect of adipose-derived mesenchymal stem cell-conditioned medium (ADSC-CM) on CTX-induced POI mice, and to provide new support for the clinical use of cell-free therapy for POI. Female mice were treated with CTX intraperitoneal injection for 2 weeks, followed by ADSCs or ADSC-CM by intravenous injection for 2 weeks. At the end of the experiment, various parameters were assessed, including ovarian interstitial fibrosis, cell proliferation, follicular count, the levels of follicle-stimulating hormone (FSH) and estradiol (E2), and the expression of gonadal hormone receptor. Additionally, we assessed the levels of oxidative stress, apoptosis, and apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK) signaling pathway-related proteins and genes in ovarian tissue. The results showed that ADSCs or ADSC-CM treatment reduced ovarian interstitial fibrosis, promoted the proliferation of cells in the follicles, and increased the number of follicles and ovarian function. In addition, ADSCs and ADSC-CM also reduced the levels of ovarian oxidative stress, decreased the apoptosis of granulosa cells (GCs), and inhibited the activation of ASK1/JNK signaling pathway. In conclusion, our study confirmed that ADSC-CM, like ADSCs, could exert therapeutic effects in POI diseases, and the underlying mechanism may be related to the inhibition of oxidative stress-mediated activation of ASK1/JNK signaling pathway. This study has important implications for the development of cell-free therapies for the clinical treatment of POI diseases.

Background: In recent years, relevant studies had shown that a large number of adipokines were involved in energy homeostasis in the body, regulating the balance of glucose and lipid metabolism. Resistin was a special type of adipose factor and its discovery and related studies had shown a close relationship between resistin and heart disease. However, there was relatively little research on the structure of heart tissue, so we conducted this present study. Methods: In order to study the effect of resistin on the heart structure of mice, 20 healthy C57BL/6 mice were randomly divided into experimental and control groups(n=10). The mice of the experimental group were injected with 20 ìl/d of resistin solution through the tail vein. The mice of the control group were injected with the same volume of double distilled water. HandE staining, Wheat Germ Agglutinin (WGA) staining, Masson’s trichrome staining and electron microscopy were used to observe the changes of microscopic structure and ultrastructure of mouse cardiomyocytes. Result: The results of HandE staining showed that the myocardial cells in the experimental group were disordered, the cytoplasm was loosely distributed and the gap between adjacent cells increased. WGA staining showed that the fluorescence green intensity of the mice in the experimental group was higherthan that of the control group. The myocardial cell membrane thickened, the average cross-sectional area of cardiomyocytes was larger than that of the control group. The results of the Masson staining showed that the staining of the cytoplasm of myocardial cells in the experimental group was significantly shallow and the blue structure was significantly increased. The electron microscopy showed that the number of mitochondria decreased and the mitochondria lightly dissolved or disappear. This study confirmed that resistin could change the content of collagen fibers and myofibrils in myocardial cells, induce cardiac hypertrophy and cause certain damage to mitochondria of cardiomyocytes. It was speculated that it could affect the physiological function of cardiomyocytes to some extent.

Probiotics effectively alleviate host diarrhoea, but the specific mechanism is not clear. Therefore, we explored the protective mechanism of Bacillus coagulans (BC) on intestinal barrier injury induced by Klebsiella pneumoniae (K. pneumoniae) in rabbits by HE, immunofluorescence and 16S rRNA. The results showed that BC pretreatment alleviated the changes in average daily gain, average daily feed intake and FCR caused by K. pneumoniae in rabbits. Moreover, BC alleviated the inflammatory cell infiltration, intestinal villus reduction, crypt deepening and goblet cell reduction caused by K. pneumoniae in rabbits. Further research revealed that BC improved the intestinal barrier by improving the mechanical barrier, chemical barrier, immune barrier and microbial barrier. Specifically, BC improved the intestinal mechanical barrier by improving the intestinal structure, increasing the protein expression of PCNA, increasing the number of goblet cells, and altering the expression of occludin, claudin-1 and ZO-1. BC improved the intestinal chemical barrier by regulating the expression of MUC1 and MUC2 and inhibited the TLR4/MyD88/NF-kappa B signalling pathway by altering the expression levels of the inflammatory factors IL-1 beta, IL-6 and TNF-alpha, thus optimizing the intestinal immune barrier. In addition, adding BC to the diet improved the intestinal microbial barrier of rabbits by reducing the abundance of harmful bacteria and increasing the abundance of beneficial bacteria. In summary, BC protects against K. pneumoniae-induced intestinal barrier damage by improving intestinal morphology, mitigating the inflammatory response and regulating the microbial composition. Among the pretreatments, the pretreatment effect of 1 x 106 CFU/g was the best. This study provides a theoretical basis for the use of BC to prevent and treat diarrhoea caused by K. pneumoniae in rabbits.

The aim of this study was to investigate the alleviating effect of selenomethionine (SeMet) on aflatoxin B1 (AFB1)-induced testicular injury in rabbits. Twenty-five 90-d-old rabbits were randomly divided into 5 groups (the control group, the AFB1 group, the 0.2 mg/kg SeMet + AFB1 group, the 0.4 mg/kg SeMet + AFB1 group and the 0.6 mg/kg SeMet + AFB1 group). After 1 d of the experiment, the SeMet-treated groups were fed 0.2 mg/kg SeMet, 0.4 mg/kg SeMet, or 0.6 mg/kg SeMet daily, and the remaining two groups were fed a normal diet for 30 d. On Day 31, all rabbits in the model group and the three treatment groups were fed 0.5 mg/kg AFB1 for 21 d. The levels of testosterone (T), luteinizing hormone (LH) and follicle stimulating hormone (FSH) in rabbit plasma were detected. Rabbit semen was collected, and its quality was evaluated. Pathological changes in rabbit testes were observed by hematoxylin-eosin (HE) staining. The expression of related proteins in testicular tissue was detected by immunohistochemistry, immunofluorescence and western blot (WB) analysis. Enzyme-linked immunosorbent assays (ELISAs) were used to detect oxidative stress-related indices and inflammatory factors in testicular tissue. The results showed that AFB1 can induce oxidative stress and inflammation to activate the p38/MSK/NF-kappa B signalling pathway, mediate apoptosis, inhibit the proliferation and differentiation of testicular cells, destroy the integrity of the blood-testis barrier (BTB) and the normal structure of the testis, and reduce the content of sex hormones and semen quality. SeMet pretreatment significantly alleviated testicular injury

The purpose of this study was to explore the protective effect of SeMet on renal injury induced by AFB1 in rabbits and its molecular mechanism. Forty rabbits of 35 days old were randomly divided into control group, AFB1 group (0.3 mg AFB1/kg b.w), 0.2 mg/kg Se + AFB1 group (0.3 mg AFB1/kg b.w + 0.2 mg SeMet/kg feed) and 0.4 mg/ kg Se + AFB1 group (0.3 mg AFB1/kg b.w + 0.4 mg SeMet/kg feed). The SeMet treatment group was fed different doses of SeMet diets every day for 21 days. On the 17-21 day, the AFB1 treatment group, the 0.2 mg/kg Se + AFB1 group and the 0.4 mg/kg Se + AFB1 group were administered 0.3 mg AFB1 /kg b.w by gavage (dissolved in 0.5 ml olive oil) respectively. The results showed that AFB1 poisoning resulted in the changes of renal structure, the increase of renal coefficient and serum biochemical indexes, the ascent of ROS and MDA levels, the descent of antioxidant enzyme activity, and the significant down-regulation of Nrf2, HO-1 and NQO1. Besides, AFB1 poisoning increased the number of renal apoptotic cells, rised the levels of PTEN, Bax, Caspase-3 and Caspase-9, and decreased the levels of PI3K, AKT, p-AKT and Bcl-2. In summary, SeMet was added to alleviate the oxidative stress injury and apoptosis of kidney induced by AFB1, and the effect of 0.2 mg/kg Se + AFB1 is better than 0.4 mg/kg Se + AFB1.

Adipose derived stem cells (ADSCs) are popular in regenerative medicine due to their easy availability, low immunogenicity and lack of controversy regarding their ethical debate use. Although ADSCs can repair nerve damage, the oxidative microenvironment of damaged tissue can induce apoptosis of transplanted stem cells, which weakens the therapeutic efficacy of ADSCs. Resveratrol (Res) is a type of natural polyphenol compound that regulates the proliferation, senescence and differentiation of stem cells. Therefore, we investigated whether incubation of ADSCs with Res improves their to promote peripheral nerve regeneration. ADSCs were cultured in vitro and treated with H2O2 to establish an apoptosis model. The control, H2O2 and Res groups were set up. The cell survival rate was detected by the CCK-8 method. The TUNEL assay was used to detect the apoptosis of the cells. qRT‒PCR was used to analyze the expression of apoptosis-related mRNA, and the effect of Res on the proliferation of ADSCs was investigated. In vivo, 40 SD rats were randomly divided into the control, model, ADSCs and ADSC + Res groups, with 13 rats in each group. The sciatic nerve injury rat model was established by the clamp method. Gait was observed on Days 7, 14, 21, and 28. Sciatic nerve regeneration was detected on Day 28. Res had no effect on the proliferation of ADSCs, and the TUNEL assay confirmed that Res pretreatment could significantly improve H2O2-induced apoptosis in ADSCs. Compared with the control group, caspase-3, Bax and Bcl-2 expression levels were significantly increased in the H2O2 group. Compared with the H2O2 group caspase-3 and Bax expression levels were significantly decreased, and Bcl-2 expression levels were significantly increased in ADSCs + Res group. At 4 weeks after surgery, the functional index of the sciatic nerve in the ADSCs + Res group was significantly higher than that in the model group. On Day 28, the average density of the sciatic nerve myelin sheath in the ADSCs + Res group was significantly increased compared with that in the model group, and Nissl staining showed that the number of motor neurons in the spinal cord was significant compared with that in the model group. Compared with the control group, the wet weight ratio of gastrocnemius muscle and muscle fiber area in ADSCs + Res group were significantly increased. Res enhanced the ability of ADSCs to promote sciatic nerve regeneration in rats.

旨在了解河南疑似兔出血症病毒2型(RHDV2)的感染情况,并对RHDV2的致病性进行初步分析.本研究采集病死兔的肝组织,利用微量血凝试验、RT-PCR扩增及测序、VP60基因系统进化树分析和动物回归试验进行病原鉴定.微量血凝试验结果显示,组织样本悬液能够凝集人"O"型血红细胞;RT-PCR扩增、测序及序列分析结果显示,检测到RHDV2特异性条带,片段大小为829 bp;系统进化树分析结果发现,分离的病毒与我国四川发现的首例RHDV2毒株SC2020/04的VP60基因相似性高达98.2％;临床病例的剖检显示病死兔胸腺、气管、肺、肝、脾、肾等实质性器官出血较为严重;动物回归试验发现攻毒组家兔死亡率为100％,平均死亡时间为65.8 h,RT-PCR扩增均检测到RHDV2特异性条带.本研究首次在河南兔场检测到RHDV2,为RHDV2的防控提供了科学参考.

以C57BL/6J雄性小鼠为试验对象,利用抵抗素重组蛋白进行尾静脉注射,模拟高循环水平抵抗素状态,探讨抵抗素对雄性小鼠生殖功能的影响.10只8周龄无特定病原体(SPF)级C57BL/6J雄性小鼠随机分为试验组和对照组,试验组小鼠注射抵抗素400 ng/(d·只),对照组小鼠注射等量的双蒸水.7 d后测定小鼠血清生殖激素水平的变化,检查精子的活动能力以及睾丸组织结构和形态变化.研究结果发现:试验组小鼠的血清雌二醇(E2)质量浓度和睾酮(T)质量浓度均显著高于对照组小鼠(P<0.05),促卵泡成熟素(FSH)质量浓度和促黄体生成素(LH)质量浓度与对照组差异不显著(P>0.05).试验组小鼠精子活力显著下降,精子形态异常现象显著增加.试验组小鼠曲精小管直径小于对照组,管腔相对较大,睾丸出现超微结构病变.抵抗素能够引起小鼠血清性激素水平变化,导致小鼠生殖功能下降.

T-2 toxin is a trichothecene mycotoxin produced by fusarium species, which is mainly prevalent in grain and livestock feed. One of the main effects of this toxin is immunodepression. Previous studies have shown that T-2 toxin can cause damage to immune organs and impaired immune function in animals. However, selenomethionine (SeMet) as an organic selenium source can not only promote the growth and development of the body but also effectively improve the body's immune function. In this study, rabbits were exposed to 0.4-mg/kg T-2 toxin, and abnormal blood routine indicators were found in the rabbits. HE staining also showed obvious lesions in the spleen and thymus tissue structures, accompanied by a large number of bleeding points. In addition, rabbits showed strong oxidative stress and inflammatory response after T-2 toxin action. 0.2 mg/kg, 0.4 mg/kg, and 0.6 mg/kg organic selenium were added to the feed. However, it was found that 0.2 mg/kg selenium can effectively improve the abnormal changes of blood routine and spleen and thymus tissue of rabbits. On the other hand, it can significantly increase the expression of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC) in the spleen and thymus, and downregulate the expression of reactive oxygen species (ROS) and malondialdehyde (MDA). In addition, inflammatory factors interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in blood were also significantly inhibited; the expression of proliferating cell nuclear antigen (PCNA) in the spleen and thymus was also significantly increased after low-dose selenium treatment. Surprisingly, 0.4 mg/kg and 0.6 mg/kg of selenium did not effectively alleviate the immunotoxic effects caused by T-2 toxin, and cause damage to a certain extent. In summary, our results show that 0.2 mg/kg of SeMet can effectively alleviate the immunotoxicity caused by T-2 toxin. Selenium may protect rabbits from T-2 toxin by improving its antioxidant and anti-inflammatory capabilities.

The aim of this study was to investigate the role of selenomethionine (SeMet) in alleviating AFB1 induced intestinal injury by inhibiting intestinal oxidative stress. Forty 35-day-old rabbits were divided randomly into 4 groups (control group, AFB1 group, 0.2 mg/kg Se + AFB1 group, 0.4 mg/kg Se + AFB1 group). From the first day of the experiment, the two treatment groups were fed 0.2 mg/kg SeMet or 0.4 mg/kg SeMet daily for 21 days. On the 17th day, all rabbits in the model group and the two treatment groups were given intragastric AFB1 daily for 5 days. The ADG, ADFI and FCR of the rabbits were examined. Rabbit jejunum tissue was collected for hematoxylin- eosin staining (HE), PCNA detection, immunofluorescence and WB. Intestinal tissue IL-1β, IL-6 and TNF-α were examined by enzyme-linked immunosorbent assay (ELISA). The results showed that the production performance was decreased, the levels of ROS and MDA were increased in intestinal tissues, the activity of antioxidant enzymes was decreased and the expression levels of Nrf2 and HO-1 were decreased in AFB1-exposed rabbits. In addition, AFB1 induces an inflammatory response in the jejunum and promotes the expression of TNF-α, IL-6 and IL-1β. SeMet pretreatment significantly improved the performance of the rabbits, alleviated intestinal oxidative stress and the inflammatory response. Therefore, we confirmed that SeMet protects against AFB1 induced oxidative damage and improves productivity in rabbits by activating the Nrf2/HO-1 signaling pathway.

为了解河南省不同地区规模化兔场的球虫发病情况及不同药物对球虫的治疗效果,对河南省13个地级市的24个规模化兔场的疑似病兔进行了粪样采集,利用饱和食盐水浮集法对样品进行检测并进行卵囊计数,使用磺胺氯吡嗪钠和妥曲珠利对球虫感染严重的肉兔进行治疗观察.结果表明:24个兔场中,有23个兔场检测出球虫,样品感染率为90％,发病率为44.3％.其中豫东地区发病率为25.0％,每克粪便囊数(OPG)值平均达1.15×104个;豫南地区发病率为27.3％,OPG值平均达2.45×104个;豫西地区发病率为28.6％,OPG值平均达0.47×104个;豫中地区发病率为55.6％,OPG值平均达2.27×104个;豫北地区感染强度最大,发病率高达61.1％,OPG值平均达1.45×106个.治疗结果显示,磺胺氯吡嗪钠组在治疗进行至第3天时OPG值已经下降到0.08×104个,在4～7 d的治疗中OPG值不再发生显著变化,但直至治疗结束仍可在粪便中检测到球虫.妥曲珠利组在治疗进行至第4天时粪便中未检测出球虫.调查结果显示,河南地区规模化兔场病兔中患球虫病的病兔多,发病情况严重,且多为混合感染,不同地区的感染情况存在差异.本次共检出9种艾美耳球虫,优势虫种为肠艾美耳球虫,斯氏艾美耳球虫和大型艾美耳球虫,占比分别为25.7％、21.3％、18.9％.在治疗时可以优先考虑使用妥曲珠利.

为了解河南疑似兔出血症病毒2型(RHDV2)的感染情况,并对RHDV2的致病性进行初步分析.研究采集病死兔的肝组织,利用微量血凝试验、RT-PCR扩增及测序、VP60基因系统进化树分析和动物回归试验进行病原鉴定.微量血凝试验结果显示,组织样本悬液能够凝集人"O"型血红细胞;RT-PCR扩增、测序及序列分析结果显示,检测到RHDV2特异性条带,片段大小为829 bp;系统进化树分析结果发现,分离的病毒与我国四川发现的首例RHDV2毒株SC2020/04的VP60基因相似性高达98.2％;临床病例的剖检显示病死兔胸腺、气管、肺、肝、脾、肾等实质性器官出血较为严重;动物回归试验发现攻毒组家兔病死率为100％,平均死亡时间为65.8 h,RT-PCR扩展均检测到RHDV2特异性条带.该研究是首次在河南兔场检测到RHDV2,为RHDV2的防控提供科学参考.

Effect of boron on development of testis in the ostrich was studied by observing the changes in the microstructure and ultrastructure. Apoptotic status of testicular cells and hormone level were examined. Compared with the control group, the experimental groups exhibited different degrees of change in the histological structure of the testis on addition of boron in different quantities. Cell apoptosis could be detected in testicular tissues of both control and experimental groups, mainly in Leydig cells and spermatocytes. Level of the follicle stimulating hormone (FSH), estradiol (E-2), luteinizing hormone (LH) and testosterone (T) of the serum in the experimental groups also varied compared with those in the control group. In the present study, 100 mg/l of boron when supplemented with drinking water was helpful for the development of testis in the ostrich. It was also observed that high doses of boron significantly inhibited cell development in the testis of the ostrich.

试验旨在研究饮水中添加不同剂量硼对肉鸡免疫功能的影响.选用1 d健康AA肉仔鸡600只,随机分为对照组和试验Ⅰ、Ⅱ、Ⅲ、Ⅳ组,每组6个重复,每个重复20只.对照组鸡饮用自来水,试验Ⅰ、Ⅱ、Ⅲ、Ⅳ组鸡的饮水中硼含量分别为40 mg/L、80 mg/L、160 mg/L、320 mg/L,试验周期42 d.在试验第21 d和42 d进行屠宰釆样,测定鸡的免疫器官指数和血清IgA、IgG、IgM的含量.结果显示:(1)在21日龄,与对照组相比,试验Ⅱ组肉鸡胸腺指数和血清中IgG含量显著(P<0.05)升高;(2)在42日龄,与对照组相比,试验Ⅱ组肉鸡血清中IgA、IgG、IgM含量均显著(P<0.05)升高.结论:饮水中添加适量硼,可以促进肉鸡的免疫器官发育、增强机体免疫功能,以80 mg/L为最佳推荐添加量.

Abstract Resistin was identified as a link between obesity and insulin resistance and is associated with many diseases in mice. Deciphering the related development and molecular mechanism is necessary for the treatment of these diseases. Previous studies have revealed that increased resistin levels are correlated with lipid accumulation and play a role in non-alcoholic fatty liver disease (NAFLD) development. However, the exact mechanisms underlying these processes remain unclear. To further clarify whether acute elevated resistin level exacerbated liver steatosis, a high-fat diet-induced NAFLD animal model was used and treated with or without resistin for 6 days. We discovered that resistin altered mitochondrial morphology, decreased mitochondrial content, and increased lipid accumulation in HFD mice. qRT-PCR and western blot analysis showed that acute elevated resistin significantly altered the gene expression of mitochondrial biogenesis and liver lipid metabolism molecules in HFD mice. Consequently, in vitro experiments verified that resistin reduced the mitochondrial content, impaired the mitochondrial function and increased the lipid accumulation of palmitate-treated HepG2 cells. Additionally, we demonstrated that resistin upregulated proinflammatory factors, which confirmed that resistin promoted the development of inflammation in NAFLD mice and palmitate-treated HepG2 cells. Signaling-transduction analysis demonstrated that acute elevated resistin aggravated liver steatosis through AMPK/PGC-1α pathway in male mice. This reveals a novel pathway through which lipogenesis is induced by resistin and suggests that maintaining mitochondrial homeostasis may be key to treatments for preventing resistin-induced NAFLD aggravation.

在动物解剖学实验教学过程中,“心脏及动脉血管主干”浸泡标本对教师的授课和学生的学习具有非常重要的地位.以绵羊为实验动物,通过耐心剥离,成功制作“心脏及动脉血管主干”浸泡标本.对制作过程进行总结和汇报,以期为动物解剖学实验课程提供教学参考.