Effect of chlorogenic acid on intestinal inflammation,antioxidant status,and microbial community of young hens challenged with acute heat stress

Heat stress in poultry is deleterious to productive performance. Chlorogenic acid (CGA) exerts antibacterial, anti-inflammatory, and antioxidant properties. This study was conducted to evaluate the effects of dietary supplemental CGA on the intestinal health and cecal microbiota composition of young hens challenged with acute heat stress. 100-day-old Hy-line brown pullets were randomly divided into four groups. The control group (C) and heat stress group (HS) received a basal diet. HS + CGA₃₀₀ group and HS + CGA₆₀₀ group received a basal diet supplemented with 300- and 600-mg/kg CGA, respectively, for 2 weeks before heat stress exposure. Pullets of HS, HS + CGA₃₀₀, and HS + CGA₆₀₀ group were exposed to 38°C for 4 h while the control group was maintained at 25°C. In this study, dietary CGA supplementation had effect on mitigate the decreased T-AOC and T-SOD activities and the increasing of IL-1β and TNFα induced by acute heat stress. Dietary supplementation with 600 mg/kg CGA had better effect on increasing the relative abundance of beneficial bacterial genera, such as Rikenellaceae RC9_gut_group, Ruminococcaceae UCG-005, and Christensenellaceae R-7_group, and deceasing bacteria genera involved in inflammation, such as Sutterella species. Therefore, CGA can ameliorate acute heat stress damage through suppressing inflammation and improved antioxidant capacity and cecal microbiota composition.     

Autophagy induces mitochondrial dysfunction in neurons from neonatal rats with hypoxic ischemic encephalopathy

AIM: To explore the influence of autophagy on the induction of mitochondrial dysfunction in the neurons in a neonatal rat hypoxic ischemic encephalopathy (HIE) model. METHODS: Ten-day-old rat pups (n=30) were randomly divided into sham group and model group. The rats in the latter group were subject to hypoxia-ischemia treatment via unilateral common carotid artery ligation. The rats were sacrificed for brain pathological examination, and the protein levels of cleaved caspase-3 and LC3B-II were detected by immunohistochemical analysis. For the in vitro experiments, the autophagy of primarily cultured rat neurons was observed after hypoxia, and Western blot and mitochondrial function testing were also performed. RESULTS: Compare with sham group, the hypoxia-ischemia treatment caused atrophy and apoptosis of neurons, and ventricular area enlargement of rat brains. Immunohistochemical results demonstrated significantly higher levels of apoptosis- and autophagy-associated proteins, such as cleaved caspase-3 and LC3B-II (P<0.01). In vitro experiments demonstrated that hypoxia induced autophagy and apoptosis in the neurons. Compared with sham group, there were higher levels of reactive oxygen species and mitochondrial superoxide, and lower mitochondrial membrane potential in the model group (P<0.01). CONCLUSION: In neonatal HIE rat model, the hypoxia-induced mitochondrial dysfunction is related to apoptosis and autophagy. It will provide a new idea for administration of autopahgy inducer agents in treatment of HIE.     

阿维菌素等三种常规渔药对卡拉白鱼的急性毒性

采用半静态法,研究了三种常规渔药阿维菌素、三氯异氰脲酸和硫酸铜对卡拉白鱼(Chalcalburnus chal coides aralensis)急性毒性效应。结果表明:阿维菌素对卡拉白鱼24、48、72、96 h的半致死浓度分别为6.25、4.66、3.66和2.82 mg/L,安全浓度为0.77 mg/L;三氯异氰尿酸对卡拉白鱼24、48、72、96 h的半致死浓度分别为3.22、2.49、2.19、1.79 mg/L,安全浓度为0.45 mg/L;硫酸铜对卡拉白鱼24、48、72、96 h的半致死浓度分别为5.56、3.96、2.03、1.74 mg/L,安全浓度为0.6 mg/L。三种药物对卡拉白鱼毒性高低依次为:硫酸铜三氯异氯尿酸阿维菌素。三种常规渔药的安全浓度近于或高于生产中常用泼洒浓度,可放心使用。     

纳米氧化锌和纳米二氧化钛对尾草履虫急性毒性效应的比较研究

[目的][方法] 本研究以原生动物尾草履虫（Paramecium caudatum）为实验对象, 对目前广泛应用的两种纳米材料，纳米二氧化钛（TiO2）和纳米氧化锌（ZnO）的24小时急性毒性进行了比较研究，分析了草履虫在两种纳米材料胁迫下抗氧化酶活性的改变，并结合两种纳米材料的超微形态，探讨了纳米材料毒性效应的机制，为两种纳米材料的环境毒性监测与评价提供依据。[结果]结果显示：对尾草履虫的24小时半数效应浓度(24h-EC50)分别为51.580mg·L-1（TiO2）、0.444mg·L-1（ZnO）；最低有影响浓度(24h-LOEC)分别为1.712mg·L-1（TiO2）、0.352mg·L-1（ZnO）；以EC50浓度24小时胁迫尾草履虫，获得抗氧化酶活性改变为：超氧化物歧化酶(SOD)，过氧化氢酶(CAT)和过氧化物酶(POD)活性与对照组相比有不同程度的改变，经成对检验分析，两种纳米材料对尾草履虫的POD酶表现出较为明显的抑制作用。[结论]上述结果表明：纳米氧化锌对草履虫的24小时急性毒性大于纳米二氧化钛，这与纳米氧化锌对草履虫抗氧化酶的抑制作用更强，以及纳米氧化锌(30nm)的超微形态相较于纳米二氧化钛(25nm)更加纤细和尖锐有关；本研究获得的24小时急性毒性指标可用于监测和评价两种纳米材料的环境毒性，并为纳米材料的环境容量和生态安全阈值确定提供参考。     

重金属Pb与抗生素对发光菌的联合毒性研究

重金属是水环境中的典型无机污染物,随着水体中抗生素检出率的增加,重金属和抗生素的复合污染及其效应已成为环境领域的研究热点。通过研究重金属和抗生素对发光菌的发光抑制作用,可以了解重金属和抗生素的毒性效应,为评估重金属和抗生素复合污染在水环境中的潜在风险提供理论依据。本文利用便携式急性毒性检测仪,系统研究了重金属Pb和6种抗生素(四环素、氧四环素、氯四环素、磺胺二甲基嘧啶、磺胺甲基嘧啶和磺胺嘧啶)对费氏弧菌的单一和联合急性毒性,得到了单一污染物的半数效应浓度,并对重金属Pb和抗生素所组成的二元、三元复合污染体系的联合作用进行初步探讨。研究表明,当Pb与抗生素共存时,对发光菌的急性毒性急剧上升。因此,在评价Pb与抗生素二元或多元复合污染体系的生态风险时,应考虑其联合毒性作用。     

右美托咪定抑制NOX4缓解急性应激致大鼠肾损伤

本研究拟探索右美托咪定（dexmedetomidine,DEX）对大鼠急性应激致肾损伤的保护作用,并从氧化应激的角度探索DEX对大鼠肾的保护通路。本研究使用了急性束缚应激模型,其中,大鼠被迫游泳15 min,并束缚3 h。本试验采用生化检测、组织病理学切片观察以评估肾功能,然后测定了氧化应激以及氧化应激的相关通路蛋白。旷场试验证实成功建立了急性应激模型。急性应激引起的肾损伤增加了NOX4,降低了Nrf2/HO-1/NQO1表达水平。DEX可降低NOX4表达,同时升高Nrf2/HO-1/NQO1的表达水平。DEX治疗组与急性应激组相比的肾生化结果明显恢复正常,病理切片观察损伤显著降低。试验结果表明,DEX治疗急性应激可影响NOX4/Nrf2/HO-1/NQO1信号通路,并抑制氧化应激。因此,DEX对急性应激引起的肾损伤具有保护作用,并在应激综合征中具有潜在的临床应用。     

Use of serum amyloid A in equine medicine and surgery

Serum amyloid A (SAA) has become an indispensable part of the management of equine patients in general practice and specialized hospital settings. Although several proteins possess acute phase properties in horses, the usefulness of SAA exceeds that of other acute phase proteins. This is due to the highly desirable kinetics of the equine SAA response. SAA concentrations exhibit a rapid and pronounced increase in response to inflammation and a rapid decline after the resolution of inflammation. This facilitates the detection of inflammatory disease and real-time monitoring of inflammatory activity. SAA may be used in all stages of patient management: (1) before diagnosis (to rule in/rule out inflammatory disease), (2) at the time of diagnosis (to assess the severity of inflammation and assist in prognostication), and (3) after diagnosis (to monitor changes in inflammatory activity in response to therapy, with relapse of disease, or with infectious/inflammatory complications). By assessing other acute phase reactants in addition to SAA, clinicians can succinctly stage inflammation. White blood cell counts and serum iron concentration change within hours of an inflammatory insult, SAA within a day, and fibrinogen within 2–3 days; the interrelationship of these markers thus indicates the duration and activity of the inflammatory condition. Much research on the equine SAA response and clinical use has been conducted in the last decade. This is the prerequisite for the evidence-based use of this analyte. However, still today, most published studies involve a fairly low number of horses. To obtain solid evidence for use of SAA, future studies should be designed with larger sample sizes.