Abstract Background Sepsis-associated acute kidney injury (AKI) is a serious complication of systemic infection with high morbidity and mortality in patients. However, no effective drugs are available for AKI treatment. Dexmedetomidine (DEX) is an alpha 2 adrenal receptor agonist with antioxidant and anti-apoptotic effects. This study aimed to investigate the therapeutic effects of DEX on sepsis-associated AKI and to elucidate the role of mitochondrial dynamics during this process. Methods A lipopolysaccharide (LPS)-induced AKI rat model and an NRK-52E cell model were used in the study. This study investigated the effects of DEX on sepsis-associated AKI and the molecular mechanisms using histologic assessment, biochemical analyses, ultrastructural observation, western blotting, immunofluorescence, immunohistochemistry, qRT-PCR, flow cytometry, and si-mRNA transfection. Results In rats, the results showed that administration of DEX protected kidney structure and function from LPS-induced septic AKI. In addition, we found that DEX upregulated the α2-AR/SIRT1/PGC-1α pathway, protected mitochondrial structure and function, and decreased oxidative stress and apoptosis compared to the LPS group. In NRK-52E cells, DEX regulated the mitochondrial dynamic balance by preventing intracellular Ca2+ overloading and activating CaMKII. Conclusions DEX ameliorated septic AKI by reducing oxidative stress and apoptosis in addition to modulating mitochondrial dynamics via upregulation of the α2-AR/SIRT1/PGC-1α pathway. This is a confirmatory study about DEX pre-treatment to ameliorate septic AKI. Our research reveals a novel mechanistic molecular pathway by which DEX provides nephroprotection.

Increasing evidence has demonstrated that coenzyme Q10 (CoQ10) exhibits a range of biological properties. Herein, we explored the protective effect and potential molecular mechanism of CoQ10 on lipopolysaccharide (LPS)-induced acute lung injury (ALI). We found that medium (10 mg/kg) and high (50 mg/kg) doses of CoQ10 ameliorated LPS (50 mu g/ mu L)-induced ALI to varying degrees, as demonstrated by reduced lung coefficient, lower wet/dry weight lung tissue ratio, decreased bronchoalveolar lavage fluid protein concentration, less anatomical and histopathological damage to the lung, and increased expression of proteins related to lung epithelial barrier structure. CoQ10 also alleviated LPS-induced oxidative stress and inflammation mediated by NOD-like receptor protein 3 (NLRP3) by reducing the reactive oxygen species (ROS), malondialdehyde, and mitochondrial ROS concentrations, increasing superoxide dismutase, glutathione, and catalase activity, and decreasing NLRP3 expression at the protein and mRNA levels. Moreover, CoQ10 alleviated structural and functional damage to the mitochondria, inhibited mitochondrial fission, and promoted mitochondrial fusion, mainly by inhibiting phosphorylation of dynamin-related protein 1 (Drp1) at Ser616 and Ser637. Correlation analysis revealed that mitochondrial fission (especially Drp1) was positively correlated with oxidative stress, NLRP3-mediated inflammation, and structural damage to the lung epithelial barrier. Molecular docking analysis showed that CoQ10 binds stably to Drp1, with a binding energy of-5.9 kcal/mol. Furthermore, the use of schaftoside (a Drp1 inhibitor) has further elucidated the mechanism of action of CoQ10. Together, these results suggest that CoQ10 alleviates LPS-induced ALI by regulating mitochondrial dynamics, attenuating oxidative stress, and decreasing NLRP3-medated inflammation, thereby promoting lung epithelial barrier structural remodeling.

Objective: Abdominal aortic aneurysms (AAA) are a common critical cardiovascular disease with high morbidity and mortality rates. Quercetin, a flavonoid and a traditional Chinese medicinal ingredient commonly found in vegetables and fruits, has a favorable inhibitory effect on experimental aneurysms without side effects. This study aimed to model elastase AAA and investigate the mechanism of action of quercetin in alleviating AAA. Methods: Quercetin was administered at a dose of 60 mg/kg once daily starting on the day of AAA induction for 5 weeks. The therapeutic effect of quercetin on AAA was demonstrated using biochemical assays, observation of pathological tissue sections, Elastic Van Gieson staining, immunohistochemistry, molecular docking simulations, and Western blot protein validation. Results: Our study showed that quercetin treatment significantly alleviated abdominal aortic vessel wall dilatation, elastin degradation and adhesion to surrounding tissues caused by elastase. Additionally, quercetin significantly inhibited the mRNA and protein expression of the receptor for advanced glycation end products(RAGE)/ phosphatidylinositol 3-kinase (PI3K)/ phosphatidylinositol 3-kinase (AKT) / mammlian target of rapamycin (mTOR) pathway. Conclusion: Quercetin can alleviate abdominal aortic injury caused by elastase via RAGE/PI3K/AKT/mTOR and provide experience in clinical use.

Trauma is a common cause of cutaneous surgical disease with an increased risk of secondary infection in cat clinics. Platelet-rich fibrin (PRF), a platelet and leukocyte concentrate containing multiple cytokines and growth factors, is known to accelerate the healing of wounds. However, how PRF affects wound healing in the cat trauma model has not been fully investigated. The study aimed to examine the impact of PRF on skin wound healing in the cat trauma model. In this study, PRF from cats was successfully produced for our investigation. The models of feline trauma were effectively established. A total of 18 cats were randomly divided into 3 groups (n = 6): (1) Control group (CON); (2) PRF group; (3) Manuka honey group (MAN, as a positive control). Experiments were performed separately on days 7, 14, 21, and 28. Our results showed that PRF was a safe and efficient method of wound healing that did not influence the cat’s body temperature, respiration rate, and heart rate (HR). PRF accelerated skin wound healing in the cat trauma model based on the rate and histological observation of wound healing. In addition, PRF promoted the production of growth factors and suppressed inflammation during wound healing. PRF accelerated wound healing by increasing the formation of collagen fibers, as shown by Masson-trichrome staining. The outcomes of the PRF and MAN groups were comparable. In conclusion, PRF improves the healing of skin wounds in cats by boosting the synthesis of growth factors, reducing inflammation, and enhancing the synthesis of collagen fibers.

This study aimed to investigate the potential protective effects of Dexmedetomidine (DEX) against acute kidney injury (AKI) induced by acute stress (AS). Wistar rats were divided into five groups: Control, DEX, AS, AS + DEX, and AS + A438079. The results showed that AS led to AKI by increasing inflammatory biomarkers and oxidative stress-related indicators. The acute stress model in rats was successfully established. Renal function, histopathology, oxidative stress, and inflammation were assessed. Localization of P2X7 receptor (P2X7R) was determined by immunofluorescence. Additionally, the key inflammatory proteins of the P2X7R/NF-κB/NLRP3 signaling pathway were measured by Western blotting. DEX significantly improved kidney function, alleviated kidney injury, and reduced oxidative stress and inflammation. DEX inhibited the activation of the P2X7R, decreased the expression of NF-κB, NLRP3 inflammasome, and Caspase-1, and inhibited the expression of interleukin-1β (IL-1β) and tumor necrosis factor α (TNFα). Furthermore, DEX also alleviated AS-induced AKI by inhibiting the excessive production of reactive oxygen species (ROS) and reducing oxidative stress. In conclusion, DEX attenuates AS-induced AKI by mitigating inflammation and oxidative stress through the inhibition of the P2X7R/NF-κB/NLRP3 pathway in rats.

随着我国现代养禽业的快速发展,更多现代化技术应用于养鸡业,鸡单位养殖密度与日俱增,同时疾病发生的风险也在成倍增长.鸡大肠杆菌病是养鸡场常发的一种细菌性疾病,临床上常与其它疾病并发或混合感染,加大治疗难度,严重危害养鸡业的发展,给养鸡场带来严重的经济损失;而且长期大量使用抗生素,导致养殖环境中致病性大肠杆菌耐药菌株大量产生和威胁食品安全.中草药及其复方制剂治疗动物疾病具有副作用小、药物残留少且防治效果显著的优势,近几年在临床疾病防治中得到广泛应用.中草药是具有抗菌和消炎作用的天然植物,粉粹添加在饲料中或提取的活性成分直接应用于机体,能够提高动物机体免疫力和抗病力,减少了临床抗生素使用量及菌株耐药性问题.

犬肾衰竭在临床中十分常见,治疗过程一般较长,对机体损害大,且发病率呈逐年上升趋势.1例中华田园犬经临床诊断及血常规、血清生化、血气、B超检查等诊断为由膀胱结石导致尿闭,造成肾脏损伤,进而引起急性肾衰竭.经过14d治疗,患犬精神状态恢复良好,饮食正常,各项指标趋于正常.文章介绍该病例的诊断及治疗过程,以期帮助宠物医生和宠主更好地了解犬急性肾衰竭,为该病的预防和诊治提供一定参考.

文章记录1例犬因误食玩具而导致的胃内异物的诊断及治疗过程.患犬表现为呕吐、食欲废绝,腹部疼痛感强烈.经临床诊断、血常规检测、血清生化检测、X射线检查、内窥镜检查确定为胃内异物;通过手术、术后药物治疗等方式对其进行治疗,最终痊愈.文章提示宠主日常饲养应注意观察犬类的异常行为,发现病情及时就医、尽快治疗;宠物医生临床中应注意辨别诊断,避免产生更大的危险.

鹅副黏病毒病是由Ⅰ型鹅副黏病毒(Goose Paramyxovirus,GPMV)感染引起,是一种急性、烈性高度接触性传染病.鹅群感染本病后会引起消化系统、神经系统和免疫系统的病变.该病感染性极强,各季节均有发生;不同日龄的鹅均可感染,日龄越小的雏鹅,发病率和死亡率越高.

猫传染性腹膜炎(FIP)是一种严重的疾病,具有很高的致死率,在宠物临床中应引起大家的重视.该文报道一例布偶猫通过血常规、生化、X光、荧光定量PCR检测后确诊为FIP.运用保肝、消炎、特效药等方式治疗,该猫病情转好,后期回访显示未出现病情复发,精神状态恢复正常.

为建立一种可同时检测鹅星状病毒(GoAstV)、鹅细小病毒(GPV)和鹅坦布苏病毒(TMUV)的方法,根据GenBank上公布的GoAstV、GPV和TMUV的保守基因序列设计3对特异性引物,通过优化反应条件和反应体系,建立了能够同时检测GoAstV、GPV和TMUV的三重PCR方法,并初步应用于临床.结果显示:所建立的三重PCR检测方法能特异性扩增GoAstV、GPV和TMUV三种病毒的目的片段,对鹅副黏病毒、禽流感病毒、禽腺病毒和鹅圆环病毒的检测结果均为阴性,对GoAstV、GPV和TMUV的最低检出浓度分别为1.26×105、1.26×103和1.26×105 copies/μL.利用三重PCR和单项PCR方法同时对黑龙江省部分鹅场的32份临床样品进行检测,3种病毒的阳性检出率分别为56.25％、6.25％和6.25％,2种方法的检测结果一致.结果表明,本试验中建立的三重PCR检测方法快捷、敏感、特异,能够用于GoAstV、GPV和TMUV的流行病学调查和临床检测.

犬口腔肿瘤主要包括恶性黑色素瘤、纤维肉瘤、鳞状细胞癌、齿龈瘤,而纤维肉瘤在临床上发病少,主要发生在大型犬中,一般发病年龄在8岁左右,有一定的性别趋向多发于雄性犬.纤维肉瘤源于口腔颌面部成纤维细胞的肿瘤,多发生于犬齿和裂齿之间的硬腭、上颌弓,肿瘤生长速度慢,但是最终会侵害黏膜导致黏膜溃疡引起继发感染.

为研究过瘤胃葡萄糖(RPG)对泌乳早期奶牛产奶量以及血清生化指标的影响,试验将 64 头年龄、胎次、泌乳量接近,产后 11～19 d奶牛随机分为对照组、150 g RPG组、225 g RPG组和 300 g RPG组,试验周期 7d.结果表明:在试验第 7 天,300 g RPG组较对照组平均产奶量显著增加 15.99%(P＜0.05);225 g RPG组和 300 g RPG组与对照组相比血糖水平极显著增加 53.39%和 107.62%(P＜0.01);300 g RPG组血清β-羟丁酸水平较对照组降低81.81%(P＜0.05);各试验组乳成分差异均不显著(P＞0.05);300 g RPG组产奶利润有所增长,增长为 8.87 元/d.上述试验表明,饲喂RPG 300 g/(d·cow)时,对奶牛健康和养殖场效益最有利.

鸭病毒性肝炎(Duck virus hepatits,DVH)的病原是鸭肝炎病毒(DHV),属微RNA病毒科,直径约为20～40 nm,在电镜下观察感染病毒细胞,细胞胞浆呈晶格状排列.DVH在加热56℃条件下加热60 min仍可存活,在62℃条件下加热30 min即可灭活,4℃下可存活2年,-20℃可存活9年.DVH是危害幼龄雏鸭的急性传染病,具有扩散速度快、发展速度快、死亡率高等显著特点.临床表现多集中为角弓性反张,病理表现常见肝炎及出血.近年来,我方各地区均有DVH发生,发病率呈逐年大幅度快速上升,给我国鸭养殖业带来了巨大的经济损失.

自2010年中国首次在规模养鸭场发生鸭坦布苏病毒病以来,该病对养殖业造成了巨大的经济损失.本研究对坦布苏病毒的免疫反应、免疫逃避机制以及疫苗开发等内容进行综述,以期为后续研究坦布苏病毒的发病机制和促进新型候选疫苗开发提供参考.

Vitamins are a class of organic substances necessary to maintain the healthy growth and nor-mal physiological function of animals.Most vitamin cannot be synthesized in animals or are not produced in sufficient quantities,so they need to be obtained by dietary supplementation.The supplementation of vitamin B in goose diet plays an active role in improving the growth performance,reproductive perfor-mance,slaughter performance,meat/egg quality and immunity of goose.This article reviewed the physi-ological functions of seven vitamins(vitamins B1,B2,B3,B5,B6,B9,B12)and their allowance in different production stages of geese were elaborated in detail,so as to provide reference for the application of B vi-tamins in goose breeding.

为研究中草药添加剂对小尾寒羊生长性能、血清生化指标、免疫指标以及胃肠道线虫驱虫效果的影响,试验选择3 月龄左右母小尾寒羊48 只,随机分为4 组,每组12 只羊.对照组饲喂基础日粮,Ⅰ、Ⅱ、Ⅲ组饲喂的日粮中分别添加0.5％、1.0％、2.0％的中草药添加剂,试验为期14 d.结果表明:与对照组比较,日粮中添加不同比例中草药添加剂对小尾寒羊生产性能无显著影响(P＞0.05).在试验第14 天,与对照组相比,Ⅱ组和Ⅲ组总蛋白(TP)显著提高了5.47％(P＜0.05)、5.38％(P＜0.05),白蛋白(ALB)显著提高了8.72％(P＜0.05)、6.18％(P＜0.05),IgA显著提高了20.00％(P＜0.05)、19.05％(P＜0.05),IgG显著提高了11.04％(P＜0.05)、9.82％(P＜0.05),驱虫效果显示试验第7 天疗效为33.11％～54.67％,第14天疗效为39.13％～55.59％.综上所述,日粮中添加中草药添加剂对小尾寒羊的生产性能无显著影响,可以有效地改善部分血清生化指标和免疫指标,具有一定的驱虫作用,临床中推荐的添加量为1％.

雏鹅痛风是由鹅星状病毒(Gooseastrovirus,GoAstV)感染引起的一种以内脏和关节尿酸盐沉积为主要特征的传染病.近几年,鹅星状病毒病在我国多省份养鹅地区暴发,感染该病的鹅群发病率高达80％,死亡率可高达50％,未死亡雏鹅生长受到抑制,体重减轻,易感染其他病原.目前针对该病缺乏有效的防控措施,给我国鹅养殖业造成巨大经济损失.本文通过对鹅星状病毒的病原、致病机理等进行综述,以期为鹅星状病毒病的相关研究及有效防控等提供参考.

鬼针草(Bidens bipinnata L.)又称鬼钗草,全国分布广泛,产量很多,是菊科草本植物.鬼针草中富含多糖、黄酮、皂苷等活性成分,具有清热解毒、抗氧化、消肿、止泻等作用,可作为饲草应用到畜牧养殖中,但菊科植物本身具有特殊气味,会影响动物采食,对其主要活性成分进行提取,能改善其适口性与消化性.

为了获得莫西菌素和左旋咪唑单独及联合用药在小尾寒羊体内的药物代谢动力学数据,并比较单独用药及联合用药时药动学参数差异,选择36只健康小尾寒羊,随机分为左旋咪唑皮下8 mg/kg组(LEVSC8)、莫西菌素皮下0.2 mg/kg组(MXDSC0.2)、联合用药组(LEVSC8+MXDSC0.2)皮下注射给药,每组12只小尾寒羊.给药后的不同时间段于颈静脉采集血液,离心获得血浆样本,通过高效液相色谱方法测定血浆中药物浓度,并通过Wlinnonlin软件获得药动学参数,通过统计学分析软件进行显著性差异比较.结果显示,左旋咪唑单独应用时,在小尾寒羊体内的达峰浓度为(1.79±0.69)μg/mL,达峰时间为(1.29±0.68)h,药时曲线下面积为(8.69±2.69)μg·h/mL,消除半衰期为(3.37±1.57)h;左旋咪唑和莫西菌素联合应用时,左旋咪唑在小尾寒羊体内的达峰浓度为(1.64±0.72)μg/mL,达峰时间为(1.35±0.73)h,药时曲线下面积为(8.03±2.69)μg·h/mL,消除半衰期为(3.69±1.71)h.左旋咪唑和莫西菌素联合用药时的药动学参数与左旋咪唑单独用药时相比,无显著性差异(P>0.05).莫西菌素单独用药时,在小尾寒羊体内的达峰浓度为(40.57±10.06)ng/mL,达峰时间为(1.08±0.53)d,药时曲线下面积为(168.76±29.39)ng·d/mL,消除半衰期为(5.76±1.36)d;与左旋咪唑联合应用时,莫西菌素在小尾寒羊体内的达峰浓度为(39.89±13.49)ng/mL,达峰时间为(1.36±0.46)d,药时曲线下面积为(152.69±35.96)ng·d/mL,消除半衰期为(6.36±1.79)d.莫西菌素和左旋咪唑联合用药时的药动学参数与莫西菌素单独用药时,无显著性差异(P>0.05).表明左旋咪唑和莫西菌素联合应用时,莫西菌素与左旋咪唑在小尾寒羊体内无动力学相互作用.研究结果可为左旋咪唑和莫西菌素在小尾寒羊上的联合应用提供依据.