Deoxynivalenol is a widespread feed contaminant that leads to vomit, which results in serious symptom such as increased intestinal permeability and even intestinal mucosal necrosis. Recent studies have reported the role of quercetin in alleviating deoxynivalenol-induced intestinal injury; however, the mechanisms and targets remain unclear. Thus, we aimed to identify the mechanisms of action by using a combination of network pharmacology and molecular docking. We identified 151 quercetin targets, 235 deoxynivalenol targets and 47 porcine intestinal injury targets by searching compound database and PubMed database, among which there were two common targets. The PPI network showed that the key proteins involved are NQO1 and PPAR-γ. The PPI network showed that the key proteins involved were NQO1 and PPARG. GO analysis found that genes were enriched primarily in response to oxidative stress. The PPI network showed that the key proteins involved are NQO1 and PPAR-γ. The genes are enriched primarily in response to oxidative stress. KEGG analysis showed enrichment of the HIF, reactive oxygen species and other signaling pathways. The molecular docking results indicated key binding activity between NQO1–quercetin and PPAR-γ–quercetin. By using network pharmacology, we have revealed the potential molecular mechanisms by which quercetin alleviates deoxynivalenol-induced porcine intestinal injury, which lays the foundation for the development of drugs to treat deoxynivalenol-induced intestinal injury in pigs.

为探讨黄芩素治疗猪链球菌脑膜炎的分子机制,应用网络药理学的方法,在Pubchem和SwissTarget Prediction数据库获取黄芩素490个潜在作用靶点,并在NCBI等平台中检索猪链球菌脑膜炎的靶点.运用STRING数据库构建"中药-疾病"共同靶点的PPI网络图;利用DAVID数据库进行GO功能注释和KEGG通路富集分析,并使用Cytoscape3.8.2软件构建"中药-靶点"通路图.结果显示黄芩素和猪链球菌脑膜炎有9个共同靶点(MMP2、SYK、FN1、MAPK14、HSPCB、CASP3、CCL2、APOD、EGFR),其中MMP2、SYK和FN1是脑损伤的核心靶点.GO富集分析发现,黄芩素可能通过影响细胞凋亡的调控过程、细胞外间隙、细胞氧化应激的过程缓解猪链球菌脑膜炎的症状;KEGG通路主要富集在IL-17信号通路、MAPK信号通路等41条相关通路.基于网络药理学的结果,本研究探讨了黄芩素潜在治疗链球菌引起的脑膜炎的作用,推测该中药成分可以作为开发抗猪链球菌疾病的先导化合物,为开发治疗猪链球菌病的药物奠定研究基础.

目的:探讨采取自制袋式减压约束带用于防止神经外科非计划性拔管(UEX)的价值.方法:选取300例神经外科烦躁病人并随机分成A、B、C三组,每组100例,三组均使用约束带进行固定,A组用传统约束带固定,B组用球拍式约束带固定,C组用自制袋式减压约束带固定,比较三组不良事件发生情况.结果:在非计划拔管次数、自解约束带次数及损坏床单元次数、约束部位皮肤损伤、经济成本上,C组均明显低于A组与B组,对比差异显著(P<0.05).结论:对神经外科烦躁病患,使用自制袋式减压约束带进行肢体固定,可有效预防UEX的发生,值得推广.

<正>神经纤维缠结(NFT)是阿尔茨海默病的特征性病理标志。据报道糖原合成酶激酶-3β(GSK-3β)在tau蛋白形成NFT中起着重要作用,而自噬障碍可能有助于tau蛋白聚集体形成。最近,韩美科学家报道了他们针对GSK-3β介导的tau蛋白磷酸化在自噬降解中的作用的研究。他们分别将T4(野生型tau蛋白)、T4C3(由caspase-3在Asp421位点对tau蛋白切割成的片段)和T4-2EC(在Ser396/Ser404位点低磷酸化的tau蛋白)转染至中国仓鼠卵巢(CHO)细胞,用激活的或被酶灭活的

Objective To study the effects of aqueous extract of cinnamon on·OH and GSH-Px in the whole cerebral ischemia reperfusion injury rats.Methods Model of cerebral ischemia reperfusion injury was established by four-vessel occlusion(4-VO).The inhibited ability of ·OH and the activity of GSH-Px in the brain,heart,liver,kidney tissues were determined by the Ultraviolet Spectrophotometer.Results Compared with the cerebral ischemia reperfusion group,aqueous extract of cinnamon could decrease·OH(P<0.01 or P<0.05),and enhance the activity of GSH-Px remarkably(P<0.01 or P<0.05).Conclusions Aqueous extract of cinnamon could enhance the activities of GSH-Px,scavenge·OH.It is a good scavenger of free radicals and had good anti-oxidation effects.

<正>肾脏是能量需求高、微循环丰富的器官,对缺血再灌注损伤极为敏感。在缺血再灌注损伤过程中,肾脏的内皮细胞活化属于微血管的炎症应答反应;磷脂酰丝氨酸(PS)迁移于内皮细胞外,成为白细胞与活化的内皮细胞黏附的结合位点,可使促

Objective To study the detection on DNA damage by single cell gel clectrophoresis assay technology during rats'neural tube defect process.Methods Twenty pregnant rats were randomly divided into control group and NTDs model group according to their weight.On the 13 d of gestation,the pregnant rats of the model group were given cyclophsphamide 12.5 mg/(kg·bw) via intraperitoneal administration,the control group was given 0.3 ml N.S in the same way.On the 14 d of gestation,two rats of each group were executed.The DNA damage of three embryo's brain tissue in each pregnant rat was checked through single-cell gel electrophoresis technology.Furthermore,influence factors of SCGE were analyzed.Results Comet cells were found in the model group but were not found in control group.The comet cells showed small head and big tail.Tail length of comet cells in model group [(16.35±5.59)μm] was longer significantly than that of neuron cells in control group [(7.28+1.76)μm].Ratio of abnormity in model group(67%) was significantly increased(P<0.05) and the developmental index was significantly decreased in model group(P<0.05).There were some factors affecting the experiment including concentration of cell suspension and gel,time of split as well as fluorescent staining.Conclusion DNA damage in NTDs can be checked by single cell gel electrophoresis assay technology.Besides,some details should be emphasize in order to improve the sensitivity and specificity.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">目的　探讨细胞凋亡在环磷酰胺致大鼠神经管畸形发生中的作用。方法　利用环磷酰胺致大鼠神经管畸形的模型 ,体内实验利用光镜、透射电镜的方法进行检测 ,而在体外实验中利用倒置相差显微镜、流式细胞仪和单细胞凝胶电泳的技术检测细胞凋亡在其发生中的作用。结果　 （1 ）光镜病理切片观察到 ,细胞核浓缩深染并碎解成许多碎片 ;（2 ）透射电镜观察可见细胞核固缩以及染色质分布欠均匀等细胞凋亡的特征性变化 ;（3）倒置相差显微镜观察发现加有环磷酰胺的组别漂浮细胞增多 ,神经突触变短 ,存活细胞数减少 ,网络变稀疏 ;（4）流式细胞仪检测发现有明显的“凋亡峰”的出现 ;而通过单细胞凝胶电泳实验检测时出现明显的“彗星状细胞”。结论　细胞凋亡是导致神经管畸形发生的重要作用机制之一。</span>

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">目的　研究环磷酰胺致大鼠胚胎神经管畸形的作用及可能机理 ,并为其防治奠定基础。方法　将大鼠按体重随机分为正常对照组及 4个不同剂量的实验组 ,其剂量分别为 7 5 ,10 5 ,12 5和 15mg/kg ,均于孕 13天腹腔一次性注射相应剂量的环磷酰胺 ,于孕 14天各组随机处死 3只 ,胎鼠进行光镜形态学观察 ;其余动物均于孕 2 0天时处死 ,进行孕鼠血清生化指标的检测、胎鼠外形及病理检测和骨骼标本的观察。结果　胎鼠神经管畸形发生率及颅骨缺损、孕鼠血清的MDA、NO含量与环磷酰胺的剂量呈正相关 ;孕鼠血清的SOD、胎鼠的生长发育指标与剂量呈负相关 ;胎鼠畸形发生处有大量的凋亡细胞存在 ;以 12 5mg/kg的剂量组致畸率高且致死率低。 结论　利用环磷酰胺制备大鼠神经管畸形模型以 12 5mg/kg的剂量效果最佳 ;畸形的发生与孕鼠机体抗氧化能力降低及胚胎神经管细胞过度凋亡有关</span>