BACKGROUND:Depression-associated memory impairment is a clinically significant comorbidity that responds poorly to conventional antidepressants. Dihydromyricetin (DHM), a natural dihydroflavonoid, exhibits neuroprotective and antidepressant-like effects, but its impact on stress-induced memory deficits and the underlying mechanisms remain unclear. METHODS:A chronic restraint stress (CRS) mouse model was employed. DHM was intraperitoneally administered daily (20 mg/kg bodyweight) for 8 consecutive days. Depression-like behavior and memory functions were assessed with the tail suspension test, the object recognition memory (ORM) task, and the Y-maze test. Network pharmacology, molecular docking, and molecular dynamics (MD) simulations were integrated to predict potential targets and associated signal pathways. Expression of hippocampal PKA, p-CREB, CREB, and BDNF was measured through Western blotting. RESULTS:CRS significantly increased immobility time in the tail suspension test and impaired both recognition memory (ORM) and spatial working memory (Y-maze), without affecting locomotor activity. DHM treatment effectively reversed behavioral despair and memory deficits. Network pharmacology identified 47 intersecting targets between DHM and depression-related memory impairment, with CREB1, ESR1 and NOS1 as core hub nodes. KEGG enrichment particularly implicated the involvement of the cAMP signaling pathway and other signaling pathways, which are associated with depression and/or memory impairment. Molecular docking predicted strong binding affinities of DHM to CREB1 (-9.225 kcal/mol), NOS1 (-9.113 kcal/mol) and ESR1 (-7.903 kcal/mol). MD simulations confirmed the thermodynamic stability of DHM-ESR1 and DHM-NOS1 complexes. Western blot analysis demonstrated that DHM treatment significantly increased the levels of hippocampal PKA, p-CREB and BDNF, without altering total CREB expression in CRS mice. CONCLUSIONS:DHM alleviated CRS-induced depression-like behaviors and memory deficits, possibly through regulation of multiple signaling pathways, including the hippocampal PKA-CREB-BDNF signaling pathway. These findings highlight DHM as a promising natural therapeutic candidate for depression-associated cognitive impairment.

Esketamine, the right-handed optical isomer of racemic ketamine, is a rapidly acting antidepressant approved by the FDA for treatment-resistant depression in 2019. However, few studies have investigated esketamine's role in learning and memory, particularly in the context of memory reconsolidation. Herein, we evaluated esketamine's role in memory reconsolidation in 7-week-old male Institute of Cancer Research mice subjected to the novel object recognition (NOR) memory task. The NOR reconsolidation procedure comprised three phases: sampling, reactivation, and testing. Esketamine-enhanced NOR memory performance when injected into mice 0 h after reactivation rather than following a 6 h delay. Conversely, administering esketamine 24 h after sampling without reactivation did not enhance NOR memory performance. Notably, esketamine exhibited no discernible effects on nonspecific responses, such as locomotor activity and exploratory behavior. Furthermore, the α-amino-3‑hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type receptor antagonist NBQX effectively blocked the esketamine-induced enhancement of memory reconsolidation. In conclusion, esketamine treatment markedly improves memory reconsolidation in NOR tasks, and this effect is linked to AMPA receptor activity.

There is a body of evidence to suggest that chronic stress modulates neurochemical homeostasis, alters neuronal structure, inhibits neurogenesis and contributes to development of mental disorders. Chronic stress-associated mental disorders present common symptoms of cognitive impairment and depression with complex disease mechanisms. P-coumaric acid (p-CA), a natural phenolic compound, is widely distributed in vegetables, cereals and fruits. p-CA exhibits a wide range of health-related effects, including anti-oxidative-stress, anti-mutagenesis, anti-inflammation and anti-cancer activities. The current study aims to evaluate the therapeutic potential of p-CA against stress-associated mental disorders. We assessed the effect of p-CA on cognitive deficits and depression-like behavior in mice exposed to chronic restraint stress (CRS); we used network pharmacology, biochemical and molecular biological approaches to elucidate the underlying molecular mechanisms. CRS exposure caused memory impairments and depression-like behavior in mice; p-CA administration attenuated these CRS-induced memory deficits and depression-like behavior. Network pharmacology analysis demonstrated that p-CA was possibly involved in multiple targets and a variety of signaling pathways. Among them, the protein kinase A (PKA) - cAMP-response element binding protein (CREB) - brain derived neurotrophic factor (BDNF) signaling pathway was predominant and further characterized. The levels of PKA, phosphorylated CREB (pCREB) and BDNF were significantly lowered in the hippocampus of CRS mice, suggesting disruption of the PKA-CREB-BDNF signaling pathway; p-CA treatment restored the signaling pathway. Furthermore, CRS upregulated expression of proinflammatory cytokines in hippocampus, while p-CA reversed the CRS-induced effects. Our findings suggest that p-CA will offer therapeutic benefit to patients with stress-associated mental disorders.

The interactions and secretions within the tumour have a pivotal role in tumour growth and therapy. Immunosuppressive cells such as regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), tumour-associated macrophages (TAMs), and cancer-associated fibroblasts (CAFs) secrete some substances, which can result in the exhaustion of anti-tumour immunity. To stimulate anti-tumour immunity, suppression of the secretion and interactions of immunosuppressive cells, on the other hand, stimulation of proliferation and activation of natural killer (NK) cells and CD8+ T lymphocytes are required. Apigenin is a flavone with anticancer properties. Emerging evidence shows that not only does apigenin modulate cell death pathways in cancer cells but it also can stimulate anti-tumour immune cells to release death signals and suppress the release of tumour-promoting molecules. In this review, we discuss the interactions between apigenin and various cells within the tumour microenvironment (TME). These interactions may enhance anti-tumour immunity to improve the efficiency of anticancer remedies such as immunotherapy.

Depression, a mood disorder, affects one in fifteen adults, has multiple risk factors and is associated with complicated underlying pathological mechanisms. P-coumaric acid (p-CA), a phenolic acid, is widely distributed in vegetables, fruits and mushrooms. P-CA has demonstrated a protective role against oxidative stress and inflammation in various diseases, including cardiovascular disease, diabetes and cancer. In the current study, we investigated the protection of p-CA against depression and memory impairment in a corticosterone (CORT)-induced chronic depressive mouse model. CORT administration resulted in depression-like behaviors and memory impairment. P-CA treatment alleviated CORT-induced depression-related behaviors and memory impairment. Network pharmacology predicted that p-CA had multiple targets and mediated various signaling pathways, of which inflammation-associated targets and signaling pathways are predominant. Western blotting showed CORT-induced activation of the advanced glycation end product (AGE)-receptor of AGE (RAGE) (AGE-RAGE) signaling and increased expression of the proinflammatory cytokines interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNFα) in the hippocampus, while p-CA treatment inactivated AGE-RAGE signaling and decreased the levels of IL-1β and TNFα, suggesting that protection against depression and memory impairment by p-CA is mediated by the inhibition of inflammation, mainly via the AGE-RAGE signaling pathway. Our data suggest that p-CA treatment will benefit patients with depression.

目的 探索对香豆酸(p-coumaric acid,p-CA)对嗅球切除小鼠抑郁样行为的作用及其可能机制.方法 采用嗅球摘除术建立小鼠嗅球切除(olfactory bulbectomy,OBX)模型,分别采用旷场测试观察小鼠活动度,强迫游泳测试和悬尾测试检测小鼠抑郁样行为.结果 OBX小鼠强迫游泳和悬尾测试中抑郁样行为及旷场测试中激越行为显著性增加,而p-CA改善了OBX小鼠强迫游泳和悬尾测试中的抑郁样行为及旷场测试中的激越行为.此外,AMPA受体拮抗剂NBQX处理阻断了p-CA的这种改善作用,AMPA受体激动剂CX546处理增强了p-CA的这种改善作用.结论 P-CA改善OBX小鼠抑郁样行为,AMPA受体可能介导了此作用.

在高等学校教育教学管理中,实验室管理是学校教学体系的关键组成部分,也是其进行科学研究、实践教学的主要基地.高校实验室的管理水平对保证高校重点科研项目顺利实施、培养学生实际动手和解决问题、提升教学质量能力等有重要的意义.文章主要探究高校实验室管理存在的问题及对策,对高校实验室管理的基本内涵与主要内容进行系统分析和总结.通过对高校实验室管理现状的介绍,对其所存在的问题进行研究和归纳,分析当前需要解决的核心问题,探究高校实验室管理对策,以期能够促进高校实验室的建设和管理.

目的:探究表膜蛋白(SjOST48)DNA疫苗对日本血吸虫感染的免疫保护效果.方法:通过PCR扩增将OST48基因序列连接到pcDNA3.1(+)质粒上,将构建成功的日本血吸虫表膜蛋白SjOST48的真核质粒pcDNA3.1/SjOST48(100μg)分别于0、2、4、6、8周免疫雌性BALB/c小鼠(小鼠左后腿股四头肌肌肉注射);末次免疫2周后,检测各组小鼠血清IgG及其亚类水平;无菌分离小鼠脾淋巴细胞,CCK-8法评估pcDNA3.1/SjOST48免疫小鼠脾淋巴细胞增殖情况;ELISA法检测小鼠脾淋巴细胞上清中TNF-α、INF-γ、IL-4和IL-10水平;末次免疫2周后血吸虫尾蚴(20±1条)感染小鼠,感染6周后处死小鼠并无菌分离肝脏组织行HE染色,显微镜下观察肝脏虫卵肉芽肿大小及虫卵周围胶原沉积情况,计算肝组织减卵率.结果:pcDNA3.1/SjOST48转染HeLa细胞后成功在真核细胞内表达;ELISA结果显示,pcDNA3.1/SjOST48免疫小鼠在第2周即产生SjOST48特异性抗体,随后抗体水平逐渐增加,第8周达到峰值,且各实验组IgG2a/IgG1的比值均大于1;pcDNA3.1/SjOST48免疫小鼠脾淋巴细胞增殖水平最为显著(P<0.05),并且上清中TNF-α、IL-10和INF-γ分泌水平明显增加(P<0.05),但IL-4分泌水平则无统计学差异(P>0.05);日本血吸虫感染6周后,与SjOST48免疫小鼠相比,pcDNA3.1/SjOST48免疫小鼠肝脏炎症浸润较轻,表面虫卵结节较少、虫卵肉芽组织数量及周围胶原含量明显减少,肝脏减卵效果显著.结论:SjOST48 DNA疫苗能诱导高水平的特异性SjOST48抗体以及Th1型细胞免疫应答反应,显著增强其抗感染保护作用.

目的 探讨白细胞介素18(IL-18)是否能增强DNA疫苗候选抗原pcDNA3.1/SjOST48对日本血吸虫病感染的免疫保护效果. 方法 构建pcDNA3.1/SjOST48和pcDNA3.1/IL-18真核载体,表达重组蛋白.Western blotting检测HeLa细胞内重组质粒pcDNA3.1/SjOST48和pcDNA3, 1/IL-18表达情况,ELISA检测细胞培养基中IL-18的表达情况.100只雌性BALB/c小鼠随机均分为PBS组(空白对照组)、pcDNA3.1组(空质粒组)、pcDNA3.1/IL-18组、pcDNA3.1/SjOST48组和pcDNA3.1/SjOST48+pcDNA3.1/IL-18组等5组,各组小鼠左后腿股四头肌肌内注射相应的重组质粒(30μg),共免疫3次,每次间隔14 d.末次免疫后2周,各组取5只小鼠采集血样,ELISA检测各组小鼠血清IgG抗体及其亚类(IgG1和IgG2a)水平.末次免疫后3周,各组取5只小鼠脾组织,无菌分离小鼠脾淋巴细胞,ELISA检测小鼠脾淋巴细胞上清中TNF-α、INF-γ、IL-2、IL-4、IL-6和IL-17含量及脾淋巴细胞增殖水平.末次免疫后2周,各组取15只免疫小鼠感染血吸虫尾蚴(20±1)条/鼠.感染后6周处死小鼠,无菌分离肝,计算减卵率;门静脉灌注法收集成虫,计算减虫率;另取肝组织,切片后行HE染色,显微镜下观察肝虫卵肉芽肿数量及炎症浸润情况. 结果 末次免疫后2周,ELISA结果显示,pcDNA3.1/SjOST48+p cDNA3.1/IL-18组、pcDNA3.1/SjOST48组、pcDNA3.1/IL-18组小鼠的IgG抗体水平分别为0.82±0.07、0.41±0.06、0.16±0.05,均高于pcDNA3.1组的0.12±0.03(P＜0.05);pcDNA3.1/SjOST48 +pcDNA3.1/IL-18组较pcDNA3.1/SjOST48组和pcDNA3.1/IL-18组均增高 (P＜0.05);pcDNA3.1/SjOST48 +pcDNA3.1/IL-18组和pcDNA3.1/SjOST48组的IgG2a/IgG1比值分别为4.02±0.01、2.51±0.01 (P＜ 0.05),均＞1,其他3组均＜1.末次免疫后3周,pcDNA3.1/SjOST48+pcDNA3.1/IL-18组小鼠脾淋巴细胞上清中的IL-2、TNF-α、INF-γ、IL-6和IL-17含量分别为(101.82±8.90)、 (738.02±146.22)、 (593.41±51.07)、 (685.64±171.2)、 (261.32±48.19)pg/ml,高于pcDNA3.1/SjOST48组[(55.82±9.69)、 (538.21±85.26)、 (393.41±51.07)、 (335.64±62.63)、(118.32±8.91) pg/ml] (P＜0.05)和pcDNA3.1/IL-18组[(35.16±6.43)、 (284.40±69.96) (141.91±24.48)、(198.44±38.15)、 (47.66±14.33) pg/ml] (P＜0.05),三者均高于pcDNA3.1组[(12.91±8.01)、 (74.86±6.64)(23.75±6.06)、 (82.75±10.96)、 (22.91±13.80) pg/ml] (P＜ 0.05);IL-4含量为(12.28±7.08) pg/ml,与pcDNA3.1/SjOST48组[(15.03±10.12)pg/ml]、pcDNA3.1/IL-18组[(13.59±4.42) pg/ml]、pcDNA3.1组[(16.13±10.08) pg/ml]比较差异无统计学意义(P＞0.05).pcDNA3.1/SjOST48+ pcDNA3.1/IL-18组脾淋巴细胞增殖水平为11.84±0.16,高于pcDNA3.1/SjOST48组(5.93±0.25) (P＜0.05)和pcDNA3.1/IL-18组(3.19±0.36) (P＜0.05),三者均高于pcDNA3.1组(2.08±0.16) (P＜0.05).末次免疫后2周,经日本血吸虫感染后6周,pcDNA3.1/SjOST48 +pcDNA3.1/IL-18组小鼠的平均检获成虫数为(14.33±1.08);与pcDNA3.1组比较,减虫率和减卵率分别为46.19％和44.68％,高于pcDNA3.1/SjOST48免疫组(32.18％和35.78％)和pcDNA3.1/IL-18组(13.22％和16.68％) (P＜0.05).各组小鼠肝组织切片HE染色结果显示,与其他4组比较,pcDNA3.1/SjOST48+pcDNA3.1/IL-18组小鼠肝组织虫卵结节较少,虫卵肉芽组织数量明显减少,炎症浸润不明显. 结论 IL-18能使pcDNA3.1/SjOST48免疫小鼠诱导较高水平的Th1型和Th17型免疫应答,并且增强其抗血吸虫感染的免疫保护效果.

目的 探讨谷氨酸转运体抑制剂二氢红藻氨酸(dihydrokainic acid,DHK)对旷场测试中小鼠焦虑样行为的影响.方法 将18只ICR小鼠随机分为溶媒组和DHK组每组9只.2组小鼠分别进行连续2 d的旷场测试,每天各10 min.在第1次旷场测试(OFT 1)前30 min小鼠侧脑室注射DHK或溶媒,OFT 1后24 h进行第2次旷场测试(OFT 2),观察2次旷场测试中小鼠直立样行为时间、理毛时间、进入中央区时间和穿越格子数.结果 在OFT 1和OFT 2中,与溶媒组相比,DHK组小鼠直立样行为时间、理毛时间、进入中央区时间和穿越格子数均无统计学意义(均P>0.05).结论 DHK注射30 min或24 h不影响旷场测试中小鼠焦虑样行为及活动水平.

目的: 探索对香豆酸(p-CA)对慢性束缚应激(CRS)诱导小鼠抑郁样行为的作用。方法: 实验分两批进行,第一批小鼠随机分成对照组(Control),慢性束缚应激组(CRS)和慢性束缚应激+p-CA组(CRS+p-CA),每组8只,其中慢性束缚应激小鼠每天接受4 h的束缚应激,连续束缚21 d,而对照组小鼠留在笼中不被打扰。第22日小鼠腹腔注射溶媒(10%吐温80)或p-CA(100 mg/kg),注射后1 h进行自发活动测试(LMA),注射后4 h进行强迫游泳测试(FST),注射后24 h进行悬尾测试。第二批小鼠随机分成慢性束缚应激组(CRS) ,慢性束缚应激+ANA-12(原肌球蛋白激酶B拮抗剂)组(CRS+ANA-12)和慢性束缚应激+p-CA组(CRS+ p-CA)慢性束缚应激+p-CA +ANA-12组(CRS+ p-CA +ANA-12),每组8只,4组小鼠每天接受4 h的束缚应激,连续束缚21 d。第22日小鼠腹腔注射溶媒(10%吐温80)或p-CA(100 mg/kg),ANA-12(0.5 mg/kg)在p-CA注射前30 min给药。注射后1 h进行自发活动测试(LMA),注射后2 h进行强迫游泳测试(FST),注射后24 h进行悬尾测试。结果: ①在实验一中,与Control组相比,CRS组小鼠强迫游泳和悬尾测试中不动时间显著性增多(P＜0.05);而与CRS组相比,CRS+ p-CA组小鼠不动时间显著性减少(P＜0.05,P＜0.01)。②在实验二中,与CRS组相比,CRS+ p-CA组小鼠强迫游泳和悬尾测试中不动时间显著性减少(P＜0.05);而与CRS+ p-CA组相比,CRS+ p-CA +ANA-12组小鼠强迫游泳和悬尾测试中不动时间显著性增多(P＜0.05)。结论: P-CA改善慢性束缚应激诱导小鼠抑郁样行为,TrkB受体可能介导了此作用。.

目的:探索对香豆酸(p-CA)对慢性束缚应激(CRS)小鼠记忆障碍的作用及其可能机制.方法:实验分两批进行,第一批小鼠随机分成对照组(Control)、慢性束缚应激+溶媒组(CRS)和慢性束缚应激+p-CA组(CRS+p-CA),每组8只,其中CRS小鼠每天接受4 h的束缚应激,连续束缚10 d,而对照组小鼠留在笼中不被打扰.第11日小鼠腹腔注射溶媒(10％吐温80)或p-CA(100 mg/kg),注射后2 h进行Y迷宫测试,注射后24 h进行新颖物体识别(NOR)采样,采样后2 h进行新颖物体识别测试.实验结束后断头取脑剥离海马并检测BDNF蛋白表达.第二批小鼠随机分成慢性束缚应激组(CRS),慢性束缚应激+ANA-12(原肌球蛋白激酶B拮抗剂)组(CRS+ANA-12),慢性束缚应激+p-CA组(CRS+p-CA)和慢性束缚应激+p-CA+ANA-12组(CRS+p-CA+ANA-12),每组8只,四组小鼠每天接受4 h的束缚应激,连续束缚10 d.第11日小鼠腹腔注射溶媒(10％吐温80)或p-CA(100 mg/kg),ANA-12在p-CA注射前30 min给药.注射后2 h进行Y迷宫测试,注射后24 h进行新颖物体识别采样,采样后2 h进行新颖物体识别测试.结果:①在实验一中,与Control组相比,CRS组小鼠Y迷宫和NOR测试的记忆显著性降低(P<0.05),BDNF蛋白表达显著性降低(P<0.01);而与CRS组相比,CRS+p-CA组小鼠记忆显著性提高(P<0.05),BDNF蛋白表达显著提高(P<0.01).②在实验二中,与CRS组相比,CRS+p-CA组小鼠Y迷宫和NOR测试中记忆显著提高(P<0.05);而与CRS+p-CA组相比,CRS+p-CA+ANA-12组小鼠Y迷宫和NOR测试中记忆显著性降低(P<0.05).结论:P-CA可改善CRS诱导的小鼠记忆障碍,这种作用可能依赖于BDNF蛋白表达的上调.

目的: 探索对香豆酸(p-CA)对慢性束缚应激(CRS)小鼠记忆障碍的作用及其可能机制。方法: 实验分两批进行,第一批小鼠随机分成对照组(Control)、慢性束缚应激＋溶媒组(CRS)和慢性束缚应激+ p-CA组(CRS+ p-CA), 每组8只,其中CRS小鼠每天接受4 h的束缚应激,连续束缚10 d,而对照组小鼠留在笼中不被打扰。第11日小鼠腹腔注射溶媒(10%吐温80)或p-CA(100 mg/kg),注射后2 h进行Y迷宫测试,注射后24 h进行新颖物体识别(NOR)采样,采样后2 h进行新颖物体识别测试。实验结束后断头取脑剥离海马并检测BDNF蛋白表达。第二批小鼠随机分成慢性束缚应激组(CRS) ,慢性束缚应激+ANA-12(原肌球蛋白激酶B拮抗剂)组(CRS+ANA-12),慢性束缚应激+p-CA组(CRS+ p-CA)和慢性束缚应激+p-CA +ANA-12组(CRS+ p-CA +ANA-12),每组8只,四组小鼠每天接受4 h的束缚应激,连续束缚10 d。第11日小鼠腹腔注射溶媒(10%吐温80)或p-CA(100 mg/kg),ANA-12在p-CA注射前30 min给药。注射后2 h进行Y迷宫测试,注射后24 h进行新颖物体识别采样,采样后2 h进行新颖物体识别测试。 结果: ①在实验一中,与Control组相比,CRS组小鼠Y迷宫和NOR测试的记忆显著性降低(P＜0.05),BDNF蛋白表达显著性降低(P＜0.01);而与CRS组相比,CRS+ p-CA组小鼠记忆显著性提高(P＜0.05),BDNF蛋白表达显著提高(P＜ 0.01)。②在实验二中,与CRS组相比,CRS+ p-CA组小鼠Y迷宫和NOR测试中记忆显著提高(P＜0.05);而与CRS+p-CA组相比,CRS+p-CA +ANA-12组小鼠 Y迷宫和NOR测试中记忆显著性降低(P＜0.05)。结论: P-CA可改善CRS诱导的小鼠记忆障碍,这种作用可能依赖于BDNF蛋白表达的上调。.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">目的探索对香豆酸（p-coumaric acid,p-CA）对急性应激小鼠记忆提取障碍的作用及其可能机制。方法采用1 h急性束缚应激（acute stress,AS）建立小鼠记忆提取障碍模型,分别运用新颖物体识别（novel object recognition,NOR）记忆提取范式和（或）物体位置识别记忆（object location recognition,OLR）提取范式检测各组小鼠记忆表现。结果 NOR和OLR测试显示,与Control组相比,AS组小鼠记忆提取障碍,而p-CA可改善AS小鼠的这一现象。此外,在NOR测试中,胞外调节蛋白激酶（extracellular signal-regulated kinase,ERK）信号抑制剂PD98059和蛋白激酶A（protein kinase A,PKA）信号抑制剂H89分别阻断了p-CA对AS小鼠记忆提取的改善作用。结论 p-CA改善AS诱导小鼠记忆提取障碍,并且这种作用可能依赖于ERK和PKA信号。</span>

目的:探索对香豆酸(p-CA)对慢性束缚应激(CRS)诱导小鼠抑郁样行为的作用.方法:实验分两批进行,第一批小鼠随机分成对照组(Control),慢性束缚应激组(CRS)和慢性束缚应激+p-CA组(CRS+p-CA),每组8只,其中慢性束缚应激小鼠每天接受4 h的束缚应激,连续束缚21 d,而对照组小鼠留在笼中不被打扰.第22日小鼠腹腔注射溶媒(10％吐温80)或p-CA(100 mg/kg),注射后1 h进行自发活动测试(LMA),注射后4 h进行强迫游泳测试(FST),注射后24 h进行悬尾测试.第二批小鼠随机分成慢性束缚应激组(CRS),慢性束缚应激+ANA-12(原肌球蛋白激酶B拮抗剂)组(CRS+ANA-12)和慢性束缚应激+p-CA组(CRS+p-CA)慢性束缚应激+p-CA+ANA-12组(CRS+p-CA+ANA-12),每组8只,4组小鼠每天接受4 h的束缚应激,连续束缚21 d.第22日小鼠腹腔注射溶媒(10％吐温80)或p-CA(100 mg/kg),ANA-12(0.5 mg/kg)在p-CA注射前30 min给药.注射后1 h进行自发活动测试(LMA),注射后2 h进行强迫游泳测试(FST),注射后24 h进行悬尾测试.结果:①在实验一中,与Control组相比,CRS组小鼠强迫游泳和悬尾测试中不动时间显著性增多(P<0.05);而与CRS组相比,CRS+p-CA组小鼠不动时间显著性减少(P<0.05,P<0.01).②在实验二中,与CRS组相比,CRS+p-CA组小鼠强迫游泳和悬尾测试中不动时间显著性减少(P<0.05);而与CRS+p-CA组相比,CRS+p-CA+ANA-12组小鼠强迫游泳和悬尾测试中不动时间显著性增多(P<0.05).结论:P-CA改善慢性束缚应激诱导小鼠抑郁样行为,TrkB受体可能介导了此作用.

随着我国医疗事业及医学的发展,有关医学的课程也有着很大的改革,特别是人体解剖学,人体解剖学是医学的基础课程,通过人体解剖学能够更加清晰明了的研究人体内器官及骨骼的构造,是医学院学生了解人体机构的主要途径.但是传统的人体解剖学课程存在诸多的弊端,在高速发展的医疗事业潮流中渐渐跟不上步伐,因此,探索新的人体解剖学教学模式是当今阶段所应该主要重视的.其中互动教学模式是人体解剖学教学的新趋势,能够更好的帮助学生学习人体解剖学课程.所以,本文就关于互动教学模式下提高人体解剖学课程质量展开研讨,并针对如何特高教学质量提出相应的建设性意见.

目的 探讨金黄色葡萄球菌通过P38 MAPK信号通路诱导U937细胞凋亡中机制.方法 100株金黄色葡萄球菌均自实验室中获取,使用不同浓度P38 MAPK抑制剂对U937细胞进行处理,后借助双染分析感染后不同时间内U937细胞凋亡的情况.结果 U937细胞凋亡率与时间之间呈正比例相关性.结论 P38 MAPK信号通路是金黄色葡萄球菌诱导U937细胞凋亡的重要传导.

目的 探讨金黄色葡萄球菌肠毒素B对人鼻黏膜上皮细胞分泌黏蛋白MUC5AC的促进作用及机制.方法 对人鼻黏膜上皮细胞进行体外培养,采用不同浓度的金黄色葡萄球菌肠毒素B孵育细胞0～24 h,采用ELISA法检测培育上清中的MUC5AC分泌水平,检测培育上清中的MUC5AC分泌水平,p38的磷酸化采用Western blotting进行分析,采用p38抑制剂SB203580(20μmol/L)对人鼻黏膜上皮细胞进行处理,观察其在介导MUC5AC分泌中的作用.结果 与经金黄色葡萄球菌肠毒素处理的人鼻黏膜上皮细胞分泌黏蛋白MUC5AC水平比较,经金黄色葡萄球菌肠毒素处理的人鼻黏膜上皮细胞分泌黏蛋白MUC5AC水平更高,且浓度越高,鼻黏膜上皮细胞分泌黏蛋白MUC5AC水平越高,组间对比差异显著(P<0.05);100μg/l的金黄色葡萄球菌肠毒素B刺激鼻黏膜上皮细胞30 min后,即可测出p38磷酸化,且时间越久,浓度越高,60 min后到达峰值,细胞内总p38水平无显著变化,磷酸化p38及总p38比值,处理30 min及60 min与未经金黄色葡萄球菌肠毒素B处理的人鼻黏膜上皮细胞比较差异显著,且时间越长,比值越高(P<0.05);人鼻黏膜上皮细胞采用1、10及20μmol/L p38抑制剂SB203580预处理半小时后,分泌MUC5AC水平显著低于而未经抑制剂SB203580预处理的细胞分泌MUC5AC水平,且浓度越高,分泌量越少(P<0.05).结论 金黄色葡萄球菌肠毒素B通过p38促使人鼻黏膜上皮细胞分泌黏蛋白MUC5AC.

以自建“邵院解剖”微信公众平台为例,介绍该微信公众平台的组建、内容板块及在医学生第二课堂中的应用,提出微信公众号运营中存在的问题及未来完善的方向,对高校医学生第二课堂建设和医学科普活动的开展具有参考价值.

为改善组织胚胎学的教学现状,提升教学效果,提高学生课堂学习的兴趣和积极性,将PBL教学直接引入教学实践中,旨在提高学生的学习效率.