Glucocorticoid (GCs), as an adjuvant drug, is widely used for alleviating chemotherapy or immunotherapy-induced adverse events, such as nausea and immune-related diseases in lung cancer treatment. However, whether GCs directly affects lung cancer progression remains unclear. This study focused on the effects of dexamethasone (DEX) on the proliferation and migration of lung cancer cells as well as the related potential mechanisms using EdU, CCK8, Transwell, Wound healing, TCGA database, HPA database, qPCR and Western blotting. Additionally, subcutaneous tumor and tail vein tumor injection models were established for investigating DEX action in vivo. Further, to confirm the key functional of Smad2/3 for DEX regulating lung cancer cells proliferation and migration. Mechanistic assays explored the upstream regulatory molecules TGFβ1, TGFβR1 and p-TGFβR1 expression after DEX treatment. Moreover, DEX modulates lung cancer cell proliferation and migration on a glucocorticoid receptor (GR)-independent manner and the association with Smad2/3 activation were investigated. Results: The results showed that DEX (1 µM) treatment significantly inhibited the proliferation and the migration of lung cancer cells A549 and LLC cells. TCGA and HPA databases showed Smad2/3 expression was positively correlated with lung cancer progression. Mechanistically, DEX treatment significantly inhibited Smad2/3 activation in vitro and in vivo, manifested as a decrease in the expression of p-Smad2 (Ser465/467), Smad2, p-Smad3 (Ser423/425), and Smad3. Smad2/3 knockdown significantly inhibit the proliferation, migration and Smad2/3 activity of A549 and LLC cells. Creatine, the agonist of Smad2/3 activation, markedly reversed the inhibitory effects of DEX on the proliferation and migration of A549 and LLC cells. Smad2/3 overexpression also reversed the inhibitory effects of DEX on A549 cell proliferation and migration. Further studies showed DEX inhibited the expression of TGFβR1 and p-TGFβR1(Ser165) and the levels of TGFβ1. Moreover, GR knockout significantly promoted the proliferation, migration and Smad2/3 activity in A549 cell. DEX can inhibits A549 cell proliferation and migration through suppressing Smad2/3 activation independent of GR. Conclusion: DEX inhibited the proliferation and migration of lung cancer cells by suppressing Smad2/3 activation, providing a theoretical basis and experimental data for clinical practice.

Porcine reproductive and respiratory syndrome virus (PRRSV) has caused significant economic losses in the swine industry. In this study, the high-throughput sequencing, microRNAs (miRNAs) mimic, and lentivirus were used to screen for potential miRNAs that can promote PRRSV infection in porcine alveolar macrophages or Marc-145 cells. It was observed that novel-216, a previously unidentified miRNA, was upregulated through the p38 signaling pathway during PRRSV infection, and its overexpression significantly increased PRRSV replication. Further analysis revealed that novel-216 regulated PRRSV replication by directly targeting mitochondrial antiviral signaling protein (MAVS), an upstream molecule of type Ⅰ IFN that mediates the production and response of type Ⅰ IFN. The proviral function of novel-216 on PRRSV replication was abolished by MAVS overexpression, and this effect was reversed by the 3′UTR of MAVS, which served as the target site of novel-216. In conclusion, this study demonstrated that PRRSV-induced upregulation of novel-216 served to inhibit the production and response of typeⅠ IFN and facilitate viral replication, providing new insights into viral immune evasion and persistent infection.

Background : A stable and standardized source of mesenchymal stem cells is a prerequisite for bone repair tissue engineering research and application. We aimed to establish a stable cell line of bone marrow mesenchymal stem cells from New Zealand rabbits and explore their osteogenic differentiation capacity.Methods : Primary rabbit bone marrow mesenchymal stem cells(RBMSCs) were isolated and immortalized via retroviral expression of SV40 Large T antigen(LTA). To assess the osteogenic differentiation capacity of the cells in vitro, we studied the alkaline phosphatase(ALP) expression level and calcium deposition in bone morphogenetic protein 9(BMP9)-i nduced immortalized cells using ALP staining and quantification, as well as alizarin red staining. Ectopic bone formation by the cells was assessed using micro-computed tomography(μCT) and histological examination.Results : The immortalized cell line we established using SV40 LTA, which we termed iRBMSCs, was non-tumorigenic and maintained long-term proliferative activity. We further discovered that BMP9(MOI = 30) effectively induced the osteogenic differentiation capacity of iRBMSCs in vitro, and there was a synergy with GelMA hydrogel in inducing osteogenic differentiation of the iRBMSCs in vivo.Conclusion : We confirmed that iRBMSCs are promising as a stable cell line source for bone defect repair engineering.

The chromodomain helicase DNA binding domain 5 (CHD5) is required for neural development and plays an important role in the regulation of gene expression. Although CHD5 exerts a broad tumor suppressor effect in many tumor types, its specific functions regarding its expression levels, and impact on immune cell infiltration, proliferation and migration in glioma remain unclear. Here, we evaluated the role of CHD5 in tumor immunity in a pan-cancer multi-database using the R language. The Cancer Genome Atlas (TCGA), Genotype Tissue Expression (GTEx), and Cancer Cell Lines Encyclopedia (CCLE) datasets were utilized to determine the role of CHD5 in 33 types of cancers, including the expression level, prognosis, tumor progression, and immune microenvironment. Furthermore, we explored the effect of CHD5 on glioma proliferation and migration using the cell counting kit 8 (CCK-8) assay, transwell assays and western blot analysis. The findings from our pan-cancer analysis showed that CHD5 was differentially expressed in the tumor tissues as compared to the normal tissues. Survival analysis showed that CHD5 was generally associated with the prognosis of glioblastoma (GBM), low Grade Glioma (LGG) and neuroblastoma, where the low expression of CHD5 was associated with a worse prognosis in glioma patients. Then, we confirmed that the expression level of CHD5 was associated with tumor immune infiltration and tumor microenvironment, especially in glioma. Moreover, si-RNA mediated knockdown of CHD5 promoted the proliferation and migration of glioma cells in vitro. In conclusion, CHD5 was found to be differentially expressed in the pan-cancer analysis and might play an important role in antitumor immunity. CHD5 is expected to be a potential tumor prognostic marker, especially in glioma.

目的 通过慢性温和不可预知刺激(chronic unpredictable and mild stress,CUMS)建立SD大鼠抑郁模型,初步探讨不同风格音乐改善SD大鼠抑郁样行为的效果和机制.方法 通过孤养后持续4周慢性不可预知刺激来构建CUMS大鼠,以糖水偏好实验(sucrose preference test,SPT)和强迫游泳实验(forced swimming test,FST)筛选出39只CUMS抑郁大鼠,随机均分为模型组、轻音乐组、古典音乐组,并另设一组不做任何刺激的对照组作空白对照.轻音乐组,古典音乐组各自每天播放久石让音乐、莫扎特音乐4 h,持续3周后立即进行SPT,FST和O迷宫实验(O-maze)测试.测试结束后立即取材.HE染色观察海马组织的结构变化、免疫组化和Western Blot检测脑源性神经营养因子(brain derived neurotrophic factor,BDNF)的表达水平、液相色谱串联质谱(liquid chromatography-tandem mass spectrometry,LC-MS/MS)检测海马组织中皮质酮(corticosterone,CORT)、五羟色胺(5-hydroxytryptamine,5-HT)含量.ELISA法检测外周血BDNF、CORT、5-HT和IL-1β的浓度变化.结果 与模型组相比,轻音乐组与古典音乐组大鼠的糖水偏好百分比均上升(P<0.05)、FST不动时间均缩短(P<0.01)、进入O迷宫开放臂的次数与停留时间均增加(P<0.05).与模型组相比,轻音乐组和古典音乐组的海马组织结构完整、排列整齐,BDNF表达水平均升高(P<0.01).两组音乐干预后,血清BDNF水平均显著升高(P<0.01).两音乐组海马中CORT含量均降低(P<0.01),古典音乐组血清CORT含量在古典音乐组显著降低(P<0.01).血清5-HT含量在轻音乐组升高(P<0.01),但在古典音乐组无显著性差异.两音乐组血清IL-1β 浓度均显著降低(P<0.01).结论 古典音乐和轻音乐均可以在一定程度上改善抑郁模型大鼠的行为.

Neuroblastoma (NB) is an extracranial solid tumor in children with poor prognosis in high-risk patients and its pathogenesis and prognostic markers urgently need to be explored. This study aimed to explore potential biomarkers related to NB from the aspect of lipid metabolism. Fifty-eight lipid metabolism-related differentially expressed genes between high-risk NB and non-high-risk NB in the GSE49710 dataset were analyzed using bioinformatics, including 45 down-regulated genes and 13 up-regulated genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis identified steroid hormone biosynthesis as an abnormal metabolic pathway in high-risk NB. Survival analysis established a three-gene prognostic model, including ACHE, GDPD5 and PIK3R1. In the test data, the AUCs of the established prognostic models used to predict patient survival at 1, 3 and 5 years were 0.84, 0.90 and 0.91, respectively. Finally, in the SH-SY5Y cell line, it was verified that overexpression of GDPD5 can inhibit cell proliferation and migration, as well as affect the lipid metabolism of SH-SY5Y, but not the sugar metabolism. hsa-miR-592 was predicted to be a potential target miRNA of GDPD5 by bioinformatics. In conclusion, this study develops a lipid-metabolism-related gene-based prognostic model for NB and demonstrates that GDPD5 inhibits SH-SY5Y proliferation and migration and may be targeted by hsa-miR-592 and inhibit SH-SY5Y fat synthesis.

Teeth arise from the tooth germ through sequential and reciprocal interactions between immature epithelium and mesenchyme during development. However, the detailed mechanism underlying tooth development from tooth germ mesenchymal cells (TGMCs) remains to be fully understood. Here, we investigate the role of Wnt/β‐catenin signalling in BMP9‐induced osteogenic/odontogenic differentiation of TGMCs. We first established the reversibly immortalized TGMCs (iTGMCs) derived from young mouse mandibular molar tooth germs using a retroviral vector expressing SV40 T antigen flanked with the FRT sites. We demonstrated that BMP9 effectively induced expression of osteogenic markers alkaline phosphatase, collagen A1 and osteocalcin in iTGMCs, as well as in vitro matrix mineralization, which could be remarkably blunted by knocking down β‐catenin expression. In vivo implantation assay revealed that while BMP9‐stimulated iTGMCs induced robust formation of ectopic bone, knocking down β‐catenin expression in iTGMCs remarkably diminished BMP9‐initiated osteogenic/odontogenic differentiation potential of these cells. Taken together, these discoveries strongly demonstrate that reversibly immortalized iTGMCs retained osteogenic/odontogenic ability upon BMP9 stimulation, but this process required the participation of canonical Wnt signalling both in vitro and in vivo. Therefore, BMP9 has a potential to be applied as an efficacious bio‐factor in osteo/odontogenic regeneration and tooth engineering. Furthermore, the iTGMCs may serve as an important resource for translational studies in tooth tissue engineering.

Embryo implantation and decidualization are crucial for successful pregnancy, which include multiple genes and signaling pathways, while the precise mechanism regarding embryo implantation and decidualization has yet to be explored. The GABA which activates GABAA or GABAB receptors has been found playing an important role in early pregnancy. Here we seek to investigate whether GABAB receptors participate in embryo implantation in mice. This study first characterized the spatiotemporal expression pattern of GABAB receptors in the uterus during the peri-implantation period and found that GABAB1 expression was drastically upregulated in stromal cells on days 4–6, a period of embryo implantation and early stages of decidualization. Embryo delayed implantation and oil-induced decidualization models were further used to confirm that the GABAB1 was associated with embryo implantation and decidualization. We also found estrogen or progesterone had no directly effect on expression of GABAB1 in ovariectomized model. Because we were unable to detect significant GABAB2 which couples with GABAB1 to form whole GABAB receptors, and the agonist and antagonist of whole GABAB receptors had weak effect on the proliferation and differentiation of stromal cells as well, we excluded the possibility whole GABAB receptors function, and concluded it should be non-classical signals of GABAB1 involving in embryo implantation and decidualization. Future studies should focus on investigating the roles and mechanisms of GABAB1 during embryo implantation and decidualization.

Objective Nuclear technology has been widely used in military and civilian fields, and radiotherapy is an effective and common form of treatment for cancer. However, acute radiation disease caused by high doses of radiation is a serious complication. The aim of this study was to investigate the chance of mitigating radiation-triggered hematopoiesis failure using human umbilical cord mesenchymal stem cell (HUCMSC) transplantation. Methods Umbilical cords were obtained from three full-term female neonatus through cesarean section at Xinqiao Hospital. Bone marrow mesenchymal stem cells (BMSCs) were cultivated as depicted before. Briefly, monocytes were collected from bone marrow blood by means of density separation columns. An acute radiation disease mouse model was established to compare the restoration effect of HUCMSCs and BMSCs transplanted via the tail vein. The hematopoietic stem cell transplantation (HSCT) mouse model was obtained through bone marrow cell transplantation (BMCT) from C57BL/6 mice (H-2b, donor) to female CB6F1 mice (H-2b×d, recipient) after irradiation. The mice were divided into five groups, including control (saline), irradiated (radiation), bone marrow (HSCT, transplanted 1×106 BM cells), HUCMSC (transplanted a mixture of 1×106 HUCMSCs and 1×106 BM cells), and BMSC group (transplanted a mixture of 1×106 BMSCs and 1×106 BM cells). The blood condition results were used to test the radiation-induced inflammatory reaction, and bone marrow pathological staining (H&E) was used to determine the radiation-induced bone marrow hematopoiesis failure. Results After radiation, HUCMSC transplantation significantly improved the survival rate. By analyzing the blood condition test, colony formation, and bone marrow pathology, it was found that the HUCMSC group demonstrated significant functional improvements in terms of the recovery from hematopoiesis failure and reduction of inflammatory reaction. Conclusions HUCMSCs have more advantages over BMSCs in restoring and promoting the recovery of radiation-induced hematopoietic damage, thus having a new therapeutic potential for patients with acute radiation disease.

Hypobaric hypoxia as an extreme environment in a plateau may have deleterious effects on human health. Studies have indicated that rush entry into a plateau may reduce male fertility and manifest in decreased sperm counts and weakened sperm motility. RNA modifications are sensitive to environmental changes and have recently emerged as novel post-transcriptional regulators in male spermatogenesis and intergenerational epigenetic inheritance. In the present study, we generated a mouse hypoxia model simulating the environment of 5500 m in altitude for 35 days, which led to compromised spermatogenesis, decreased sperm counts, and an increased sperm deformation rate. Using this hypoxia model, we further applied our recently developed high-throughput RNA modification quantification platform based on liquid chromatography with tandem mass spectrometry, which exhibited the capacity to simultaneously examine 25 types of RNA modifications. Our results revealed an altered sperm RNA modifications signature in the testis (6 types) and mature sperm (11 types) under the hypoxia model, with 4 types showing overlap (Am, Gm, m7G, and m22G). Our data first drew the signature of RNA modification profiles and comprehensively analyzed the alteration of RNA modification levels in mouse testis and sperm under a mouse hypoxia model. These data may be highly related to human conditions under a similar hypoxia environment.

CULLIN1 (CUL1) protein, as a scaffold protein in Skp1-CUL1-F box (SCF) E3 ligases complex, was reported involved in different cellular functions to regulate the early embryonic development. In our previous study, we have demonstrated that CUL1 promote trophoblast cell invasion at the maternal–fetal interface in human and the CUL1 protein significantly decreased in preeclampsia (PE) placenta, but how CUL1 involved in placentation is still obscure. Due to the embryo lethal in CUL1 knockout mice, the lentivirus mediated placenta-specific CUL1 knockdown mice model was constructed to uncover the potential role of CUL1 in placentation. In this study, CUL1 was first detected in mouse placenta. CUL1 mainly expressed in trophoblast giant cell at E9.5, and spongiotrophoblast at E11.5 and E13.5 by using immunohistochemistry and int situ hybridization. In lentivirus mediated placenta specific mouse model, the number of implanted embryos was reduced in CUL1 shRNA group at E13.5 and E18.5 compared to control group. Based on the morphological analysis of histologic staining, we observed that spongiotrophoblast layer is expanded, fetal angiogenesis in labyrinth was obstructed and fetus blood cells were accumulated in vessels. These results indicated that decreased expression of CUL1 affect placentation of mice, which give new insights into the cause of gestational diseases, but the exactly mechanism still needs further study.

L-type amino acid transporter 1 (LAT1) is a neutral amino acid transporter expressed in trophoblast giant cells onembryonic day 8 in mice. LAT1 is responsible for metabolism in blastocysts and cancer cells. Despite research concerning the aberrant high expression and indispensable function of LAT1 in various cancers, little is known about the role of LAT1 in regulating the behaviors of human trophoblast cells under different physiological and pathological conditions. The HTR8-SVneo human trophoblast cell line and JEG-3 and JAR choriocarcinoma cell lines are used as models for trophoblast cell biological research. The proliferation and apoptosis of these cells were assayed using the CCK-8 assay and flow cytometry, respectively. Transwell-chambers were used to observed migration and invasion of the cells. Immunofluorescent staining, western blot, and RT-PCR assays were used to determine the possible mechanism of LAT1 on human trophoblast cell behaviors with small interfering RNA or signal agonists and antagonist treatments. LAT1 was expressed in the trophoblast and choriocarcinoma cells. LAT1 was involved in regulating behaviors of these cells, such as cell proliferation, apoptosis, migration, and invasion. Detailed results suggested that LAT1 modulated trophoblast cell functions by mediation of mTORC1 signaling pathways. Our results implicate LAT1 as a very important regulator in human trophoblast cell behaviors at the maternal-fetal interface.

γ‐Aminobutyrate (GABA) is commonly used as a food supplement and a health care product by young females, due to its positive roles in relieving stress, alleviating anxiety, and improving sleep. However, its recommended daily dose in different products varies widely. Besides, it is unknown whether, and how, GABA consumption during early pregnancy influences pregnancy establishment. In this study, we found that when pregnant mice were treated with a high (12.5 mg/g) dose of GABA (orally) during preimplantation, there was a reduction in the number of implantation sites on day 5 of pregnancy. Also, among these unimplanted embryos, most exhibited morphological degeneration and developmental retardation, and only a few of them developed into blastocysts but could not implant into the uterus. Moreover, the expression of uterine receptivity–related factors—LIF, E‐cadherin, and HOXA10—were all downregulated, while the number of uterine glands was reduced in the high GABA dose group. Finally, in vitro results demonstrated that GABA (ranging from 10 to 50 μg/μL) markedly inhibited preimplantation embryo development in a dose‐response manner. However, this inhibitory effect was not observed when the embryos were pretreated with 40 μΜ 2‐hydroxysaclofen, a GABAB antagonist, indicating that GABA exerts its inhibitory effects via its B‐type receptor. Our results suggest that exposure to certain GABA concentrations, during early pregnancy, can impair preimplantation embryo development via its B‐type receptor, and endometrial receptivity, which greatly disturbs early embryo implantation in mice. These findings could raise concerns about GABA consumption during the early stages of pregnancy.

Background:The chronic unpredictable mild stress（CUMS） model has long been considered the best model for exploring the pathophysiological mechanisms underlying depression.However,there are no widely recognised standards for strategies for modeling and for behavioral testing.The present study aimed to optimize the protocols for food deprivation and the sucrose preference test（SPT） for the CUMS model.Methods:We first evaluated the effects of different long periods of food deprivation on the body weight of Sprague Dawley（SD） rats by testing food deprivation for 24 hours（8:00-8:00+）,food deprivation for 12 hours during the daytime（8:00-20:00） and food deprivation for 12 hours at night（20:00-8:00+）.Next,we established a SD rat CUMS model with 15 different stimulations,and used body weight measurement,SPT,forced swim test（FST）,open field test（OFT） and Morris water maze（MWM） test to verify the success of the modeling.In the SPT,consumption of sucrose and pure water within 1 and 12 hours was measured.Results:Twelve hours of food deprivation during the daytime（8:00-20:00） had no effect on body weight,while 12 hours of food deprivation at night（20:00-8:00+） and 24 hours of food deprivation（8:00-8:00+） significantly reduced the mean body weight of the SD rats.When SPT was used to verify the successful establishment of the CUMS rat model,sucrose consumption measured within 12 hours was less variable than that measured within 1 hour.Conclusions:Twelve hours of food deprivation in the daytime（8:00-20:00） may be considered a mild stimulus for the establishment of a CUMS rat model.Measuring sucrose consumption over 12 hours is recommended for SPT.

目的:为阿尔茨海默病(AD)发病机制的阐释、早期预防与诊断以及治疗靶点的筛选提供参考.方法:从美国国立生物技术信息中心公共数据平台基因表达数据库中下载基因芯片数据集GSE28146,使用GEO2R在线分析工具筛选出AD相关差异表达基因(DEGs);使用DAVID 6.8生物信息学资源数据库进行基因本体(GO)分析和KEGG通路富集分析;使用STRING数据库和Cytoscape 3.2.1软件进行蛋白-蛋白相互作用(PPI)网络分析.结果与结论:筛选出AD相关DEGs共1478个,其中上调913个、下调565个.GO分析结果显示,DEGs主要分布于细胞质、膜、细胞外隙中,主要通过转录的正/负调节、核因子κB活性的正调节、Rho蛋白信号转导的调节、蛋白质磷酸化的调节等生物学过程以及蛋白质结合、DNA结合、转录因子活性(序列特异性DNA结合)等分子功能来诱导AD的发生.KEGG通路富集分析结果显示,DEGs显著富集于癌症途径、肺结核、破骨细胞分化、Janus激酶/信号传导及转录激活因子信号通路、叉头转录因子信号通路、EB病毒感染等信号通路上.DEGs编码蛋白的PPI网络含节点蛋白共1205个、边3931条;其中的关键核心基因为SOCS3、NEDD4、CBLB,可能是AD发生发展的潜在靶点.

目的:建立实时荧光定量RT-PCR检测方法,普查重庆市实验小鼠诺如病毒(munne Norovirus,MNv)的感染情况及其对BABL/c-nu小鼠免疫功能影响的初步研究.方法:①根据GenBank中收录的MNV全基因组序列,设计MNV特异性引物,检测其特异性、灵敏度、重复性和稳定性,并和两个实验动物质量检测单位对123份小鼠临床样本开展比对检测,以最终构建荧光定量RT-PCR检测方法.②应用该方法比较小鼠不同肠道排泄物(盲肠内容物、新鲜粪便和排出体外24h粪便)中MNV的检出情况.③应用该方法普查重庆市实验小鼠感染MNV的情况.④6～8周的BABL/c-nu小鼠被随机分为3组(n=3):正常对照组、MNV感染30 d组、MNV感染60d组,收集各组小鼠血清及肝、肺、脾、结肠,HE染色观察各脏器的病理变化;酶联免疫吸附法(enzyme linked immunosorbent assay,ELISA)检测血清、脾和结肠肿瘤坏死因子-α(tumor necrosis factor-alpha,TNF-α)及干扰素-γ(interfemn gamma,IFN-γ的含量.结果:①建立的荧光定量RT-PCR方法特异性强,与同种属其他病毒均不发生交叉反应,方法的灵敏度、重复性和稳定性良好,与另外两个实验动物质检单位的检测结果吻合度高达98％.②新鲜粪便与盲肠内容物中MNV的检出结果完全一致;24 h的陈旧粪便也能准确反映出该笼小鼠MNV的感染情况.③重庆市实验小鼠存在较高的MNV感染率,且封闭群和近交系小鼠MNV感染率无品系特异性(68.3％ vs.70.6％,x2=0.116,P=0.733),但基因修饰小鼠比普通小鼠更易感染MNV(78％ vs.64％,x2=6.434,P=0.011).④与正常对照组小鼠相比,BABL/c-nu小鼠自然感染MNV后肝、肺、脾和结肠均出现不同程度的炎症细胞浸润和明显的组织病理变化,且结肠组织的TNF-α、IFN-γ水平明显升高(F=21.682,P=0.002;F=77.223,P=0.000).结论:本研究建立的实时荧光定量PCR方法可靠,且可通过小鼠粪便样本,日常监测MNV的感染情况等;重庆市实验小鼠有较高的MNV感染率,且BABL/c-nu小鼠感染MNV会对动物实验结果造成干扰.因此,各实验动物单位应该重视MNV的传播和防控,加强实验动物的饲养管理,降低实验动物感染MNV的风险.

目的 研究富硒米糠代替有机硒添加对仔兔生长性能和抗氧化功能的影响.方法 将60只35日龄断奶仔兔随机分为普通米糠组、有机硒组、富硒米糠组,每组20只,雌雄各半,分别饲喂普通米糠饲料、普通米糠加有机硒饲料、富硒米糠饲料,共饲喂30 d,记录每日饲料消耗量.分别于实验第0、5、10、15、20、25、30天称量实验兔体重,计算每组实验兔料重比.饲喂结束后,采集各组实验兔血清,检测血糖、尿酸、总蛋白、白蛋白、球蛋白含量、白蛋白/球蛋白比及血清谷胱甘肽过氧化物酶(GSH-Px)活性、超氧化物歧化酶活性(SOD)、过氧化氢酶(CAT)活性和丙二醛(MDA)含量;采集各组实验兔肝、脾、肾并称重,计算各组组内脏器指数,并检测肾硒含量.结果 有机硒组和富硒米糠组的日增重、料重比、脏器指数、肾硒含量以及上述血液生化指标同普通米糠组相比,差异均无显著性(P>0.05),但富硒米糠组的GSH-Px和SOD活性、有机硒组的GSH-Px和CAT活性较普通米糠组均有显著增加(P<0.05),两组的MDA含量较普通米糠组均有明显降低(P<0.05),且富硒米糠组和有机硒组的抗氧化能力相当.结论 富硒米糠对仔兔生长性能和抗氧化功能的促进作用与有机硒相当,可代替有机硒作为仔兔饲料硒的来源.

tRNA-derived small RNAs (tsRNAs) is a type of newly discovered non-coding small RNA, which is derived from mature tRNA or tRNA precursor and exists in various organisms. tsRNAs exhibit tissue- and cell-specific expression and are involved in various biological functions such as stress response, protein translation regulation, ribosomes biogenesis, intergenerational transmission of acquired epigenetic information, tumorgenesis, cell proliferation and apoptosis. This review briefly discussed the biogenesis, classification, biological functions and molecular mechanisms of tsRNAs, as well as the roles of tsRNA modifications in tsRNA regulation and in diseases diagnosis.

目的 建立C57BL/6小鼠抑郁模型,初步探究莫扎特K448奏鸣曲中的高频段声波改善C57BL/6小鼠抑郁症状的效果.方法 1)慢性应激模型的建立:小鼠依据自主活动实验结果剔除活动次数差异较大者,其余分为空白组(n=10)、模型组(n=36),模型组经历5周慢性温和不可预知刺激(chronic unpredictable and mild stress,CUMS),建立小鼠抑郁模型.(2)治疗干预:造模成功后,将模型组小鼠随机均衡分为模型对照组(n=12)、氟西汀组(n=12)和音乐组(n=12).氟西汀组每天腹腔注射盐酸氟西汀溶液(10 mg/kg),其余两组注射等量的生理盐水.音乐组每天进行2 h高频音乐干预,其余两组不进行音乐干预.干预持续2周.(3)效果评价:实验前3 d及实验中每周称量体重并记录,实验第1周、第5周、第7周进行悬尾实验(tail suspension test,TST)和强迫游泳实验(forced swimming test,FST).第7周行为学实验结束后,取小鼠脑组织制备匀浆,通过酶联免疫吸附法(enzyme-linked immunosorbent assay,ELISA)测定脑源性神经营养因子(brain derived neurotrophic factor,BDNF)含量.结果 1)成功构建CUMS小鼠模型.第5周模型组小鼠悬尾不动时间明显增加,差异有显著性(P<0.01),强迫游泳不动时间增加,差异有显著性(P<0.05).(2)氟西汀组与模型对照组相比,悬尾实验不动时间明显缩短,差异有显著性(P<0.01),强迫游泳实验不动时间缩短,差异无显著性(P>0.05);音乐组与模型对照组相比,悬尾不动时间缩短,差异有显著性(P<0.05),强迫游泳实验不动时间无明显改变,差异无显著性(P>0.05).模型对照组与空白组小鼠相比,脑组织匀浆中的BDNF含量明显降低,差异有显著性(P<0.01);氟西汀组与模型对照组相比,脑组织匀浆中的BDNF含量明显回升,差异有显著性(P<0.01),但音乐组与模型对照组相比,其差异无显著性(P>0.05).结论 莫扎特K448奏鸣曲高频段声波可一定程度优化小鼠抑郁模型的治疗作用.