褪黑激素对绒山羊皮肤中毛囊周期相关miRNAs表达模式的影响

褪黑激素(Melatonin, MT)和miRNAs在毛囊的生长发育过程中发挥重要的作用, 但MT对绒山羊皮肤毛囊miRNAs表达模式的影响尚未见报道。为探索MT从miRNAs层次影响山羊绒生长的机制, 文章在内蒙古绒山羊中实施了褪黑激素埋植试验：5只青年母羊作为实验组埋植褪黑激素, 另外5只青年母羊作为对照。利用荧光定量PCR检测褪黑激素埋植前后毛囊周期相关miRNAs的表达变化。结果表明, 埋植MT明显改变了6个绒毛相关miRNAs的表达规律：在一个绒毛周期内, 除let-7a外, miR-203、miR-205、miR-96、miR-183和miR-199a的表达量均发生3次跃迁;埋植MT改变了miRNAs之间的共表达模式。对照组各miRNA之间相关系数范围为0.87~0.99(P<0.01)。与对照组相比, 埋植组中let-7a与miR-96、miR-199a、miR-205, miR-203与miR-96、miR-199a, miR-96与miR-183, miR-183与miR-199a之间的相关系数被明显消弱;MT通过下调6月份埋植组各miRNA的表达量提早诱发二次生绒。     

外源褪黑素对小麦幼苗生理及光合荧光特性的影响

为探讨不同浓度外源褪黑素对小麦幼苗生理及光合荧光特性的影响，该研究以良星99为供试材料，测定不同浓度褪黑素处理下小麦幼苗生长形态、光合及荧光参数以及抗氧化酶活性等关键指标。结果表明：(1)0.1μmol·L^-1的褪黑素处理显著提高了小麦植株的光合能力，叶绿素Chl a、Chl b和Chl (a+b)以及叶绿素荧光参数调节性能量耗散的量子产额Y(NPQ)、表观光合传递速率(ETR)和非光化学淬灭(NPQ)均在褪黑素浓度为0.1μmol·L^-1时达到增加最大值；PSⅡ最大光合效率(Fv/Fm)、最大光能转化潜力(Fv/Fo)随褪黑素浓度升高逐渐降低；光化学淬灭(qL)随褪黑素浓度增加先下降后上升。(2)与CK(0μmol·L^-1)相比，低浓度褪黑素显著降低小麦根和叶中过氧化物酶(POD)及小麦叶中过氧化氢酶(CAT)的活性，高浓度褪黑素处理显著增加小麦POD的活性；小麦根中丙二醛(MDA)含量随褪黑素浓度的增加先下降后上升。综上表明，适量褪黑素处理可促进小麦的生长，使小麦光合能力维持在较高水平，并通过POD和CAT调节不同褪...     

中西医观解读时间生物学

时间生物学是一门研究生命活动节律的科学。在西方医学中,研究时间生物学是利用分子生物学实验来阐释其机制,以西医的思维方法解释时间生物学的生理及病理过程;中医对时间生物学的记载有两千多年的历史,阴阳理论、子午流注学说以及五运六气学说一直以来都在指导中医的诊断和治疗。中西医观的不同对时间生物学的研究提供了新的研究思路,同时时间生物学也为研究中西医结合提供了广阔的前景。     

褪黑素受体激动剂改善高糖高脂喂养大鼠脂联素敏感性

目的观察褪黑素受体激动剂（NEU-P11）对高糖高脂饲养大鼠脂联素敏感性的影响。方法将30只SD大鼠随机分为对照组（CD组）,高糖高脂组（HFSD组）,褪黑素组（Mel组）,褪黑素受体激动剂组（NEU-P11组）。CD组饲以正常饲料;其余3组饲以高糖高脂饲料。6个月后,给药治疗2个月。治疗期间,Mel组每天注射Mel（4mg／kg）;NEU—P11组每天注射NEU-P11（10mg／kg）;CD组以及HFSD组注射生理盐水（5ml／kg）。测定糖脂代谢指标并做口服葡萄糖耐量实验（oral glucose tolerant test,OG-TY）,Western印迹检测脂联素（adiponectin,APN）在脂肪组织及脂联素受体（AdipoR）在骨骼肌组织中的表达变化。结果高糖高脂饮食可诱导SD大鼠产生胰岛素抵抗,脂联素表达增加。Neu-P11治疗后,胰岛素敏感性增强．脂联素表达降低至正常水平。结论Neu-P11能提高胰岛素敏感性,改善脂联素抵抗。     

Fibroblast growth factor 9 prevents MPP+-induced death of dopaminergic neurons and is involved in melatonin neuroprotection in vivo and in vitro

Oxidative stress and down-regulated trophic factors are involved in the pathogenesis of nigrostriatal dopamine(DA)rgic neurodegeneration in Parkinson's disease. Fibroblast growth factor 9 (FGF9) is a survival factor for various cell types; however, the effect of FGF9 on DA neurons has not been studied. The antioxidant melatonin protects DA neurons against neurotoxicity. We used MPP⁺ to induce neuron death in vivo and in vitro and investigated the involvement of FGF9 in MPP⁺ intoxication and melatonin protection. We found that MPP⁺ in a dose- and time-dependent manner inhibited FGF9 mRNA and protein expression, and caused death in primary cortical neurons. Treating neurons in the substantia nigra and mesencephalic cell cultures with FGF9 protein inhibited the MPP⁺-induced cell death of DA neurons. Melatonin co-treatment attenuated MPP⁺-induced FGF9 down-regulation and DA neuronal apoptosis in vivo and in vitro . Co-treating DA neurons with melatonin and FGF9-neutralizing antibody prevented the protective effect of melatonin. In the absence of MPP⁺, the treatment of FGF9-neutralizing antibody-induced DA neuronal apoptosis whereas FGF9 protein reduced it indicating that endogenous FGF9 is a survival factor for DA neurons. We conclude that MPP⁺ down-regulates FGF9 expression to cause DA neuron death and that the prevention of FGF9 down-regulation is involved in melatonin-provided neuroprotection.     

Melatonin protects against defects induced by malathion during porcine oocyte maturation

Malathion (MAL) is a common organophosphorus pesticide and affects both animal and human reproduction. However, the mechanisms regarding how MAL affects the mammalian oocyte quality and how to prevent it have not been fully investigated. In this study, we used porcine oocyte as a model and proved that MAL impaired porcine oocyte quality in a dose-dependent manner during maturation. MAL decreased the first polar body extrusion, disrupted spindle assembly and chromosome alignment, impaired cortical granules (CGs) distribution, and increased reactive oxygen species (ROS) level in oocytes. RNA-seq analysis showed that MAL exposure altered the expression of 2,917 genes in the porcine maturated oocytes and most genes were related to ROS, the lipid droplet process, and the energy supplement. Nevertheless, these defects could be remarkably ameliorated by adding melatonin (MLT) into the oocyte maturation medium. MLT increased oocyte maturation rate and decreased the abnormities of spindle assembly, CGs distribution and ROS accumulation in MAL-exposed porcine oocytes. More important, MLT upregulated the expression of genes related to lipid droplet metabolism (PPARγ and PLIN2), decreased lipid droplet size and lipid peroxidation in MAL-exposed porcine oocytes. Finally, we found that MLT increased the blastocysts formation and the cell numbers of blastocysts in MAL-exposed porcine oocytes after parthenogenetic activation, which was mediated by reduction of ROS levels and maintaining lipid droplet metabolism. Taken together, our results revealed that MLT had a protective action against MAL-induced deterioration of porcine oocyte quality.     

褪黑素受体

褪黑素是松果体分泌的主要激素,其功能活动通过特异的Ｇ蛋白耦联受体介导,本文综述褪黑素受体 分布、药理学特性,受体的克隆及受体基因结构特点。     

Twenty-four-hour rhythm patterns of plasma melatonin in short-day and long-day breeders maintained under natural environmental conditions

ABSTRACT

Photoperiodic treatments have been of practical interest in controlling seasonal reproduction in sheep, goats and horses. Melatonin is the principal mediator of the environmental photoperiodic message. To investigate the intra- and inter-subject variability of melatonin 24 h rhythm, ten female Italian Saddle horses (8–10 yrs old, mean body weight 525 ± 30 kg), ten female Sarda breed sheep (2–3 yrs old, mean body weight 40.5 ± 2.8 kg) and ten female Sarda breed goats (3–4 yrs old, mean body weight 38.9 ± 4.1 kg), housed individually in a 4 × 4 m soundproof box equipped with 50 × 100 cm opening windows, were subjected to a natural photoperiod of the vernal equinox (sunrise 06:00 h; sunset 18:00 h). Blood samples were collected from each animal, every 3 h over a 48 h period starting at 00:00 h of day 1 and ending at 00:00 h of day 3. Plasma melatonin concentrations were determined by direct radioimmunoassay (MelatoninDirect RIA, Labor Diagnostika Nord GmbH, Nordhorn, Germany). The application of single cosinor method substantiated a circadian rhythm of melatonin with a nocturnal peak in all studied species. The application of two-way ANOVA on the rhythmic parameters indicated statistically significant differences between the three species in all of the cosinor analysis-derived parameters of MESOR, amplitude, acrophase and robustness of rhythm. Analyses of intra- and inter-subject variability indicate that organization of the melatonin 24 h rhythm is characterized by great accuracy of control within and between the individuals of a breed. In conclusion, features of the 24 h rhythm of melatonin among species; however, the 24 h rhythmicity of melatonin each species showed high stability within the various subjects and within the same subject. These findings must be taken into consideration when applying photoperiod and melatonin treatments for breeding purposes.     

Melatonin against acute ischaemic stroke dependently via suppressing both inflammatory and oxidative stress downstream signallings

This study tested the hypothesis that melatonin (Mel) therapy preserved the brain architectural and functional integrity against ischaemic stroke (IS) dependently through suppressing the inflammatory/oxidative stress downstream signalling pathways. Adult male B6 (n = 6 per each B6 group) and TLR4 knockout (ie TLR4^?/?) (n = 6 per each TLR4^?/? group) mice were categorized into sham control (SC^B6), SC^TLR4?/?, IS^B6, IS^TLR4?/?, IS^B6 + Mel (i.p. daily administration) and IS^TLR4?/? + Mel (i.p. daily administration). By day 28 after IS, the protein expressions of inflammatory (HMBG1/TLR2/TLR4/MAL/MyD88/RAM TRIF/TRAF6/IKK‐α/p‐NF‐κB/nuclear‐NF‐κB/nuclear‐IRF‐3&7/IL‐1β/IL‐6/TNF‐α/IFN‐γ) and oxidative stress (NOX‐1/NOX‐2/ASK1/p‐MKK4&7/p‐JNK/p‐c‐JUN) downstream pathways as well as mitochondrial‐damaged markers (cytosolic cytochrome C/cyclophilin D/SRP1/autophagy) were highest in group IS^B6, lowest in groups SC^B6 and SC^TLR4?/?, lower in group IS^TLR4?/? + Mel than in groups IS^TLR4?/? and IS^B6 + Mel and lower in group IS^B6 + Mel than in group IS^TLR4?/? (all P < .0001). The brain infarct volume, brain infarct area and the number of inflammatory cells in brain (CD14/F4‐88) and in circulation (MPO+//Ly6C+/CD11b+//Ly6G+/CD11b+) exhibited an identical pattern, whereas the neurological function displayed an opposite pattern of inflammatory protein expression among the six groups (all P < .0001). In conclusion, TLR inflammatory and oxidative stress signallings played crucial roles for brain damage and impaired neurological function after IS that were significantly reversed by Mel therapy.