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Melatonin Regulates Rheumatoid Synovial Fibroblasts-Related Inflammation: Implications for Pathological Skeletal Muscle Treatment 褪黑激素调节类风湿滑膜成纤维细胞相关炎症:病理骨骼肌治疗的意义》。
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-09-24 DOI: 10.1111/jpi.13009
Chen-Ming Su, Chun-Hao Tsai, Hsien-Te Chen, Yi-Syuan Wu, Shun-Fa Yang, Chih-Hsin Tang

Melatonin has been reported to regulate circadian rhythms and have anti-inflammatory characteristics in various inflammatory autoimmune diseases, but its effects in diseases-associated muscle atrophy remain controversial. This study is aimed to determine the evidence of melatonin in rheumatoid arthritis (RA)-related pathological muscle atrophy. We used initially bioinformatics results to show that melatonin regulated significantly the correlation between pro-inflammation and myogenesis in RA synovial fibroblasts (RASF) and myoblasts. The conditioned medium (CM) from melatonin-treated RASF was incubated in myoblasts with growth medium and differentiated medium to investigate the markers of pro-inflammation, atrophy, and myogenesis. We found that melatonin regulated RASF CM-induced pathological muscle pro-inflammation and atrophy in myoblasts and differentiated myocytes through NF-κB signaling pathways. We also showed for the first time that miR-30c-1-3p is negatively regulated by three inflammatory cytokines in human RASF, which is associated with murine-differentiated myocytes. Importantly, oral administration with melatonin in a collagen-induced arthritis (CIA) mouse model also significantly improved arthritic swelling, hind limb grip strength as well as pathological muscle atrophy. In conclusion, our study is the first to demonstrate not only the underlying mechanism whereby melatonin decreases pro-inflammation in RA-induced pathological muscle atrophy but also increases myogenesis in myoblasts and differentiated myocytes.

据报道,褪黑素可调节昼夜节律,并在各种炎症性自身免疫疾病中具有抗炎特性,但其在疾病相关肌肉萎缩中的作用仍存在争议。本研究旨在确定褪黑激素在类风湿性关节炎(RA)相关病理性肌肉萎缩中的作用证据。我们利用生物信息学的初步研究结果表明,褪黑激素能显著调节类风湿性关节炎滑膜成纤维细胞(RASF)和成肌细胞的促炎和肌生成之间的相关性。将褪黑素处理过的RASF的条件培养基(CM)与肌母细胞的生长培养基和分化培养基一起培养,以研究促炎、萎缩和肌生成的标志物。我们发现,褪黑激素可通过 NF-κB 信号通路调控 RASF CM 在成肌细胞和分化肌细胞中诱导的病理性肌肉促炎和萎缩。我们还首次发现,在人类 RASF 中,miR-30c-1-3p 受三种炎症细胞因子的负向调节,这与小鼠分化的肌细胞有关。重要的是,在胶原诱导的关节炎(CIA)小鼠模型中口服褪黑素也能显著改善关节炎肿胀、后肢握力以及病理性肌肉萎缩。总之,我们的研究首次证明了褪黑激素不仅能减少RA诱导的病理性肌肉萎缩中的促炎作用,还能增加成肌细胞和分化肌细胞的肌生成的内在机制。
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引用次数: 0
Melatonin Attenuates Diabetic Retinopathy by Regulating EndMT of Retinal Vascular Endothelial Cells via Inhibiting the HDAC7/FOXO1/ZEB1 Axis 褪黑激素通过抑制 HDAC7/FOXO1/ZEB1 轴调节视网膜血管内皮细胞的内切酶抑制糖尿病视网膜病变
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-09-19 DOI: 10.1111/jpi.13008
Jiayi Ning, Minghong Pan, Hanyi Yang, Zhaoyang Wang, Xiaolan Wang, Kai Guo, Yingtong Feng, Tingke Xie, Yixuan Chen, Chengming Chen, Sida Liu, Yimeng Zhang, Yuanyong Wang, Xiaolong Yan, Jing Han

Diabetic retinopathy (DR) is characterized as a microvascular disease. Nonproliferative diabetic retinopathy (NPDR) presents with alterations in retinal blood flow and vascular permeability, thickening of the basement membrane, loss of pericytes, and formation of acellular capillaries. Endothelial–mesenchymal transition (EndMT) of retinal microvessels may play a critical role in advancing NPDR. Melatonin, a hormone primarily secreted by the pineal gland, is a promising therapeutic for DR. This study explored the EndMT in retinal microvessels of NPDR and its related mechanisms. The effect of melatonin on the retina of diabetic rats was evaluated by electroretinogram (ERG) and histopathologic slide staining. Furthermore, the effect of melatonin on human retinal microvascular endothelial cells (HRMECs) was detected by EdU incorporation assay, scratch assay, transwell assay, and tube formation test. Techniques such as RNA-sequencing, overexpression or knockdown of target genes, extraction of cytoplasmic and nuclear protein, co-immunoprecipitation (co-IP), and multiplex immunofluorescence facilitated the exploration of the mechanisms involved. Our findings reveal, for the first time, that melatonin attenuates diabetic retinopathy by regulating EndMT of retinal vascular endothelial cells via inhibiting the HDAC7/FOXO1/ZEB1 axis. Collectively, these results suggest that melatonin holds potential as a therapeutic strategy to reduce retinal vascular damage and protect vision in NPDR.

糖尿病视网膜病变(DR)是一种微血管疾病。非增殖性糖尿病视网膜病变(NPDR)表现为视网膜血流和血管通透性的改变、基底膜增厚、周细胞丢失以及无细胞毛细血管的形成。视网膜微血管的内皮-间质转化(EndMT)可能在促进 NPDR 的发展中起着至关重要的作用。褪黑激素是一种主要由松果体分泌的激素,是一种很有前景的 DR 治疗药物。本研究探讨了 NPDR 视网膜微血管的 EndMT 及其相关机制。通过视网膜电图(ERG)和组织病理学切片染色评估了褪黑素对糖尿病大鼠视网膜的影响。此外,褪黑素对人视网膜微血管内皮细胞(HRMECs)的影响还通过EdU掺入试验、划痕试验、transwell试验和成管试验进行了检测。RNA测序、过表达或敲除靶基因、提取细胞质和细胞核蛋白、共免疫沉淀(co-IP)和多重免疫荧光等技术促进了对相关机制的探索。我们的研究结果首次揭示了褪黑激素通过抑制 HDAC7/FOXO1/ZEB1 轴来调节视网膜血管内皮细胞的 EndMT,从而减轻糖尿病视网膜病变。总之,这些结果表明,褪黑激素有可能作为一种治疗策略,减少NPDR患者的视网膜血管损伤并保护视力。
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引用次数: 0
Melatonin Prevents Thioacetamide–Induced Gut Leakiness and Liver Fibrosis Through the Gut–Liver Axis via Modulating Sirt1-Related Deacetylation of Gut Junctional Complex and Hepatic Proteins 褪黑素通过调节与 Sirt1 相关的肠道连接复合体和肝脏蛋白质的去乙酰化,防止硫代乙酰胺诱发的肠道渗漏和肝纤维化
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-09-13 DOI: 10.1111/jpi.13007
Wiramon Rungratanawanich, Karli Rae LeFort, Young-Eun Cho, Xiaoling Li, Byoung-Joon Song

Intestinal barrier dysfunction with high serum endotoxin is common in patients with liver fibrosis, but the mechanisms underlying liver fibrosis remain unclear. Melatonin is a well-recognized antioxidant and an anti-inflammatory agent that benefits multiple organs. However, the beneficial effects of melatonin on gut leakiness–associated liver fibrosis have not been systemically studied. Here, we investigated the protective mechanisms of melatonin against thioacetamide (TAA)–induced gut barrier dysfunction and hepatic fibrosis by focusing on posttranslational protein modifications through the gut–liver axis. Our results showed that gut leakiness markers, including decreased gut tight/adherens junction proteins (TJ/AJs) with increased intestinal deformation, apoptosis, and serum endotoxin, were observed early at 1 week after TAA exposure. Liver injury, apoptosis, and fibrosis were prominent at 2 and 4 weeks. Mechanistically, we found that gut TJ/AJs were hyper-acetylated, followed by ubiquitin-dependent proteolysis, leading to their degradation and gut leakiness. Gut dysbiosis, hepatic protein hyper-acetylation, and SIRT1 downregulation were also observed. Consistently, intestinal Sirt1 deficiency greatly enhanced protein hyper-acetylation, gut leakiness, endotoxemia, and liver fibrosis. Pretreatment with melatonin prevented or improved all these changes in both the gut and liver. Furthermore, melatonin blunted protein acetylation and injury in TAA–exposed T84 human intestinal and AML12 mouse liver cells. Overall, this study demonstrated novel mechanisms by which melatonin prevents gut leakiness and liver fibrosis through the gut–liver axis by attenuating the acetylation of intestinal and hepatic proteins. Thus, melatonin consumption can become a potentially safe supplement for liver fibrosis patients by preventing protein hyper-acetylation and gut leakiness.

肝纤维化患者常伴有肠屏障功能障碍和高血清内毒素,但肝纤维化的内在机制仍不清楚。褪黑素是一种公认的抗氧化剂和抗炎剂,对多个器官有益。然而,褪黑激素对肠道渗漏相关肝纤维化的有益作用尚未得到系统研究。在这里,我们研究了褪黑素对硫代乙酰胺(TAA)诱导的肠道屏障功能障碍和肝纤维化的保护机制,重点是通过肠道-肝脏轴的翻译后蛋白质修饰。我们的研究结果表明,在暴露于硫代乙酰胺1周后的早期就观察到了肠道渗漏标记物,包括肠道紧密/粘连接头蛋白(TJ/AJs)减少,肠道变形、细胞凋亡和血清内毒素增加。肝损伤、细胞凋亡和纤维化在 2 周和 4 周时更为突出。从机理上讲,我们发现肠道 TJ/AJs 被过度乙酰化,随后泛素依赖性蛋白水解,导致其降解和肠道渗漏。同时还观察到肠道菌群失调、肝脏蛋白质高乙酰化和 SIRT1 下调。一致的是,肠道 Sirt1 缺乏会大大增强蛋白质高乙酰化、肠道渗漏、内毒素血症和肝纤维化。褪黑激素的预处理可防止或改善肠道和肝脏的所有这些变化。此外,褪黑素还能减弱暴露于 TAA 的 T84 人肠道细胞和 AML12 小鼠肝细胞中的蛋白质乙酰化和损伤。总之,这项研究证明了褪黑素通过肠肝轴减轻肠道和肝脏蛋白质乙酰化防止肠道渗漏和肝纤维化的新机制。因此,服用褪黑素可以防止蛋白质高乙酰化和肠道渗漏,从而成为肝纤维化患者的一种潜在安全补充剂。
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引用次数: 0
Melatonin Alleviates Osteoarthritis by Regulating NADPH Oxidase 4–Induced Ferroptosis and Mitigating Mitochondrial Dysfunction 褪黑激素通过调节 NADPH 氧化酶 4 诱导的铁氧化作用和减轻线粒体功能障碍缓解骨关节炎。
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-09-04 DOI: 10.1111/jpi.12992
Qi Wang, Beijie Qi, Shi Shi, Weihao Jiang, Dejian Li, Xinhua Jiang, Chengqing Yi

Recent evidence indicates that the damaged regions in osteoarthritis are accompanied by the accumulation of iron ions. Ferroptosis, as an iron-dependent form of cell death, holds significant implications in osteoarthritis. Melatonin, a natural product with strong scavenging abilities against reactive oxygen species and lipid peroxidation, plays a crucial role in the treatment of osteoarthritis. This study aims to demonstrate the existence of ferroptosis in osteoarthritis and explore the specific mechanism of melatonin in suppressing ferroptosis and alleviating osteoarthritis. Our findings reveal that melatonin reverses inflammation-induced oxidative stress and lipid peroxidation while promoting the expression of extracellular matrix components in chondrocytes, safeguarding the cells. Our research has revealed that NADPH oxidase 4 (NOX4) serves as a crucial molecule in the ferroptosis process of osteoarthritis. Specifically, NOX4 is located on mitochondria in chondrocytes, which can induce disorders in mitochondrial energy metabolism and dysfunction, thereby intensifying oxidative stress and lipid peroxidation. LC-MS analysis further uncovered that GRP78 is a downstream binding protein of NOX4. NOX4 induces ferroptosis by weakening GRP78's protective effect on GPX4 and reducing its expression. Melatonin can inhibit the upregulation of NOX4 on mitochondria and mitigate mitochondrial dysfunction, effectively suppressing ferroptosis and alleviating osteoarthritis. This suggests that melatonin therapy represents a promising new approach for the treatment of osteoarthritis.

最近的证据表明,骨关节炎的受损区域伴随着铁离子的积累。铁变态反应是一种依赖于铁的细胞死亡形式,在骨关节炎中具有重要意义。褪黑素是一种天然产物,具有很强的清除活性氧和脂质过氧化的能力,在骨关节炎的治疗中起着至关重要的作用。本研究旨在证明骨关节炎中存在铁变态反应,并探索褪黑素抑制铁变态反应、缓解骨关节炎的具体机制。我们的研究结果表明,褪黑素能逆转炎症诱导的氧化应激和脂质过氧化反应,同时促进软骨细胞细胞外基质成分的表达,保护细胞。我们的研究发现,NADPH 氧化酶 4(NOX4)是骨关节炎铁氧化过程中的一个关键分子。具体来说,NOX4 位于软骨细胞的线粒体上,可诱导线粒体能量代谢紊乱和功能障碍,从而加剧氧化应激和脂质过氧化。LC-MS分析进一步发现,GRP78是NOX4的下游结合蛋白。NOX4 通过削弱 GRP78 对 GPX4 的保护作用并减少其表达,从而诱导铁变态反应。褪黑素可抑制线粒体上NOX4的上调,缓解线粒体功能障碍,有效抑制铁变态反应,缓解骨关节炎。这表明,褪黑素疗法是治疗骨关节炎的一种很有前景的新方法。
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引用次数: 0
Melatonin Regulates Neuronal Synaptic Plasticity in the Supramammillary Nucleus and Attenuates Methamphetamine-Induced Conditioned Place Preference and Sensitization in Mice 褪黑素调节小鼠颌上核的神经元突触可塑性并减弱甲基苯丙胺诱导的条件性位置偏好和敏感性
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-09-02 DOI: 10.1111/jpi.13006
Qingyu Ren, Weikai Han, Yanan Yue, Yaqi Tang, Qingwei Yue, Stefano Comai, Jinhao Sun

Methamphetamine (METH) is an addictive drug that threatens human health. The supramammillary nucleus (SuM) and its neural circuits play key roles in the regulation of spatial memory retrieval, and hippocampal contextual or social memory. Melatonin (MLT), a pineal hormone, can regulate hypothalamic-neurohypophysial activity. Our previous study showed that MLT attenuates METH-induced locomotor sensitization. However, whether MLT regulates SuM function and participates in METH-induced contextual memory retrieval remains unclear. Using a mouse model of METH-conditioned place preference (CPP) and sensitization, we found that METH activated c-Fos expression and elevated calcium (Ca²⁺) levels in SuM neurons. Chemogenetic inhibition of SuM attenuates CPP and sensitization. Pretreatment with MLT decreased c-Fos expression and Ca2+ levels in the SuM and reversed METH-induced addictive behavior, effects that were blocked with the selective MT2 receptors antagonist 4P-PDOT and the MT1 receptors antagonist S26131. Furthermore, MLT reduced SuM synaptic plasticity, glutamate (Glu) release, and neuronal oscillations caused by METH, which were blocked by 4P-PDOT. In conclusion, our data revealed that MLT regulates neuronal synaptic plasticity in the SuM, likely through the MLT receptors (MTs), and plays a role in modulating METH-addictive behavior.

甲基苯丙胺(METH)是一种威胁人类健康的成瘾性药物。绒毛上核(SuM)及其神经回路在调节空间记忆检索和海马情境记忆或社会记忆方面发挥着关键作用。褪黑激素(MLT)是一种松果体激素,可调节下丘脑-神经-生理活动。我们之前的研究表明,MLT 可减轻 METH 诱导的运动敏感性。然而,MLT 是否调节 SuM 功能并参与 METH 诱导的情境记忆检索仍不清楚。利用小鼠的 METH 条件性位置偏好(CPP)和致敏模型,我们发现 METH 会激活 SuM 神经元中 c-Fos 的表达并升高钙(Ca²⁺)水平。对SuM的化学抑制可减轻CPP和致敏作用。MLT预处理可降低SuM中c-Fos的表达和Ca2+的水平,并逆转METH诱导的成瘾行为,这些效应被选择性MT2受体拮抗剂4P-PDOT和MT1受体拮抗剂S26131所阻断。此外,MLT 还能降低 METH 引起的 SuM 突触可塑性、谷氨酸(Glu)释放和神经元振荡,4P-PDOT 也能阻断这些作用。总之,我们的数据揭示了 MLT 可能通过 MLT 受体(MTs)调节 SuM 中神经元突触的可塑性,并在调节 METH 上瘾行为中发挥作用。
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引用次数: 0
Criticism on the Incorrect Use of Oxygen–Ozone Therapy in Medicine 关于在医学中不正确使用氧气-臭氧疗法的批评。
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-08-23 DOI: 10.1111/jpi.13005
Marianno Franzini, Luigi Valdenassi, Francesco Vaiano, Tommaso Richelmi, Umberto Tirelli, Salvatore Chirumbolo
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引用次数: 0
Correction to “PP2C1 Fine-Tunes Melatonin Biosynthesis and Phytomelatonin Receptor PMTR1 Binding to Melatonin in Cassava” 对 "PP2C1 微调木薯中褪黑激素的生物合成和植物褪黑激素受体 PMTR1 与褪黑激素的结合 "的更正。
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-08-21 DOI: 10.1111/jpi.12983

Y. Bai, Y. Wei, H. Yin, et al., “PP2C1 Fine-Tunes Melatonin Biosynthesis and Phytomelatonin Receptor PMTR1 Binding to Melatonin in Cassava,” Journal of Pineal Research 73, no. 1 (2022): e12804. https://doi.org/10.1111/jpi.12804

After publication of the article, the authors identified inaccuracies in images in Figure 3A, namely SD-Trp-Leu-Ade-His for MePP2C1 and MeWRKY20 interaction. The authors have found the original data and corrected this error, which was due to the oversight during combing and dragging different figures in Photoshop software. It is important to emphasize that this correction does not compromise the scientific integrity of the study's conclusions. The authors sincerely apologize for any inconvenience caused by this oversight. The accurate images, obtained during the original experimental procedures, are provided below.

In addition, the authors also found inaccuracies in images in Figure 6B, namely Vector+Vector, MePMTR1+Vector, Vector+MePP2C1. The authors have found the original data and corrected these errors, which was due to the oversight that the adjacent figures were only labeled by number and stored in the same files during combing and dragging different figures in Photoshop software. It is important to emphasize that this correction does not compromise the scientific integrity of the study's conclusions. The authors sincerely apologize for any inconvenience caused by this oversight. The accurate images, obtained during the original experimental procedures, are provided below.

Y.Bai, Y. Wei, H. Yin, et al., "PP2C1 Fine-Tunes Melatonin Biosynthesis and Phytomelatonin Receptor PMTR1 Binding to Melatonin in Cassava," Journal of Pineal Research 73, no.作者找到了原始数据并纠正了这一错误,这是由于在 Photoshop 软件中梳理和拖动不同图片时的疏忽造成的。需要强调的是,这一更正并不影响研究结论的科学完整性。作者对此疏忽造成的不便表示诚挚的歉意。此外,作者还发现图 6B 中的图像存在不准确之处,即 Vector+Vector、MePMTR1+Vector、Vector+MePP2C1。作者找到了原始数据并纠正了这些错误,这是由于在 Photoshop 软件中梳理和拖动不同的图时,疏忽了相邻的图只用数字标注并存储在同一个文件中。需要强调的是,此次更正并不影响研究结论的科学性。作者对这一疏忽造成的不便表示诚挚的歉意。下文提供了在原始实验过程中获得的准确图像。
{"title":"Correction to “PP2C1 Fine-Tunes Melatonin Biosynthesis and Phytomelatonin Receptor PMTR1 Binding to Melatonin in Cassava”","authors":"","doi":"10.1111/jpi.12983","DOIUrl":"10.1111/jpi.12983","url":null,"abstract":"<p>Y. Bai, Y. Wei, H. Yin, et al., “PP2C1 Fine-Tunes Melatonin Biosynthesis and Phytomelatonin Receptor PMTR1 Binding to Melatonin in Cassava,” <i>Journal of Pineal Research</i> 73, no. 1 (2022): e12804. https://doi.org/10.1111/jpi.12804</p><p>After publication of the article, the authors identified inaccuracies in images in Figure 3A, namely SD-Trp-Leu-Ade-His for MePP2C1 and MeWRKY20 interaction. The authors have found the original data and corrected this error, which was due to the oversight during combing and dragging different figures in Photoshop software. It is important to emphasize that this correction does not compromise the scientific integrity of the study's conclusions. The authors sincerely apologize for any inconvenience caused by this oversight. The accurate images, obtained during the original experimental procedures, are provided below.</p><p>In addition, the authors also found inaccuracies in images in Figure 6B, namely Vector+Vector, MePMTR1+Vector, Vector+MePP2C1. The authors have found the original data and corrected these errors, which was due to the oversight that the adjacent figures were only labeled by number and stored in the same files during combing and dragging different figures in Photoshop software. It is important to emphasize that this correction does not compromise the scientific integrity of the study's conclusions. The authors sincerely apologize for any inconvenience caused by this oversight. The accurate images, obtained during the original experimental procedures, are provided below.</p>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":8.3,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jpi.12983","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142007925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction to “Melatonin mediates selenium-induced tolerance to cadmium stress in tomato plants” 更正 "褪黑激素介导番茄植物硒诱导的镉胁迫耐受性"。
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-08-21 DOI: 10.1111/jpi.12982

Li M-Q, Hasan MK, Li C-X, et al. Melatonin mediates selenium-induced tolerance to cadmium stress in tomato plants. J Pineal Res. 2016;61(3):291-302. https://doi.org/10.1111/jpi.12346

After the publication of the article, the authors identified inaccuracies in chlorophyll fluorescence images in Figure 4C, namely Water treatment of TRV (1st row, panel 1 from the left), Water treatment of TRV-TDC (1st row, panel 4 from the left), and Se treatment of TRV-TDC (1st row, panel 5 from the left). The accurate images, obtained during the original experimental procedures, are provided below. These corrections do not compromise the scientific integrity of the study's conclusions.

We apologize for this error.

Li M-Q, Hasan MK, Li C-X, et al. Melatonin mediates selenium-induced tolerance to cadmium stress in tomato plants.J Pineal Res. 2016;61(3):291-302。 https://doi.org/10.1111/jpi.12346After 文章发表后,作者发现图 4C 中的叶绿素荧光图像有误,即水处理 TRV(第 1 行,左起第 1 面板)、水处理 TRV-TDC(第 1 行,左起第 4 面板)和 Se 处理 TRV-TDC(第 1 行,左起第 5 面板)。以下是在原始实验过程中获得的准确图像。这些更正并不影响研究结论的科学完整性。
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引用次数: 0
A Protocol to Determine Circadian Phase by At-Home Salivary Dim Light Melatonin Onset Assessment 通过家庭唾液暗光褪黑激素起始评估确定昼夜节律阶段的方案。
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-08-19 DOI: 10.1111/jpi.12994
Jade M. Murray, Julia E. Stone, Sabra M. Abbott, Bjorn Bjorvatn, Helen J. Burgess, Christian Cajochen, Jip J. Dekker, Jeanne F. Duffy, Lawrence J. Epstein, Corrado Garbazza, John Harsh, Elizabeth B. Klerman, Jacqueline M. Lane, Steven W. Lockley, Milena K. Pavlova, Stuart F. Quan, Kathryn J. Reid, Frank A. J. L. Scheer, Tracey L. Sletten, Kenneth P. Wright Jr., Phyllis C. Zee, Andrew J. K. Phillips, Charles A. Czeisler, Shantha M. W. Rajaratnam, International Association of Circadian Health Clinics

Internal circadian phase assessment is increasingly acknowledged as a critical clinical tool for the diagnosis, monitoring, and treatment of circadian rhythm sleep−wake disorders and for investigating circadian timing in other medical disorders. The widespread use of in-laboratory circadian phase assessments in routine practice has been limited, most likely because circadian phase assessment is not required by formal diagnostic nosologies, and is not generally covered by insurance. At-home assessment of salivary dim light melatonin onset (DLMO, a validated circadian phase marker) is an increasingly accepted approach to assess circadian phase. This approach may help meet the increased demand for assessments and has the advantages of lower cost and greater patient convenience. We reviewed the literature describing at-home salivary DLMO assessment methods and identified factors deemed to be important to successful implementation. Here, we provide specific protocol recommendations for conducting at-home salivary DLMO assessments to facilitate a standardized approach for clinical and research purposes. Key factors include control of lighting, sampling rate, and timing, and measures of patient compliance. We include findings from implementation of an optimization algorithm to determine the most efficient number and timing of samples in patients with Delayed Sleep−Wake Phase Disorder. We also provide recommendations for assay methods and interpretation. Providing definitive criteria for each factor, along with detailed instructions for protocol implementation, will enable more widespread adoption of at-home circadian phase assessments as a standardized clinical diagnostic, monitoring, and treatment tool.

人们日益认识到,内部昼夜节律相位评估是诊断、监测和治疗昼夜节律睡眠-觉醒障碍以及研究其他疾病的昼夜节律时间的重要临床工具。在常规临床实践中,实验室内昼夜节律相位评估的广泛应用一直受到限制,这很可能是因为昼夜节律相位评估并非正式诊断命名所要求的,而且通常也不在保险范围内。对唾液暗光褪黑激素起始期(DLMO,一种有效的昼夜节律相位标志物)进行居家评估是一种日益被接受的昼夜节律相位评估方法。这种方法有助于满足日益增长的评估需求,而且具有成本低、更方便患者的优点。我们回顾了描述居家唾液 DLMO 评估方法的文献,并确定了成功实施的重要因素。在此,我们提供了进行居家唾液 DLMO 评估的具体方案建议,以促进临床和研究目的的标准化方法。关键因素包括对照明、采样率和时间的控制,以及对患者依从性的测量。我们纳入了优化算法的实施结果,以确定睡眠-觉醒延迟期障碍患者最有效的采样数量和时间。我们还对检测方法和解释提出了建议。提供每个因素的明确标准以及方案实施的详细说明,将有助于更广泛地采用居家昼夜节律相位评估作为标准化的临床诊断、监测和治疗工具。
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引用次数: 0
Melatonin Priming Promotes Crop Seed Germination and Seedling Establishment Under Flooding Stress by Mediating ABA, GA, and ROS Cascades 褪黑激素通过调节ABA、GA和ROS级联促进洪水胁迫下作物种子的发芽和成苗
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-08-15 DOI: 10.1111/jpi.13004
Xiaofeng Luo, Xiaojing Xu, Jiahui Xu, Xiaoting Zhao, Ranran Zhang, Yiping Shi, Mingyu Xia, Baoshan Xian, Wenguan Zhou, Chuan Zheng, Shaowei Wei, Lei Wang, Junbo Du, Weiguo Liu, Kai Shu

Both seed germination and subsequent seedling establishment are key checkpoints during the life cycle of seed plants, yet flooding stress markedly inhibits both processes, leading to economic losses from agricultural production. Here, we report that melatonin (MT) seed priming treatment enhances the performance of seeds from several crops, including soybean, wheat, maize, and alfalfa, under flooding stress. Transcriptome analysis revealed that MT priming promotes seed germination and seedling establishment associated with changes in abscisic acid (ABA), gibberellin (GA), and reactive oxygen species (ROS) biosynthesis and signaling pathways. Real-time quantitative RT-PCR (qRT-PCR) analysis confirmed that MT priming increases the expression levels of GA biosynthesis genes, ABA catabolism genes, and ROS biosynthesis genes while decreasing the expression of positive ABA regulatory genes. Further, measurements of ABA and GA concentrations are consistent with these trends. Following MT priming, quantification of ROS metabolism-related enzyme activities and the concentrations of H2O2 and superoxide anions (O2) after MT priming were consistent with the results of transcriptome analysis and qRT-PCR. Finally, exogenous application of GA, fluridone (an ABA biosynthesis inhibitor), or H2O2 partially rescued the poor germination of non-primed seeds under flooding stress. Collectively, this study uncovers the application and molecular mechanisms underlying MT priming in modulating crop seed vigor under flooding stress.

种子萌发和随后的成苗是种子植物生命周期中的关键检查点,然而洪水胁迫会明显抑制这两个过程,导致农业生产的经济损失。在这里,我们报告了褪黑激素(MT)种子萌发处理可提高大豆、小麦、玉米和紫花苜蓿等几种作物种子在洪水胁迫下的表现。转录组分析表明,褪黑激素促进种子萌发和成苗与脱落酸(ABA)、赤霉素(GA)和活性氧(ROS)生物合成和信号通路的变化有关。实时定量 RT-PCR (qRT-PCR)分析证实,MT 引物提高了 GA 生物合成基因、ABA 分解基因和 ROS 生物合成基因的表达水平,同时降低了 ABA 正调控基因的表达水平。此外,ABA 和 GA 浓度的测量结果也与这些趋势一致。在 MT 诱导后,ROS 代谢相关酶活性的定量以及 H2O2 和超氧阴离子(O2 -)的浓度与转录组分析和 qRT-PCR 的结果一致。最后,外源施用 GA、氟利酮(一种 ABA 生物合成抑制剂)或 H2O2 可部分缓解未引种种子在淹水胁迫下萌发不良的问题。总之,本研究揭示了在洪水胁迫下MT引物调节作物种子活力的应用和分子机制。
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Journal of Pineal Research
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