Peptides最新文献_第8页

Octadecaneuropeptide promotes the migration of astrocyte via ODN metabotropic receptor and calcium signaling pathway 八肽通过ODN代谢受体和钙信号通路促进星形胶质细胞的迁移。

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Peptides

Pub Date : 2025-01-01 DOI: 10.1016/j.peptides.2024.171338

Sada Al-Mashhadani , Mariem Sallemi , Amira Namsi , Yosra Hamdi , Amine Cherif , Fethia Abidi , Jérôme Leprince , Zekri Sami , David Vaudry , Masmoudi-Kouki Olfa

Migration is an essential characteristic of cells that occurs during many physiological and pathological processes. Astrocytes represent the most abundant cell type in the adult central nervous system (CNS), that play a crucial role in various functions such as guiding and supporting neuronal migration during development and maintaining brain homeostasis at adulthood. Astrocytes specifically synthesize and release endozepines, a family of regulatory peptides, including the octadecaneuropeptide (ODN). ODN is an endogenous ligand for both central-type benzodiazepine receptors and a metabotropic receptor. ODN promotes proliferation and prevents oxidative damage induced apoptosis on both neurons and astrocytes. However, little is known regarding the effect of ODN on cell migration. The purpose of the present study was to investigate the potential effect of ODN on astrocytes migration. Our results show that ODN stimulates astrocytes proliferation and migration at very low concentrations in wound healing assays, that was mimicked by the metabotropic ODN receptor agonist cyclo_1–8 octapeptide (cyclo_1–8OP, 10⁻¹⁴ M to 10⁻¹⁰ M). The effect of ODN on astrocyte migration was abrogated by the metabotropic receptor antagonist, cyclo_1–8[DLeu⁵] OP. Moreover, we have shown that ODN activates the calcium signaling pathway and increases the mammalian target of rapamycin (mTOR) gene transcription, which are both known to promote astrocyte migration. Therefore, the present results suggest that ODN regulates astroglial cell migration through the calcium/mTOR signaling pathway and provide new insight regarding the role of ODN on brain remodling after injury.

迁移是细胞在许多生理和病理过程中发生的基本特征。星形胶质细胞是成人中枢神经系统（CNS）中最丰富的细胞类型，在发育过程中指导和支持神经元迁移以及维持成年期大脑稳态等多种功能中起着至关重要的作用。星形胶质细胞特异性地合成并释放内啡肽，这是一个调节肽家族，包括十八欧肽（ODN）。ODN是中枢型苯二氮卓受体和代谢受体的内源性配体。ODN促进神经元和星形胶质细胞的增殖并防止氧化损伤诱导的细胞凋亡。然而，关于ODN对细胞迁移的影响知之甚少。本研究旨在探讨ODN对星形胶质细胞迁移的潜在影响。我们的研究结果表明，在伤口愈合实验中，ODN在非常低的浓度下刺激星形胶质细胞的增殖和迁移，这是由代谢ODN受体激动剂cyclo1-8八肽（cyclo1-8OP， 10-14M至10-10M）模拟的。ODN对星形胶质细胞迁移的影响被代谢受体拮抗剂cyclo1-8[DLeu5] op所消除。此外，我们已经证明ODN激活钙信号通路并增加哺乳动物雷帕霉素靶基因（mTOR）的转录，这两者都是已知的促进星形胶质细胞迁移的因素。因此，本研究结果提示ODN通过钙/mTOR信号通路调控星形胶质细胞的迁移，并为ODN在损伤后脑重塑中的作用提供了新的认识。

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引用次数: 0

Apelin/APJ increased renal blood flow through endothelial BKCa channel induced p-eNOS and ET-1 in diabetic conditions Apelin/APJ增加通过内皮BKCa通道的肾血流量，诱导糖尿病患者p-eNOS和ET-1。

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Peptides

Pub Date : 2025-01-01 DOI: 10.1016/j.peptides.2024.171333

Mingcong Huang , Jing Chang , Yu Liu , Jiming Yin , Xiangjun Zeng

Renal hemodynamics damage, an important driving mechanism of diabetic nephropathy (DN), is related to many abnormal endothelial released molecules, such as endothelial nitrogen monoxide synthase (eNOS) and endothelin-1 (ET-1), caused by glomerular endothelial cells dysfunction. Apelin, as the endogenous ligand for APJ, was reported to be associated with endothelial cell dysfunction in diabetes. Therefore, it is hypothesized that apelin/APJ increased renal perfusion in DN through regulating endothelial released molecules. Diabetic models were replicated via injecting STZ intraperitoneally (40 mg/kg/day) for 5 consecutive days. Apelin-13 was infused with micro-osmotic pump at 30 μg/kg/day for 4 weeks. The results showed that apelin increased renal blood flow by increasing phosphorylated eNOS and decreasing ET-1 in diabetic mice, which were cancelled in endothelial-specific APJ knockout mice or whole-body large conductance Ca^2 +-activated K⁺ (BKCa) channel knockout rats. Additionally, apelin/APJ activated BKCa channel via increasing expression of BKCa subunits through PI3K/AKT/GSK-3β/Nrf2 pathway but not increasing intracellular Ca²⁺ concentration under high glucose conditions. In conclusion, this study revealed that apelin/APJ increased renal blood flow in early phase of DN via increasing p-eNOS and decreasing ET-1 in glomerular endothelial cells dependent on PI3K/AKT/GSK-3β/Nrf2 pathway induced expression of BKCa subunits.

肾血流动力学损伤是糖尿病肾病（DN）的重要驱动机制，与肾小球内皮细胞功能障碍引起的内皮一氧化氮合酶（eNOS）、内皮素-1 （ET-1）等内皮释放分子异常有关。据报道，APJ的内源性配体Apelin与糖尿病内皮细胞功能障碍有关。因此，我们假设apelin/APJ通过调节内皮细胞释放的分子增加DN的肾灌注。通过腹腔注射STZ （40mg/kg/天）连续5天复制糖尿病模型。Apelin-13以30μg/kg/d微渗透泵滴注，连续4周。结果表明，在糖尿病小鼠中，apelin通过增加磷酸化的eNOS和降低ET-1来增加肾血流量，而在内皮特异性APJ敲除小鼠或全身大电导Ca2+激活K+ (BKCa)通道敲除大鼠中，这种作用被取消。此外，apelin/APJ通过PI3K/AKT/GSK-3β/Nrf2途径增加BKCa亚基的表达，激活BKCa通道，但在高糖条件下不增加细胞内Ca2+浓度。综上所述，本研究表明apelin/APJ通过PI3K/AKT/GSK-3β/Nrf2通路诱导BKCa亚基的表达，通过增加肾小球内皮细胞的p-eNOS和降低ET-1来增加DN早期肾血流量。

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引用次数: 0

Elevated Plasma Soluble (Pro)renin receptor as a potential indicator for heart failure 血浆可溶性肾素受体升高作为心力衰竭的潜在指标。

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Peptides

Pub Date : 2025-01-01 DOI: 10.1016/j.peptides.2024.171337

Jianhua Xiong , Huiru Yang , Xiaoli Yi , Xu Zhou , Wenting Tan , Shanshan Song , Chunju Liu , Mulan Wang , Mengzhi Zhu , Lixiang Zheng , Jun Yu , Chuanming Xu

Increasing evidence has demonstrated that sPRR [a truncated soluble form of (pro)renin receptor] levels may reflect the severity of several diseases, including kidney disease, hypertension, and heart failure (HF). Although previous studies using cohorts primarily consisting of HF patients with reduced ejection fraction revealed that increased plasma sPRR levels may be a promising evaluative indicator for HF, definitive information on the relationship between plasma sPRR levels and HF patients with preserved ejection fraction (HFpEF) is still insufficient and scarce. In the present study, we further clarified the status of plasma sPRR levels in HF patients by meta-analysis. We enrolled a cohort primarily consisting of HFpEF patients (87.8 %) to further determine the relationships between plasma sPRR levels and HFpEF. Meta-analysis showed a significant increase in plasma sPRR levels in HF patients, with substantial statistical heterogeneity. In our observational study, plasma sPRR levels were significantly higher in the HF group than in the non-HF group (17.4 ± 9.8 vs. 10.4 ± 3.4 ng/ml, p < 0.001) and positively correlated with age, B-type natriuretic peptide, creatine, urea nitrogen, plasma renin activity, angiotensin II, and left atrial diameter and negatively correlated with estimated glomerular filtration rate. Plasma sPRR levels (The average value ≥ 16.1 ± 7.2 ng/ml) and the diagnostic values (reflected by the area under the receiver operating characteristic curves ≥ 0.749) of sPRR were comparable for all subtypes of HF patients. Overall, plasma sPRR levels were significantly elevated in HF patients. Elevated plasma sPRR levels may be one of the underlying indicators for HF.

越来越多的证据表明，sPRR（肾素受体的一种截断的可溶性形式）水平可能反映几种疾病的严重程度，包括肾病、高血压和心力衰竭（HF）。虽然先前的研究主要由射血分数降低的HF患者组成，结果表明血浆sPRR水平升高可能是一个很有希望的HF评估指标，但关于血浆sPRR水平与保留射血分数（HFpEF）的HF患者之间关系的明确信息仍然不足且稀缺。在本研究中，我们通过荟萃分析进一步阐明了HF患者血浆sPRR水平的现状。我们招募了一个主要由HFpEF患者（87.8 %）组成的队列，以进一步确定血浆sPRR水平与HFpEF之间的关系。荟萃分析显示，HF患者血浆sPRR水平显著升高，具有显著的统计学异质性。在我们的观察性研究中，HF组血浆sPRR水平显著高于非HF组(17.4 ± 9.8 vs. 10.4 ± 3.4 ng/ml, p

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引用次数: 0

Estrogens impair hypophagia and hypothalamic cell activation induced by vasoactive intestinal peptide, but not by pituitary adenylate cyclase-activating polypeptide 雌激素对血管活性肠肽诱导的下咽和下丘脑细胞活化有影响，而对垂体腺苷酸环化酶激活多肽无影响。

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Peptides

Pub Date : 2025-01-01 DOI: 10.1016/j.peptides.2024.171325

Marcela Cristina Garnica-Siqueira , Andressa Busetti Martins , Érica Cristina Alves Munhoz Monteiro , Maria Heloisa Bernardes de Oliveira , Carolina dos Reis Baratto , Fabiano Takeo Komay Tsutsui , Lucas Leonardo França de Oliveira , Larissa Rugila dos Santos Stopa , Camila Franciele de Souza , Ana Luiza Machado Wunderlich , Dimas Augusto Morozin Zaia , Cristiane Mota Leite , Cássia Thaïs Bussamra Vieira Zaia , Ernane Torres Uchoa

The neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) act in arcuate (ARC) and paraventricular (PVN) hypothalamic nuclei, reducing food intake and changing plasma parameters. Estrogens (E) also regulate energy homeostasis, and loss of ovarian function leads to hyperphagia and body weight gain. This study aimed to evaluate the effects of estradiol (E) in a postmenopausal rat model, ovariectomy (OVX), on PAC1 and VPAC2 receptors in the PVN and ARC, as well as on food intake, plasma parameters, and PVN and ARC cell activation in response to intracerebroventricular microinjection of VIP and PACAP. For this, the rats underwent intracerebroventricular and OVX surgeries, being treated daily with subcutaneous injections of 0.2 mL of corn oil or 10 μg/0.2 mL of estradiol cypionate, comprising the OVX+O and OVX+E groups, respectively. OVX+E showed reduced VPAC2 mRNA expression in the PVN. PACAP reduced food intake in both groups, and VIP-induced hypophagia was not observed in OVX+E. VIP increased plasma glucose in both groups, and PACAP increased plasma glucose only in OVX+O. VIP decreased free fatty acids in OVX+E. Furthermore, PACAP increased ARC cell activation in both groups, and in the PVN only in OVX+O. Cell activation induced by VIP in ARC and PVN was blocked by estradiol. Therefore, estrogens disrupted the hypophagia induced by VIP, but not by PACAP, and these differences seem to be, at least in part, due to an impairment of the activation of the ARC-PVN pathway.

血管活性肠肽（VIP）和垂体腺苷酸环化酶激活多肽（PACAP）等神经肽作用于下丘脑弓状核（ARC）和室旁核（PVN），减少食物摄取量，改变血浆参数。雌激素(E)也调节能量稳态，卵巢功能的丧失会导致贪食和体重增加。本研究旨在评估绝经后大鼠卵巢切除模型（OVX）中雌二醇(E)对PVN和ARC中PAC1和VPAC2受体的影响，以及对脑室内微注射VIP和PACAP对食物摄入、血浆参数和PVN和ARC细胞活化的影响。为此，大鼠接受脑室和OVX手术，每天皮下注射0.2mL玉米油或10μg/0.2mL雌二醇，分别分为OVX+O组和OVX+E组。OVX+E显示PVN中vpac2mrna表达降低。PACAP减少了两组的食物摄入量，OVX+E未观察到vip诱导的吞咽不足。VIP使两组血糖升高，PACAP仅使OVX+O组血糖升高。VIP降低OVX+E游离脂肪酸。此外，PACAP在两组中均增加了ARC细胞的活化，而在PVN中仅在OVX+O中增加了ARC细胞的活化。雌二醇可阻断VIP诱导的ARC和PVN细胞活化。因此，雌激素破坏了VIP诱导的下咽，而不是PACAP诱导的下咽，这些差异似乎至少部分是由于ARC-PVN通路激活的损害。

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引用次数: 0

Nesfatin-1 is involved in hyperbaric oxygen-mediated therapeutic effects in high fat diet-induced hyperphagia in mice Nesfatin-1参与高压氧介导的高脂饮食诱导的小鼠贪食的治疗作用。

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Peptides

Pub Date : 2025-01-01 DOI: 10.1016/j.peptides.2024.171336

Yuchen Xie , Yihui Feng , Shaohua Li , Bowen Yu , Fangzheng Yang , Yanfei Li , Yuanchao Cheng , Zhouxi Yu , Chanjuan Li , Jing Dong , Junhua Yuan

Obesity is a worldwide health issue. Effective and safe methods for obesity management are highly desirable. In the current study, hyperbaric oxygen (HBO) treatment was investigated as a potential treatment against obesity-associated hyperphagia and hyperenergy intake. Diet induced obesity (DIO) mice model was established with high fat diet (HFD) feeding, HBO was then co-administered. Food and energy intake were assessed with nocturnal food intake assay. Immunohistochemistry for c-Fos was performed for neuronal activation in arcuate nucleus (ARC), paraventricular nucleus of hypothalamus (PVN) and lateral parabrachial nucleus (LPBN) of brain. Additionally, enzyme-linked immunosorbent assay (ELISA) in serum and immunofluorescence in LPBN were performed. Results indicated that HBO co-treatment effectively decreased food and energy intake in DIO mice, reverted the abnormal neuronal activation in the ARC and PVN, and enhanced both peripheral and central nesfatin-1 peptide levels without affecting serum leptin levels. While SHU9119 microinjection in LPBN effectively abolished the beneficial effects of HBO on body weight, visceral fat, nocturnal feeding and energy intake in DIO mice. In conclusion, HBO treatment could effectively protect against HFD-induced increase of food and energy intake, which is associated with its central effects against abnormal neuronal activation in ARC and PVN and enhanced peptide levels of nesfatin-1 both centrally and peripherally. The melanocortin system downstream of nesfatin-1 may exert a potential effect in this process.

肥胖是一个全球性的健康问题。有效和安全的肥胖管理方法是非常可取的。在目前的研究中，高压氧（HBO）治疗被研究作为一种潜在的治疗肥胖相关的贪食和高能量摄入的方法。采用高脂日粮（HFD）喂养建立饮食性肥胖（DIO）小鼠模型，同时给予HBO。用夜间摄食量测定法测定食物和能量的摄取量。采用免疫组化方法检测c-Fos在脑弓状核（ARC）、下丘脑室旁核（PVN）和外侧臂旁核（LPBN）的神经元活化情况。同时进行血清酶联免疫吸附试验（ELISA）和LPBN免疫荧光检测。结果表明，HBO联合治疗可有效减少DIO小鼠的食物和能量摄入，逆转ARC和PVN中异常神经元的激活，并在不影响血清瘦素水平的情况下提高外周和中枢nesfatin-1肽水平。而在LPBN中微量注射SHU9119可有效消除HBO对DIO小鼠体重、内脏脂肪、夜间摄食和能量摄入的有益作用。综上所述，HBO治疗可有效预防hfd诱导的食物和能量摄入增加，这与HBO对ARC和PVN异常神经元激活以及中枢和外周nesfatin-1肽水平升高的中枢作用有关。巢脂素-1下游的黑素皮质素系统可能在这一过程中发挥潜在作用。

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引用次数: 0

Prokineticin 2 protein is diurnally expressed in PER2-containing clock neurons in the mouse suprachiasmatic nucleus Prokineticin 2蛋白在小鼠视交叉上核含PER2的时钟神经元中每日表达。

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Peptides

Pub Date : 2025-01-01 DOI: 10.1016/j.peptides.2024.171339

Ida Stangerup , Birgitte Georg , Jens Hannibal

Expression of prokineticin 2 (PK2) mRNA in the suprachiasmatic nucleus (SCN), also known as the brain’s clock, exhibits circadian oscillations with peak levels midday, zeitgeber time (ZT) 4, and almost undetectable levels during night. This circadian expression profile has substantially contributed to the suggested role of PK2 as an SCN output molecule involved in transmitting circadian rhythm of behavior and physiology. Due to unreliable specificity of PK2 antibodies, the 81 amino acid protein has primarily been studied at the mRNA level and correlation between circadian oscillating mRNAs and protein products are infrequent. Hence, data on PK2 protein expression in the SCN is lacking. In this study a thorough validation of a commercial PK2 antibody for immunohistochemistry (IHC) was performed followed by fluorescence IHC on SCN mouse brain sections at six consecutive ZTs over a 24-h cycle (12:12 light-dark, ZT0 =light ON whereas ZT12 =light OFF). Data were visualized and processed using confocal microscopy. Results showed that PK2 protein expression diurnally oscillates with calculated peak expression ZT5:40 ± 1:40 h. Opposite than described for PK2 mRNA, PK2 immunoreactivity was detectable at all times during the 24-h cycle. PK2 was primarily located in neurons of the shell compartment and > 80 % of these neurons co-expressed the core clock protein PER2. In conclusion, PK2 protein expression oscillates as the mRNA, supporting the suggested role of PK2 as a SCN molecule involved in circadian rhythm regulation.

视交叉上核（SCN）中促动素2 (PK2) mRNA的表达，也被称为大脑的时钟，表现出昼夜节律振荡，中午达到峰值，zeitgeber时间（ZT） 4，晚上几乎检测不到水平。这种昼夜节律表达谱极大地促进了PK2作为SCN输出分子参与传递行为和生理昼夜节律的作用。由于PK2抗体的特异性不可靠，这种81个氨基酸的蛋白质主要在mRNA水平上进行研究，而昼夜振荡mRNA与蛋白质产物之间的相关性并不常见。因此，缺乏PK2蛋白在SCN中的表达数据。在这项研究中，对商业PK2抗体进行了免疫组织化学（IHC）的彻底验证，然后在SCN小鼠脑切片上进行了荧光免疫组化，在24小时周期内连续6个ZTs（12:12光暗，ZT0=亮，ZT12=灭）。使用共聚焦显微镜对数据进行可视化和处理。结果表明，PK2蛋白的表达量以计算的峰值ZT5:40±1:40小时为波动周期。与PK2 mRNA相反，PK2的免疫反应性在24小时周期内的所有时间都可以检测到。PK2主要位于壳室和>的神经元中，这些神经元中80%共表达核心时钟蛋白PER2。总之，PK2蛋白的表达作为mRNA振荡，支持PK2作为SCN分子参与昼夜节律调节的作用。

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引用次数: 0

Oxytocin attenuates cardiac hypertrophy by improving cardiac glucose metabolism and regulating OXTR/JAK2/STAT3 axis 催产素通过改善心脏糖代谢和调节OXTR/JAK2/STAT3轴来减轻心肌肥厚

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Peptides

Pub Date : 2024-12-01 DOI: 10.1016/j.peptides.2024.171323

Yuqiao Yang , Jin Liu , Lingyan Wang , Wen Wu, Quan Wang, Yu Zhao, Xi Qian, Zhuoran Wang, Na Fu, Yanqiong Wang, Jinqiao Qian

Background

The progress of cardiac hypertrophy is modulated by JAK2/STAT3 signaling pathway. Cardiac glucose metabolism derangement exacerbates the progression of cardiac hypertrophy. Oxytocin (OT) has emerged as a significant hormone involved in cardiovascular homeostasis, especially in protecting against cardiac hypertrophy. The present study aims to explore whether the anti-hypertrophy effect of oxytocin is related to the JAK2/STAT3 signaling pathway and cardiac glucose metablism.

Methods

Cardiac hypertrophy model was induced by angiotensin II (Ang II) in H9c2 cells and in mice with or without oxytocin treatment. Changes in cardiac histopathology were evaluated by hematoxylin and eosin (H&E), Masson staining, and wheat germ agglutinin (WGA) staining. The hypertrophy-related genes and JAK2/STAT3 pathway signaling molecules were analyzed by qRT-PCR and western blotting. The levels of glucose, pyruvic acid, lactic acid, and lactate dehydrogenase activity in H9c2 cells using the corresponding assay kits.

Results

The results showed that OT inhibited hypertrophic and fibrotic changes. Furthermore, OT increased intracellular levels of glucose and pyruvic acid, and decreased lactate dehydrogenase activity and lactic acid levels. Mechanistically, Ang II decreased oxytocin receptors (OXTR) expression and facilitated JAK2 and STAT3 phosphorylation. OT treatment increased OXTR expression and blocked JAK2 and STAT3 phosphorylation The OXTR-specific siRNA-mediated depleted expression could abrogate OT-induced anti-hypertrophic effects in H9c2 cells following angiotensin II insult. However, the JAK2/STAT3 inhibitor AG490 rescued the protective effects of OT against cardiac hypertrophy under OXTR downregulation.

Conclusion

OT exerts its protective effects against cardiac hypertrophy by improving cardiac glucose metabolism and regulating OXTR/JAK2/STAT3 axis.

背景心肌肥厚的进展受JAK2/STAT3信号通路的调控。心脏糖代谢紊乱加剧了心脏肥厚的进展。催产素（OT）已成为一种重要的激素，参与心血管稳态，特别是防止心脏肥厚。本研究旨在探讨催产素的抗肥厚作用是否与JAK2/STAT3信号通路和心脏糖代谢有关。方法采用血管紧张素II （Ang II）诱导H9c2细胞心肌肥厚模型，并在催产素处理和未处理小鼠心肌肥厚模型中进行比较。通过苏木精和伊红（H&；E）、Masson染色和小麦胚芽凝集素（WGA）染色评估心脏组织病理学的变化。采用qRT-PCR和western blotting分析肥大相关基因和JAK2/STAT3通路信号分子。使用相应的检测试剂盒检测H9c2细胞中葡萄糖、丙酮酸、乳酸和乳酸脱氢酶活性的水平。结果OT对大鼠大鼠增生性和纤维化有抑制作用。此外，OT增加细胞内葡萄糖和丙酮酸水平，降低乳酸脱氢酶活性和乳酸水平。在机制上，Ang II降低了催产素受体（OXTR）的表达，促进了JAK2和STAT3的磷酸化。在血管紧张素II损伤H9c2细胞后，OXTR特异性sirna介导的表达缺失可以消除OT诱导的抗肥厚作用。然而，JAK2/STAT3抑制剂AG490在OXTR下调的情况下恢复了OT对心脏肥厚的保护作用。结论ot通过改善心脏糖代谢、调节OXTR/JAK2/STAT3轴对心肌肥厚具有保护作用。

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引用次数: 0

Corrigendum to “Lasso peptides realm: Insights and applications” Peptides 182(December) (2024) 171317 Lasso peptides realm：肽 182（12 月）（2024）171317。

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Peptides

Pub Date : 2024-12-01 DOI: 10.1016/j.peptides.2024.171321

Othman Al Musaimi

引用次数: 0

The Viktor Mutt Award Lecture 2024 to Tomas Hökfelt 托马斯-霍克费尔特获得 2024 年维克多-穆特奖。

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Peptides

Pub Date : 2024-12-01 DOI: 10.1016/j.peptides.2024.171324

Karl-Heinz Herzig

引用次数: 0

The effects of corticotropin-releasing factor (CRF) and urocortins on the noradrenaline (NA) released from the locus coeruleus (LC) 促肾上腺皮质激素释放因子（CRF）和尿皮质素对脑皮质释放的去甲肾上腺素（NA）的影响。

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Peptides

Pub Date : 2024-12-01 DOI: 10.1016/j.peptides.2024.171322

Patrícia Tancsics , Aliz Kovács , Miklós Palotai , Zsolt Bagosi

Corticotropin-releasing factor (CRF) activates the hypothalamic-pituitary-adrenal (HPA) axis and stimulates the noradrenergic neurotransmission, both processes being implicated in the pathogenesis of anxiety and depression, but the intimate site and mechanism of interaction of CRF and CRF-related peptides, named urocortins (UCN1, UCN2, UCN3), with noradrenaline (NA) was not fully elucidated yet. Therefore, the aim of the present study was to investigate the actions of CRF and urocortins on the NA released from the rat locus coeruleus (LC), the primary source of NA in the brain, and the participation of CRF receptors (CRF1 and CRF2) in these actions. In order to do so, male Wistar rats were used, their LC were isolated and dissected, and the LC slices were incubated with tritium-labelled NA, superfused and stimulated electrically. During superfusion, the LC slices were treated with CRF, UCN1, UCN2 or UCN3, and, when significant effect was observed, pretreated with selective CRF1 antagonist antalarmin or selective CRF2 antagonist astressin2B. The release of tritium-labelled NA from the LC was determined by liquid scintillation counting. CRF and UCN1 increased significantly the tritium-labelled NA release from the LC, and these effects were reduced by antalarmin, but not by astressin2B. In addition, UCN2, but not UCN3, decreased significantly the tritium-labelled NA release from the LC, and this effect was reversed by astressin2B, but not antalarmin. Our results indicate the existence of two apparently opposing CRF systems in the LC, since activation of CRF1 by CRF and UCN1 stimulated, whereas activation of CRF2 by UCN2 inhibited the NA release.

促肾上腺皮质激素释放因子（CRF）能激活下丘脑-垂体-肾上腺（HPA）轴，刺激去甲肾上腺素能神经递质，这两个过程都与焦虑和抑郁的发病机制有关，但CRF和CRF相关肽（即尿皮质素（UCN1、UCN2、UCN3））与去甲肾上腺素（NA）相互作用的密切部位和机制尚未完全阐明。因此，本研究旨在探究 CRF 和尿皮质素对大鼠脑内 NA 的主要来源--大鼠脑室（LC）释放的 NA 的作用，以及 CRF 受体（CRF1 和 CRF2）在这些作用中的参与情况。为此，研究人员使用雄性 Wistar 大鼠，分离并解剖了它们的 LC，用氚标记的 NA 培养 LC 切片，并对其进行灌注和电刺激。在超灌注过程中，用 CRF、UCN1、UCN2 或 UCN3 处理 LC 切片，并在观察到显著效果时，用选择性 CRF1 拮抗剂 antalarmin 或选择性 CRF2 拮抗剂 astressin2B 进行预处理。通过液体闪烁计数测定氚标记的 NA 从 LC 中的释放量。CRF 和 UCN1 能显著增加胰岛素管中氚标记 NA 的释放，antalarmin 能降低这些效应，但 astressin2B 却不能。此外，UCN2（而非 UCN3）能显著减少 LC 中氚标记 NA 的释放，而 astressin2B（而非 antalarmin）能逆转这种效应。我们的研究结果表明，LC中存在两种明显对立的CRF系统，因为CRF和UCN1激活CRF1会刺激NA的释放，而UCN2激活CRF2会抑制NA的释放。

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引用次数: 0