Neuropeptides最新文献_第4页

GnRH protective effects against long-term potentiation impairment induced by AANAT-siRNA GnRH对AANAT-siRNA诱导的长期延时损伤的保护作用

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-09-18 DOI: 10.1016/j.npep.2024.102474

Leila Karimi-Zandi , Tahereh Ghorbandaiepour , Maryam Zahmatkesh , Esmaeil Sadroddiny

{"title":"GnRH protective effects against long-term potentiation impairment induced by AANAT-siRNA","authors":"Leila Karimi-Zandi , Tahereh Ghorbandaiepour , Maryam Zahmatkesh , Esmaeil Sadroddiny","doi":"10.1016/j.npep.2024.102474","DOIUrl":"10.1016/j.npep.2024.102474","url":null,"abstract":"<div><div>There is an interplay between the gonadotropin-releasing hormone (GnRH) and melatoninergic systems. The key enzyme of melatonin synthesis (arylalkylamine <em>N</em>-acetyltransferase, AANAT), and GnRH receptors are expressed in the hippocampus. While it has been shown that hippocampal AANAT enzyme activity is necessary for proper hippocampal cognitive function, their role in long-term potentiation (LTP) induction is not fully understood. In current study, the impact of GnRH on LTP induction was investigated, while hippocampal melatonin synthesis had been inhibited. The melatonin synthesis was inhibited by AANAT-siRNA administration, and LTP was induced using in vivo field potential electrophysiological recording.</div><div>Animals were divided into 5 groups: Intact, vehicle, siRNA, GnRH and siRNA+GnRH. All animals, except intact group, experienced the stereotaxic surgery and intra-hippocampal cannulation to receive vehicle agent, AANAT siRNA (0.5 μg/hip), GnRH (1 ng/rat), and AANAT siRNA+GnRH. The recognition memory was assessed by Novel object recognition test. The field potential electrophysiology experiment was conducted by stimulating the Schaffer collateral pathway, and LTP induction was carried out through high-frequency stimulation (HFS). After recording, animals' brain was isolated and quickly frozen for further hippocampal melatonin levels measurement by LC-MS and AANAT mRNA levels by qRT-PCR.</div><div>GnRH injection in the hippocampus increased local AANAT-mRNA expression and melatonin levels. GnRH-treated animals displayed higher LTP amplitude compared to intact, vehicle and siRNA groups. While the reduction in hippocampal melatonin levels by AANAT-siRNA inhibited LTP and impaired recognition memory, the GnRH prevented these adverse effects. The data suggests that GnRH have protective effects against AANAT-siRNA-induced LTP decline. The protective mechanism at least partially, may be related to the increased expression of local AANAT-mRNA.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102474"},"PeriodicalIF":2.5,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Phosphorylated NPY1R regulates phenotypic transition of vascular smooth muscle cells, inflammatory response and macrophage infiltration to promote intracranial aneurysm progression 磷酸化的 NPY1R 可调控血管平滑肌细胞的表型转换、炎症反应和巨噬细胞浸润，从而促进颅内动脉瘤的进展

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-09-06 DOI: 10.1016/j.npep.2024.102465

Jian He , Yonghong Duan , Yuanding Jiang , Jie Luo , Tao Wang , Richu Liang , Ting Tang

{"title":"Phosphorylated NPY1R regulates phenotypic transition of vascular smooth muscle cells, inflammatory response and macrophage infiltration to promote intracranial aneurysm progression","authors":"Jian He , Yonghong Duan , Yuanding Jiang , Jie Luo , Tao Wang , Richu Liang , Ting Tang","doi":"10.1016/j.npep.2024.102465","DOIUrl":"10.1016/j.npep.2024.102465","url":null,"abstract":"<div><h3>Background</h3><div>Rupture of intracranial aneurysm (IA) could give rise to spontaneous subarachnoid hemorrhage, leading to a high disability rate and even death. NPY1R expression was upregulated in aneurysm tissues of IA patients. However, the role and underlying mechanism of NPY1R remains unknown.</div></div><div><h3>Methods</h3><div>The IA model of mice was established using inducing systemic hypertension and injecting elastase. The expression of genes and proteins was detected by RT-qPCR and western blot. The number of T cells, macrophages, and neutrophils in IA mice was detected using flow cytometry and IF assay. The levels of inflammatory factors were measured using ELISA. Patho-morphology and inflammatory cells in aneurysm tissues were evaluated by HE staining. The interaction between TK and NPY1R was validated using Co-IP.</div></div><div><h3>Results</h3><div>NPY1R expression was greatly elevated in aneurysm tissues in IA patients and mice, which were positively related to macrophage infiltration. Besides, exogenous overexpression of NPY1R resulted in the promotion of contractile phenotype to the synthetic phenotype of vascular smooth muscle cells (VSMCs), inflammatory response and M1 macrophage polarization. In terms of the underlying mechanism, NPY1R protein could be modified by TK-mediated phosphorylation and TKI could decrease IA formation and suppresse contractile phenotype to synthetic phenotype of VSMCs, inflammatory response and M1 macrophage polarization in IA mice. Furthermore, ablating mouse macrophages abolished NPY1R overexpression-mediated promotion of IA formation and rupture in mice.</div></div><div><h3>Conclusion</h3><div>Phosphorylated NPY1R contributed to IA progression through promoting contractile phenotype to synthetic phenotype of VSMCs, inflammatory response and M1 macrophage polarization in IA.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102465"},"PeriodicalIF":2.5,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142358313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The restraint stress-induced antinociceptive effects decreased by antagonism of both orexin receptors within the CA1 region of the hippocampus 拮抗海马 CA1 区的两种奥曲肽受体可降低束缚应激引起的抗痛觉效应

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-08-22 DOI: 10.1016/j.npep.2024.102463

Elaheh Danesh , Shahin Hassanpour , Bita Vazir , Mohammad Saghafi , Mohadeseh Ghalandari-Shamami , Abbas Haghparast

{"title":"The restraint stress-induced antinociceptive effects decreased by antagonism of both orexin receptors within the CA1 region of the hippocampus","authors":"Elaheh Danesh , Shahin Hassanpour , Bita Vazir , Mohammad Saghafi , Mohadeseh Ghalandari-Shamami , Abbas Haghparast","doi":"10.1016/j.npep.2024.102463","DOIUrl":"10.1016/j.npep.2024.102463","url":null,"abstract":"<div><p>Studies have indicated that stress-related symptoms can lead to hormonal and neural changes, affecting the pain threshold and nociceptive behaviors. The precise role of orexin receptors (OX1r and OX2r) in stress-induced analgesia (SIA) remains an inquiry yet to be comprehensively elucidated. The current investigation aimed to assess the impact of acute immobilization restraint stress on pain-related behavioral responses after administering antagonists targeting OX1r and OX2r in a rat model using the tail-flick test. After a period of five to seven days post-stereotaxic surgery in CA1, the baseline tail-flick latency (TFL) was recorded for each animal. Subsequently, rats were unilaterally administered varying doses of the OX1r antagonist (SB334867; 1, 3, 10, and 30 nmol), the OX2r antagonist (TCS OX2 29; 1, 3, 10, and 30 nmol), or a vehicle (0.5 μl solution containing 12% DMSO) through an implanted cannula. Following a 5-min interval, the animals were subjected to a restraint stress (RS) lasting for 3 h. The tail-flick test was conducted after the stress exposure, and the TFLs were assessed at 60-min intervals. The findings of this study revealed that RS elicits antinociceptive responses in the tail-flick test. Microinjection of OX1r and OX2r antagonists into the CA1 attenuated RS-induced analgesia during the tail-flick test. Furthermore, the results underscored the preeminent role of OX2 receptors in modulating SIA. In conclusion, the orexin system localized within the hippocampal CA1 region may, in part, contribute to the manifestation of SIA in the context of acute pain.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102463"},"PeriodicalIF":2.5,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142050135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ninjinyoeito ameliorates anorexia and changes in peptide YY and ghrelin levels of cisplatin-treated mice 万年青能改善顺铂治疗小鼠的厌食症以及肽 YY 和胃泌素水平的变化。

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-08-22 DOI: 10.1016/j.npep.2024.102464

Akinobu Hatae, Takuya Watanabe, Chise Taniguchi, Kaori Kubota, Shutaro Katsurabayashi, Katsunori Iwasaki

{"title":"Ninjinyoeito ameliorates anorexia and changes in peptide YY and ghrelin levels of cisplatin-treated mice","authors":"Akinobu Hatae, Takuya Watanabe, Chise Taniguchi, Kaori Kubota, Shutaro Katsurabayashi, Katsunori Iwasaki","doi":"10.1016/j.npep.2024.102464","DOIUrl":"10.1016/j.npep.2024.102464","url":null,"abstract":"<div><p>We explored the effect of Ninjinyoeito (NYT) on cisplatin-induced anorexia, which reduces cancer patient survival. Both gastrointestinal motility and plasma concentrations of gastrointestinal peptides were assessed. Nine-week-old ICR female mice received intraperitoneal cisplatin injections (10 mg/kg) and daily oral NYT doses of 300 mg/kg (NYT300) or 1000 mg/kg (NYT1000). Plasma levels of gastrointestinal peptides were measured at 3 and 6 days after cisplatin injection. Gastrointestinal motility was assessed by analyzing the concentration of phenol red marker within sections of the gastrointestinal tract. Cisplatin-injected mice showed a decrease in daily food intake, but this effect was attenuated on day 5 with NYT1000 administration. Although plasma ghrelin levels were reduced on day 3 in cisplatin-treated mice, NYT1000 administration ameliorated this decrease. However, there were no differences in ghrelin levels among all groups on day 6. Levels of peptide YY (PYY) were elevated in the plasma of cisplatin-injected mice on days 3 and 6. Administration of NYT300 and NYT1000 suppressed the increase in PYY levels on day 6 but not on day 3. Gastrointestinal motility was impaired on day 6 in cisplatin-treated mice, but NYT1000 administration attenuated this effect. Our results suggest that NYT improves cisplatin-induced anorexia by suppressing alterations in ghrelin and PYY levels and by increasing gastrointestinal motility. Therefore, NYT may be a promising candidate for alleviating cisplatin-induced anorexia.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102464"},"PeriodicalIF":2.5,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143417924000635/pdfft?md5=e9234acd11366797dd1a70bafb18c233&pid=1-s2.0-S0143417924000635-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142056175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Melittin protects against neural cell damage in rats following ischemic stroke Melittin 可防止大鼠缺血性中风后神经细胞受损

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-08-13 DOI: 10.1016/j.npep.2024.102462

Xiang Yao , Junlong Kang , Yufei Li , Haoran Zhang , Zhibin Yang , E. Chen

{"title":"Melittin protects against neural cell damage in rats following ischemic stroke","authors":"Xiang Yao , Junlong Kang , Yufei Li , Haoran Zhang , Zhibin Yang , E. Chen","doi":"10.1016/j.npep.2024.102462","DOIUrl":"10.1016/j.npep.2024.102462","url":null,"abstract":"<div><h3>Objective</h3><p>In this study, we explored the neuroprotective effect of melittin (MEL) after brain ischemia using a rat model.</p></div><div><h3>Methods</h3><p>The rats underwent middle cerebral artery occlusion (MCAO) for 60 min and were randomly divided into the control group, saline group, and MEL group. Rats in each group were injected intraperitoneally with MEL one day before MCAO until sacrificed. Morris water maze and rotation test were used to assess locomotor function and cognitive ability. The 9.4 Tesla MRI was used to scan and assess the infarct volume of the rat brains. Immunohistochemistry was used to detect the sites of action of MEL on microglia. Western blot and ELISA were used to measure the effect of MEL on the production of pro-inflammatory cytokines. The effect of MEL on neuronal cell apoptosis was observed by flow cytometry.</p></div><div><h3>Results</h3><p>Compared with the saline group, MEL treatment significantly increased the density of neurons in the cerebral cortical and reduced the cerebral infarct size after MCAO (33.9 ± 8.8% vs. 15.8 ± 3.9%, <em>P</em> < 0.05). Meanwhile, the time for MEL-treated rats to complete the water maze task on the 11th day after MCAO was significantly shorter than that of rats in the saline group (<em>P</em> < 0.05). MEL treatment also prolonged the rotarod retention time on day 14 after MCAO. Immunohistochemistry analysis showed that MEL inhibited the activation of microglia and suppressed the expression of TNF-α, IL-6, and IL-1β in the brain after ischemia. MEL treatment resulted in a significant decrease in TLR4, MyD88, and NF-κB p65 levels in extracts from the ischemic cerebral cortex. Finally, MEL reduced neuronal apoptosis induced by ischemic stroke (<em>P</em> < 0.05).</p></div><div><h3>Conclusion</h3><p>MEL treatment promotes neurological function recovery after cerebral ischemia in rats. These effects are potentially mediated through anti-inflammatory and anti-apoptotic mechanisms.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102462"},"PeriodicalIF":2.5,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142083410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Upregulation of Xbp1 in NPY/AgRP neurons reverses diet-induced obesity and ameliorates leptin and insulin resistance 上调 NPY/AgRP 神经元中的 Xbp1 可逆转饮食引起的肥胖，并改善瘦素和胰岛素抵抗。

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-08-06 DOI: 10.1016/j.npep.2024.102461

Jason Ajwani, Eunsang Hwang, Bryan Portillo, Linh Lieu, Briana Wallace, Anita Kabahizi, Zhenyan He, Yanbin Dong, Kyle Grose, Kevin W. Williams

引用次数: 0

Expression and localization of the neuropeptide Y-Y4 receptor in the chick spleen: mRNA upregulation by high ambient temperature 神经肽Y-Y4受体在雏鸡脾脏中的表达和定位：高环境温度对mRNA的上调。

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-08-05 DOI: 10.1016/j.npep.2024.102459

Haruka Nishimura , Mohamed Z. Elhussiny , Yoshimitsu Ouchi , Shogo Haraguchi , Taichi Q. Itoh , Elizabeth R. Gilbert , Mark A. Cline , Shotaro Nishimura , Yoshinao Z. Hosaka , Eiki Takahashi , John F. Cockrem , Takashi Bungo , Vishwajit S. Chowdhury

{"title":"Expression and localization of the neuropeptide Y-Y4 receptor in the chick spleen: mRNA upregulation by high ambient temperature","authors":"Haruka Nishimura , Mohamed Z. Elhussiny , Yoshimitsu Ouchi , Shogo Haraguchi , Taichi Q. Itoh , Elizabeth R. Gilbert , Mark A. Cline , Shotaro Nishimura , Yoshinao Z. Hosaka , Eiki Takahashi , John F. Cockrem , Takashi Bungo , Vishwajit S. Chowdhury","doi":"10.1016/j.npep.2024.102459","DOIUrl":"10.1016/j.npep.2024.102459","url":null,"abstract":"<div><p>High ambient temperatures (HT) can increase diencephalic neuropeptide Y (NPY) expression, and central injection of NPY attenuates heat stress responses while inducing an antioxidative state in the chick spleen. However, there is a lack of knowledge about NPY receptor expression, and its regulation by HT, in the chick spleen. In the current study, male chicks were used to measure the expression of NPY receptors in the spleen and other immune organs under acute (30 vs. 40 ± 1°C for 3 h) or chronic (30 vs. 40 ± 1°C for 3 h/day for 3 days) exposure to HT and in response to central injection of NPY (47 pmol, 188 pmol, or 1 nmol). We found that NPY-Y4 receptor mRNA was expressed in the spleen, but not in other immune organs studied. Immunofluorescence staining revealed that NPY-Y4 receptors were localized in the splenic pulp. Furthermore, NPY-Y4 receptor mRNA increased in the chick spleen under both acute and chronic exposure to HT. Central NPY at two dose levels (47 and 188 pmol) and a higher dose (1 nmol) did not increase splenic NPY-Y4 receptor mRNA expression or splenic epinephrine under HT (35 ± 1°C), and significantly increased 3-methoxy-4-hydroxyphenylglycol (MHPG) concentrations under HT (40 ± 1°C). In conclusion, increased expression of NPY-Y4 receptor mRNA in the spleen under HT suggest that Y4 receptor may play physiological roles in response to HT in male chicks.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102459"},"PeriodicalIF":2.5,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143417924000581/pdfft?md5=f52d9e73c00f9c5dca1139e53cf90a94&pid=1-s2.0-S0143417924000581-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141913411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Trefoil factor 1 (TFF1) reduces cerebral edema and gastric mucosal injury by regulating the EGFR/Src/FAK pathway in an intracerebral hemorrhage rat model 三叶草因子 1（TFF1）通过调节表皮生长因子受体/Src/FAK 通路减轻脑出血大鼠模型的脑水肿和胃黏膜损伤

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-08-03 DOI: 10.1016/j.npep.2024.102460

Chao Huang , Likun Wang , Guofeng Wu

{"title":"Trefoil factor 1 (TFF1) reduces cerebral edema and gastric mucosal injury by regulating the EGFR/Src/FAK pathway in an intracerebral hemorrhage rat model","authors":"Chao Huang , Likun Wang , Guofeng Wu","doi":"10.1016/j.npep.2024.102460","DOIUrl":"10.1016/j.npep.2024.102460","url":null,"abstract":"<div><p>The destruction of the blood-brain barrier and damage to the gastrointestinal mucosa after intracerebral hemorrhage (ICH) are important reasons for its high disability and mortality rates. However, the exact etiology is not yet clear. In addition, there are currently no effective treatments for improving cerebral edema and gastric mucosal damage after ICH. Trefoil factor 1 (TFF1) is a secretory protein that plays a crucial role in maintaining the integrity and barrier function of the gastric mucosa, and it has been reported to have a protective effect on brain damage induced by various causes. This study utilized a rat model of ICH induced by type IV collagenase was utilized, and intervened with recombinant TFF1 protein from an external institute to investigate the protective mechanisms of TFF1 against brain edema and gastric mucosal damage after ICH. The results demonstrated that TFF1 alleviated the neurological function and gastric mucosal damage in the rat model of ICH induced by type IV collagenase. TFF1 may ensure the integrity of the blood-brain and gastric mucosal barriers by regulating the EGFR (epidermal growth factor receptor)/Src (non-receptor tyrosine kinase)/FAK (focal adhesion kinase) pathway. Clearly, the disruption of the blood-brain barrier and the destruction of the gastric mucosal barrier are key pathological features of ICH, and TFF1 can improve the progression of blood-brain barrier and gastric mucosal barrier disruption in ICH by regulating the EGFR/Src/FAK pathway. Therefore, TFF1 may be a potential target for the treatment of ICH.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102460"},"PeriodicalIF":2.5,"publicationDate":"2024-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143417924000593/pdfft?md5=e91a9ee599634bd01394d82cfcaedaf9&pid=1-s2.0-S0143417924000593-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141978268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

The protective effects of orexin B in neuropathic pain by suppressing inflammatory response 奥曲肽 B 通过抑制炎症反应对神经病理性疼痛的保护作用

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-07-30 DOI: 10.1016/j.npep.2024.102458

Zuqing Zhu , Gang Chen , Jiangtao He , Yuanting Xu

{"title":"The protective effects of orexin B in neuropathic pain by suppressing inflammatory response","authors":"Zuqing Zhu , Gang Chen , Jiangtao He , Yuanting Xu","doi":"10.1016/j.npep.2024.102458","DOIUrl":"10.1016/j.npep.2024.102458","url":null,"abstract":"<div><p>Chronic pain induced by pathological insults to the sensorimotor system is a typical form of neuropathic pain (NP), and the underlying mechanism is complex. Currently, there are no successful therapeutic interventions for NP. Orexin B is a neuropeptide with a wide range of biological functions. However, the pharmacological function of orexin B in chronic neuropathic pain has been less studied. Here, we aim to examine the neuroprotective effects of orexin B in chronic constriction injury (CCI)- induced NP. Firstly, we found that orexin type 2 receptor (OX2R) but not orexin type 1 receptor (OX1R) was reduced in the spinal cord (SC) of CCI-treated rats. Mechanical withdrawal threshold and thermal withdrawal latency assays display that administration of orexin B clearly ameliorated CCI-evoked neuropathic pain dose-dependently. Notably, orexin B treatment also effectively prevented microglia activation by reducing the levels of IBA1. Additionally, orexin B was also found to suppress the inflammatory response in the SC tissue by reducing the levels of IL-6, TNF-α, iNOS, and COX-2 as well as the production of NO and PGE<sub>2</sub> in CCI-treated rats. Furthermore, orexin B administration attenuated oxidative stress (OS) by increasing the activity of SOD and the levels of GSH. Mechanically, orexin B prevented activation of JNK/NF-κB signaling in the SC of CCI-treated rats. Based on these findings, we conclude that orexin B might have a promising role in ameliorating CCI-evoked neuropathic pain through the inhibition of microglial activation and inflammatory response.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102458"},"PeriodicalIF":2.5,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142162195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Research progress on the protection and mechanism of active peptides in Alzheimer's disease and Parkinson's disease 关于阿尔茨海默病和帕金森病中活性肽的保护作用和机制的研究进展。

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-07-25 DOI: 10.1016/j.npep.2024.102457

Xuying Ding , Yutong Chen , Xiaojun Zhang , Yanming Duan , Guojing Yuan , Chang Liu

{"title":"Research progress on the protection and mechanism of active peptides in Alzheimer's disease and Parkinson's disease","authors":"Xuying Ding , Yutong Chen , Xiaojun Zhang , Yanming Duan , Guojing Yuan , Chang Liu","doi":"10.1016/j.npep.2024.102457","DOIUrl":"10.1016/j.npep.2024.102457","url":null,"abstract":"<div><p>Neurodegenerative diseases are the main causes of death and morbidity among elderly people worldwide. From the pathological point of view, oxidative stress, neuroinflammation, mitochondrial damage and apoptosis are the causes of neuronal diseases, and play a harmful role in the process of neuronal cell death and neurodegeneration. The most common neurodegenerative diseases are Alzheimer's disease(AD) and Parkinson's disease(PD), and there is no effective treatment. The physiological role of active peptides in the human body is significant. Modern medical research has found that animal and plant peptides, natural peptides in human body, can act on the central nervous system, and their active components can improve learning and memory ability, and play the roles of antioxidation, anti-inflammation, anti-apoptosis and maintaining the structure and function of mitochondria. This review reviews the reports on neurodegenerative diseases such as AD and PD by active peptides from animals and plants and natural peptides from the human body, and summarizes the neuroprotective mechanism of peptides. A theoretical basis for further research and development of active peptides was provided by examining the research and application of peptides, which provided a theoretical basis for further research and development.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102457"},"PeriodicalIF":2.5,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141788742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0