首页 > 最新文献

Archives of Physiology and Biochemistry最新文献

英文 中文
Hsa_circ_0004776 regulates the retina neovascularization in progression of diabetic retinopathy via hsa-miR-382-5p/BDNF axis. Hsa_circ_0004776通过hsa-miR-382-5p/BDNF轴调节糖尿病视网膜病变进展过程中视网膜新生血管的形成。
IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-12-01 Epub Date: 2024-07-08 DOI: 10.1080/13813455.2024.2375981
Lu Ye, Yixiu Chen, Wendong Gu, Jun Shao, Yu Xin

The aim of this work was to identify the regulatory function of hsa_circ_0004776 in the progression of diabetic retinopathy (DR). The direct interactions between hsa_circ_0004776 and hsa-miR-382-5p and between hsa-miR-382-5p and BDNF, were confirmed via dual-luciferase reporter assays. Quantitative Real-Time PCR analysis indicated that hsa_circ_0004776 was highly expressed in aqueous humour samples of DR patients and human retinal microvascular epithelial cells (hRECs) under a high-glucose environment, whereas hsa-miR-382-5p showed the opposite trend. Overexpressed hsa_circ_0004776 significantly enhanced DNA synthesis, proliferation, migration, and tube formation in hRECs in hyperglycaemia, while hsa-miR-382-5p mimics reversed these changes. Additionally, in a streptozotocin-induced Sprague-Dawley rat model of DR, vitreous microinjection of rno-miR-382-5p agomir reversed the pathologic features in the progression of DR, including retinal vascular leakage, capillary decellularization, loss of pericytes, fibrosis, and gliosis. Our results indicated that under hyperglycaemic conditions, hsa_circ_0004776 influences the progression of DR via hsa-miR-382-5p and thus represents a potential therapeutic target.

这项研究旨在确定 hsa_circ_0004776 在糖尿病视网膜病变(DR)进展过程中的调控功能。通过双荧光素酶报告实验证实了 hsa_circ_0004776 与 hsa-miR-382-5p 之间以及 hsa-miR-382-5p 与 BDNF 之间的直接相互作用。定量实时 PCR 分析表明,在高葡萄糖环境下,hsa_circ_0004776 在 DR 患者的水样和人视网膜微血管上皮细胞(hRECs)中高表达,而 hsa-miR-382-5p 则呈现相反的趋势。过表达的 hsa_circ_0004776 能显著增强高血糖环境下 hRECs 的 DNA 合成、增殖、迁移和管形成,而 hsa-miR-382-5p 模拟物则能逆转这些变化。此外,在链脲佐菌素诱导的 Sprague-Dawley 大鼠 DR 模型中,玻璃体显微注射 rno-miR-382-5p 激动剂可逆转 DR 进展过程中的病理特征,包括视网膜血管渗漏、毛细血管脱细胞、周细胞丧失、纤维化和胶质增生。我们的研究结果表明,在高血糖条件下,hsa_circ_0004776通过hsa-miR-382-5p影响DR的进展,因此是一个潜在的治疗靶点。
{"title":"Hsa_circ_0004776 regulates the retina neovascularization in progression of diabetic retinopathy <i>via</i> hsa-miR-382-5p/<i>BDNF</i> axis.","authors":"Lu Ye, Yixiu Chen, Wendong Gu, Jun Shao, Yu Xin","doi":"10.1080/13813455.2024.2375981","DOIUrl":"10.1080/13813455.2024.2375981","url":null,"abstract":"<p><p>The aim of this work was to identify the regulatory function of hsa_circ_0004776 in the progression of diabetic retinopathy (DR). The direct interactions between hsa_circ_0004776 and hsa-miR-382-5p and between hsa-miR-382-5p and <i>BDNF</i>, were confirmed <i>via</i> dual-luciferase reporter assays. Quantitative Real-Time PCR analysis indicated that hsa_circ_0004776 was highly expressed in aqueous humour samples of DR patients and human retinal microvascular epithelial cells (hRECs) under a high-glucose environment, whereas hsa-miR-382-5p showed the opposite trend. Overexpressed hsa_circ_0004776 significantly enhanced DNA synthesis, proliferation, migration, and tube formation in hRECs in hyperglycaemia, while hsa-miR-382-5p mimics reversed these changes. Additionally, in a streptozotocin-induced Sprague-Dawley rat model of DR, vitreous microinjection of rno-miR-382-5p agomir reversed the pathologic features in the progression of DR, including retinal vascular leakage, capillary decellularization, loss of pericytes, fibrosis, and gliosis. Our results indicated that under hyperglycaemic conditions, hsa_circ_0004776 influences the progression of DR <i>via</i> hsa-miR-382-5p and thus represents a potential therapeutic target.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"921-933"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Development of pancreatic islet cells in the extrahepatic bile ducts of rats with experimentally-induced metabolic syndrome. 实验性代谢综合征大鼠肝外胆管胰岛细胞的发育。
IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-12-01 Epub Date: 2023-08-31 DOI: 10.1080/13813455.2023.2252205
Maya Gulubova, Anna Tolekova, Dimitar Berbatov, Nurettin Aydogdu

Context: There is data about the existence of some endocrine cells in the epithelial layer of the bile duct in humans and rats.

Objective: We evaluated Ghrelin-, Insulin-, Glucagon- and Somatostatin-positive cells in peribiliary glands, mast cells, and nerve fibres.

Materials and methods: Wistar rats were used for dietary manipulation with a 15% fructose solution for 12 weeks. Tissue samples were elaborated with immunohistochemistry for Insulin, Glucagon, Ghrelin, and Somatostatin. Glucose and lipid parameters were studied.

Results: In treated animals, Ghrelin+ and Insulin+ cells in perybiliary glands (PBGs) were significantly increased. In the male fructose group there was a significant increase of the homeostasis model assessment insulin resistance (HOMA-IR).

Conclusions: Stem/progenitor cells in extrahepatic bile tree (EHBT) could be a source of Insulin-producing cells in metabolic syndrome. Fructose treatment induces the increase of Ghrelin+ and Insulin+ cells in PBGs and the elevation of Insulin and Ghrelin plasma concentration.

背景:有资料表明,人类和大鼠胆管上皮中存在一些内分泌细胞。目的:我们评估了生长素、胰岛素、胰高血糖素和生长抑素阳性细胞在胆道周围腺、肥大细胞和神经纤维中的作用。材料与方法:Wistar大鼠采用15%果糖溶液进行饮食操纵,为期12周。用免疫组化方法对组织样本进行胰岛素、胰高血糖素、生长素和生长抑素的检测。研究了葡萄糖和脂质参数。结果:治疗组小鼠胆道周围腺(PBGs)中Ghrelin+和胰岛素+细胞显著升高。在雄性果糖组中,评估胰岛素抵抗的稳态模型(HOMA-IR)显著增加。结论:肝外胆管树(EHBT)干细胞/祖细胞可能是代谢综合征中胰岛素生成细胞的来源。果糖处理诱导pbg中Ghrelin+和胰岛素+细胞增加,胰岛素和Ghrelin血浆浓度升高。
{"title":"Development of pancreatic islet cells in the extrahepatic bile ducts of rats with experimentally-induced metabolic syndrome.","authors":"Maya Gulubova, Anna Tolekova, Dimitar Berbatov, Nurettin Aydogdu","doi":"10.1080/13813455.2023.2252205","DOIUrl":"10.1080/13813455.2023.2252205","url":null,"abstract":"<p><strong>Context: </strong>There is data about the existence of some endocrine cells in the epithelial layer of the bile duct in humans and rats.</p><p><strong>Objective: </strong>We evaluated Ghrelin-, Insulin-, Glucagon- and Somatostatin-positive cells in peribiliary glands, mast cells, and nerve fibres.</p><p><strong>Materials and methods: </strong>Wistar rats were used for dietary manipulation with a 15% fructose solution for 12 weeks. Tissue samples were elaborated with immunohistochemistry for Insulin, Glucagon, Ghrelin, and Somatostatin. Glucose and lipid parameters were studied.</p><p><strong>Results: </strong>In treated animals, Ghrelin<sup>+</sup> and Insulin<sup>+</sup> cells in perybiliary glands (PBGs) were significantly increased. In the male fructose group there was a significant increase of the homeostasis model assessment insulin resistance (HOMA-IR).</p><p><strong>Conclusions: </strong>Stem/progenitor cells in extrahepatic bile tree (EHBT) could be a source of Insulin-producing cells in metabolic syndrome. Fructose treatment induces the increase of Ghrelin<sup>+</sup> and Insulin<sup>+</sup> cells in PBGs and the elevation of Insulin and Ghrelin plasma concentration.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"669-677"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10128034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Ellagic acid reduces hepatic lipid contents through regulation of SIRT1 and AMPK in old rats. Ellagic酸通过调节SIRT1和AMPK降低老年大鼠肝脏脂质含量。
IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-12-01 Epub Date: 2023-10-10 DOI: 10.1080/13813455.2023.2262165
Mahdis Rahimi Naiini, Beydolah Shahouzehi, Mohammad Khaksari, Shahrzad Azizi, Niloufar Naghibi, Mahdieh Nazari-Robati

Objective: Ellagic acid is used in traditional medicine for the treatment of lipid disorders. In this study, the effects of ellagic acid on key regulators of lipid metabolism, and histopathological alterations in aged liver were examined.

Methods: A total of 21 male Wistar rats were divided into three groups, including young control, old control, and old ellagic acid. After one month of treatment with ellagic acid, the expression levels of hepatic SIRT1, AMPK, SREBP-1c, PPAR-α, and phosphorylated AMPK (p-AMPK) were evaluated. The levels of several serum biochemical factors, and hepatic triglyceride, and cholesterol contents were assessed.

Results: Ellagic acid elevated the levels of SIRT1, p-AMPK, and PPAR-α and reduced SREBP-1c level in the liver of old rats. It decreased triglyceride and cholesterol contents in the aged liver and improved histopathological changes.

Conclusions: The results demonstrated that ellagic acid can exert protective effects against hepatic lipid metabolism disorders induced by ageing.

前言:目的:艾拉吉酸在传统医学中用于治疗脂质紊乱。在本研究中,研究了鞣花酸对衰老肝脏脂质代谢关键调节因子的影响以及组织病理学变化。方法:将21只雄性Wistar大鼠分为三组,分别为青年对照组、老年对照组和老年鞣花酸组。鞣花酸治疗一个月后,评估肝脏SIRT1、AMPK、SREBP-1c、PPAR-α和磷酸化AMPK(p-AMPK)的表达水平。评估了几种血清生化因子、肝甘油三酯和胆固醇含量的水平。结果:Ellagic acid使老年大鼠肝脏SIRT1、p-AMPK和PPAR-α水平升高,SREBP-1c水平降低。它降低了老年肝脏中甘油三酯和胆固醇的含量,改善了组织病理学变化。结论:鞣花酸对衰老引起的肝脏脂质代谢紊乱具有保护作用。
{"title":"Ellagic acid reduces hepatic lipid contents through regulation of SIRT1 and AMPK in old rats.","authors":"Mahdis Rahimi Naiini, Beydolah Shahouzehi, Mohammad Khaksari, Shahrzad Azizi, Niloufar Naghibi, Mahdieh Nazari-Robati","doi":"10.1080/13813455.2023.2262165","DOIUrl":"10.1080/13813455.2023.2262165","url":null,"abstract":"<p><strong>Objective: </strong>Ellagic acid is used in traditional medicine for the treatment of lipid disorders. In this study, the effects of ellagic acid on key regulators of lipid metabolism, and histopathological alterations in aged liver were examined.</p><p><strong>Methods: </strong>A total of 21 male Wistar rats were divided into three groups, including young control, old control, and old ellagic acid. After one month of treatment with ellagic acid, the expression levels of hepatic SIRT1, AMPK, SREBP-1c, PPAR-α, and phosphorylated AMPK (p-AMPK) were evaluated. The levels of several serum biochemical factors, and hepatic triglyceride, and cholesterol contents were assessed.</p><p><strong>Results: </strong>Ellagic acid elevated the levels of SIRT1, p-AMPK, and PPAR-α and reduced SREBP-1c level in the liver of old rats. It decreased triglyceride and cholesterol contents in the aged liver and improved histopathological changes.</p><p><strong>Conclusions: </strong>The results demonstrated that ellagic acid can exert protective effects against hepatic lipid metabolism disorders induced by ageing.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"686-693"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41181909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Reverse pharmacology approach to validate the diabetic wound-healing activity of Jatyadi thailam formulations in vitro on diabetic mimic environment. 反向药理学方法验证Jatyadi thailam制剂在糖尿病模拟环境中的糖尿病伤口愈合活性。
IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-12-01 Epub Date: 2023-10-28 DOI: 10.1080/13813455.2023.2264536
Kandasamy Swathi, Sundaravadivelu Sumathi, Kumar Somit, Sripathi K Shubashini

Objective: Jatyadi thailam, an Ayurvedic preparation, is renowned for its efficacy in diabetic wound healing and inflammation. This study aimed to validate and compare the diabetic wound-healing potential of two Jatyadi thailam formulations - Ayurvedic formulary of India Jatyadi thailam (JT-AFI) and Yogagrantha formulation of Jatyadi thailam (JT-YG), in a diabetic environment using L929 fibroblast cells in vitro.

Methodology: The effects on cell survival, proliferation, migration, angiogenesis, cell cycle progression, apoptosis, ROS generation, and mitochondrial function were evaluated.

Results: The formulations promoted cell proliferation, migration, angiogenesis, while also regulating cell cycle and apoptosis. They effectively suppressed ROS generation and modulated mitochondrial function. JT-AFI exhibited superior efficacy in accelerating diabetic wound healing compared to JT-YG.

Conclusion: These findings provide substantial support for the mechanistic role of Jatyadi thailam in diabetic wound healing.

目的:阿育吠陀制剂Jatyadi thailam以其对糖尿病伤口愈合和炎症的疗效而闻名。本研究旨在使用L929成纤维细胞体外验证和比较两种Jatyadi thailam配方——印度阿育吠陀配方Jatyadi-thailam(JT-AFI)和Jatyadi-thailam的Yogagrantha配方(JT-YG)——在糖尿病环境中的糖尿病伤口愈合潜力。方法:评估对细胞存活、增殖、迁移、血管生成、细胞周期进展、细胞凋亡、ROS生成和线粒体功能的影响。结果:该制剂促进细胞增殖、迁移、血管生成,同时调节细胞周期和凋亡。它们有效抑制ROS的产生并调节线粒体功能。与JT-YG相比,JT-AFI在加速糖尿病伤口愈合方面表现出优异的疗效。结论:这些发现为Jatyadi thailam在糖尿病伤口愈合中的机制作用提供了实质性支持。
{"title":"Reverse pharmacology approach to validate the diabetic wound-healing activity of Jatyadi thailam formulations <i>in vitro</i> on diabetic mimic environment.","authors":"Kandasamy Swathi, Sundaravadivelu Sumathi, Kumar Somit, Sripathi K Shubashini","doi":"10.1080/13813455.2023.2264536","DOIUrl":"10.1080/13813455.2023.2264536","url":null,"abstract":"<p><strong>Objective: </strong>Jatyadi thailam, an Ayurvedic preparation, is renowned for its efficacy in diabetic wound healing and inflammation. This study aimed to validate and compare the diabetic wound-healing potential of two Jatyadi thailam formulations - Ayurvedic formulary of India Jatyadi thailam (JT-AFI) and Yogagrantha formulation of Jatyadi thailam (JT-YG), in a diabetic environment using L929 fibroblast cells <i>in vitro</i>.</p><p><strong>Methodology: </strong>The effects on cell survival, proliferation, migration, angiogenesis, cell cycle progression, apoptosis, ROS generation, and mitochondrial function were evaluated.</p><p><strong>Results: </strong>The formulations promoted cell proliferation, migration, angiogenesis, while also regulating cell cycle and apoptosis. They effectively suppressed ROS generation and modulated mitochondrial function. JT-AFI exhibited superior efficacy in accelerating diabetic wound healing compared to JT-YG.</p><p><strong>Conclusion: </strong>These findings provide substantial support for the mechanistic role of Jatyadi thailam in diabetic wound healing.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"710-723"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61560178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
In vitro inhibitor effect and molecular docking of thiamine (vitamin B1), riboflavin (vitamin B2), and reference inhibitor captopril on angiotensin-converting enzyme purified from sheep plasma. 硫胺素(维生素 B1)、核黄素(维生素 B2)和参考抑制剂卡托普利对从羊血浆中纯化的血管紧张素转换酶的体外抑制作用和分子对接。
IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-12-01 Epub Date: 2024-07-10 DOI: 10.1080/13813455.2024.2376814
Muhammed Haluk Ciftci, Vedat Turkoglu, Zehra Bas, Fatih Caglar Celikezen

Objective: Angiotensin-converting enzyme (ACE, EC 3.4.15.1) is a very important factor in the regulation of blood pressure. Also, the inhibition of ACE with natural compounds has been a very important research area in the treatment of high blood pressure. ACE was purified and characterized from sheep plasma. Molecular docking studies and the inhibition effect of thiamine, riboflavin, and captopril on ACE were investigated.

Methods: Herein, ACE was purified from sheep plasma by affinity chromatography. The effect of thiamine and riboflavin on ACE was researched. Molecular docking studies were performed to understand the molecular interactions between thiamine, riboflavin, and captopril with ACE.

Results: The purification coefficient was found to be 8636 fold. The binding energy of thiamine, riboflavin, and captopril was found to be -6.7 kcal/mol, -8.1 kcal/mol, and -5.5 kcal/mol, respectively. Thiamine conformed to three conventional hydrogen bonds with ASP:415, HIS:513, and LYS:454. Riboflavin formed four conventional hydrogen bonds with GLN:281, GLU:376, THR:282, and TYR:520. Captopril formed two conventional hydrogen bonds with ARG:124, one conventional hydrogen bond with TYR:62 and ASN:85, and one carbon-hydrogen bond with ASN:66. Molecular docking results showed that thiamine, riboflavin, and captopril interacted with ACE through hydrogen bonding and hydrophobic interactions. Thiamine and riboflavin indicated significant inhibition effects on ACE. The IC50 values of thiamine, riboflavin, and captopril were found as 960.56 µM, 11.02 µM, and 1.60 nM, respectively. Ki values for thiamine, riboflavin, and captopril were determined as 1352.04 µM, 12.30 µM, and 1.06 nM, respectively.

Conclusion: In this work, it was concluded that thiamine and riboflavin may have preventive and therapeutical impacts against high blood pressure with their ACE inhibitor effect. Thiamine and riboflavin showed a lower inhibitory effect with a higher IC50 than captopril. However, when the inhibitory effect of thiamine and riboflavin vitamins is compared to captopril, it is concluded that they may be natural inhibitors with fewer side effects.

目的:血管紧张素转换酶(ACE,EC 3.4.15.1)是调节血压的一个非常重要的因素。此外,用天然化合物抑制 ACE 也是治疗高血压的一个非常重要的研究领域。我们从绵羊血浆中纯化并鉴定了 ACE。方法:采用亲和层析法从绵羊血浆中纯化出 ACE。研究了硫胺素和核黄素对 ACE 的影响。进行了分子对接研究,以了解硫胺素、核黄素和卡托普利与 ACE 的分子相互作用:结果:硫胺素、核黄素和卡托普利与 ACE 的纯化系数为 8636 倍。硫胺素、核黄素和卡托普利的结合能分别为-6.7 kcal/mol、-8.1 kcal/mol和-5.5 kcal/mol。硫胺素与 ASP:415、HIS:513 和 LYS:454 形成三个常规氢键。核黄素与 GLN:281、GLU:376、THR:282 和 TYR:520 形成四个常规氢键。卡托普利与 ARG:124 形成了两个常规氢键,与 TYR:62 和 ASN:85 形成了一个常规氢键,与 ASN:66 形成了一个碳氢键。分子对接结果显示,硫胺素、核黄素和卡托普利通过氢键和疏水作用与 ACE 相互作用。硫胺素和核黄素对 ACE 有明显的抑制作用。硫胺素、核黄素和卡托普利的 IC50 值分别为 960.56 µM、11.02 µM 和 1.60 nM。硫胺素、核黄素和卡托普利的 Ki 值分别为 1352.04 µM、12.30 µM 和 1.06 nM:这项研究认为,硫胺素和核黄素具有抑制 ACE 的作用,对高血压有预防和治疗作用。与卡托普利相比,硫胺素和核黄素的抑制作用较低,其 IC50 值较高。不过,如果将硫胺素和核黄素维生素的抑制作用与卡托普利进行比较,可以得出结论,它们可能是副作用较小的天然抑制剂。
{"title":"In vitro inhibitor effect and molecular docking of thiamine (vitamin B<sub>1</sub>), riboflavin (vitamin B<sub>2</sub>), and reference inhibitor captopril on angiotensin-converting enzyme purified from sheep plasma.","authors":"Muhammed Haluk Ciftci, Vedat Turkoglu, Zehra Bas, Fatih Caglar Celikezen","doi":"10.1080/13813455.2024.2376814","DOIUrl":"10.1080/13813455.2024.2376814","url":null,"abstract":"<p><strong>Objective: </strong>Angiotensin-converting enzyme (ACE, EC 3.4.15.1) is a very important factor in the regulation of blood pressure. Also, the inhibition of ACE with natural compounds has been a very important research area in the treatment of high blood pressure. ACE was purified and characterized from sheep plasma. Molecular docking studies and the inhibition effect of thiamine, riboflavin, and captopril on ACE were investigated.</p><p><strong>Methods: </strong>Herein, ACE was purified from sheep plasma by affinity chromatography. The effect of thiamine and riboflavin on ACE was researched. Molecular docking studies were performed to understand the molecular interactions between thiamine, riboflavin, and captopril with ACE.</p><p><strong>Results: </strong>The purification coefficient was found to be 8636 fold. The binding energy of thiamine, riboflavin, and captopril was found to be -6.7 kcal/mol, -8.1 kcal/mol, and -5.5 kcal/mol, respectively. Thiamine conformed to three conventional hydrogen bonds with ASP:415, HIS:513, and LYS:454. Riboflavin formed four conventional hydrogen bonds with GLN:281, GLU:376, THR:282, and TYR:520. Captopril formed two conventional hydrogen bonds with ARG:124, one conventional hydrogen bond with TYR:62 and ASN:85, and one carbon-hydrogen bond with ASN:66. Molecular docking results showed that thiamine, riboflavin, and captopril interacted with ACE through hydrogen bonding and hydrophobic interactions. Thiamine and riboflavin indicated significant inhibition effects on ACE. The IC<sub>50</sub> values of thiamine, riboflavin, and captopril were found as 960.56 µM, 11.02 µM, and 1.60 nM, respectively. K<sub>i</sub> values for thiamine, riboflavin, and captopril were determined as 1352.04 µM, 12.30 µM, and 1.06 nM, respectively.</p><p><strong>Conclusion: </strong>In this work, it was concluded that thiamine and riboflavin may have preventive and therapeutical impacts against high blood pressure with their ACE inhibitor effect. Thiamine and riboflavin showed a lower inhibitory effect with a higher IC<sub>50</sub> than captopril. However, when the inhibitory effect of thiamine and riboflavin vitamins is compared to captopril, it is concluded that they may be natural inhibitors with fewer side effects.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"974-983"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141578840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Behaviour of Tunisian Psammomys obesus fed high-calorie diets: biochemical disturbance and histopathological alterations. 喂食高热量食物的突尼斯狒狒的行为:生化紊乱和组织病理学改变。
IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-12-01 Epub Date: 2024-07-10 DOI: 10.1080/13813455.2024.2375983
Souhaieb Chrigui, Sihem Mbarek, Sameh Hadj Taieb, Zohra Haouas, Monssef Feki, Maha Benlarbi, Ayachi Zemmel, Fatiha Chigr, Nourhène Boudhrioua, Rafika Ben Chaouacha-Chekir

This work investigated the biochemical disturbances and histological alteration in Psammomys obesus animal model fed different high calorie diets (HCDs) during three months. Four diets were used: a low-calorie natural diet, Chenopodiaceae halophyte plant used as control (LCD), a high standard carbohydrate diet rich in protein, HCD 0, a high carbohydrate diet rich in two concentrations of fat, HCD 1 and HCD 2. All animals having received HCDs developed dyslipidemia after one month of experiment with distinction of different sub-groups developing or not obesity and diabetes. HCDs induced a remarkable increasing in blood cholesterol, LDL-cholesterol and triglyceride levels indicating a fast induction of dyslipidemia and a significant increase of aminotransaminases activities revealing a pronounced hepatotoxicity. Animal developing diabetes showed a severe hepatic injury, a degeneration of the adipose tissue and a significant reduction of retinal thickness. P. obesus seems to be an excellent animal model to investigate nutritional metabolic diseases.

这项研究调查了在三个月内喂食不同高热量饮食(HCD)的肥胖松鼠动物模型的生化紊乱和组织学改变。研究使用了四种饮食:低热量天然饮食(Chenopodiaceae Halophyte 植物作为对照)(LCD)、富含蛋白质的高标准碳水化合物饮食(HCD 0)、富含两种浓度脂肪的高碳水化合物饮食(HCD 1 和 HCD 2)。实验一个月后,所有接受高碳水化合物饮食的动物都出现了血脂异常,不同亚组的动物会出现或不出现肥胖和糖尿病。HCDs 导致血液中胆固醇、低密度脂蛋白胆固醇和甘油三酯水平显著升高,这表明它能快速诱导血脂异常,同时转氨酶活性显著升高,显示出明显的肝毒性。患糖尿病的动物表现出严重的肝损伤、脂肪组织变性和视网膜厚度明显降低。肥胖猪似乎是研究营养代谢疾病的极佳动物模型。
{"title":"Behaviour of Tunisian <i>Psammomys obesus</i> fed high-calorie diets: biochemical disturbance and histopathological alterations.","authors":"Souhaieb Chrigui, Sihem Mbarek, Sameh Hadj Taieb, Zohra Haouas, Monssef Feki, Maha Benlarbi, Ayachi Zemmel, Fatiha Chigr, Nourhène Boudhrioua, Rafika Ben Chaouacha-Chekir","doi":"10.1080/13813455.2024.2375983","DOIUrl":"10.1080/13813455.2024.2375983","url":null,"abstract":"<p><p>This work investigated the biochemical disturbances and histological alteration in <i>Psammomys obesus</i> animal model fed different high calorie diets (HCDs) during three months. Four diets were used: a low-calorie natural diet, <i>Chenopodiaceae</i> halophyte plant used as control (LCD), a high standard carbohydrate diet rich in protein, HCD 0, a high carbohydrate diet rich in two concentrations of fat, HCD 1 and HCD 2. All animals having received HCDs developed dyslipidemia after one month of experiment with distinction of different sub-groups developing or not obesity and diabetes. HCDs induced a remarkable increasing in blood cholesterol, LDL-cholesterol and triglyceride levels indicating a fast induction of dyslipidemia and a significant increase of aminotransaminases activities revealing a pronounced hepatotoxicity. Animal developing diabetes showed a severe hepatic injury, a degeneration of the adipose tissue and a significant reduction of retinal thickness. <i>P. obesus</i> seems to be an excellent animal model to investigate nutritional metabolic diseases.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"934-950"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141562473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Hydrogen sulfide protects the endometrium in a rat model of type 1 diabetes via modulation of PPARγ/mTOR and Nrf-2/NF-κb pathways. 硫化氢通过调节 PPARγ/mTOR 和 Nrf-2/NF-κb 通路保护 1 型糖尿病大鼠模型的子宫内膜。
IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-12-01 Epub Date: 2024-04-29 DOI: 10.1080/13813455.2024.2347239
Heba A Abdel-Hamid, Heba Marey, Manar Fouli Gaber Ibrahim

Diabetes is one of the leading causes of endometrial diseases in women. No study has addressed the influence of hydrogen sulphide (H2S) donors on endometrial injury on top of type 1 diabetes. This research was conducted to study either the effect of sodium hydrosulphide (NaHS), the H2S donor, or DL-propargylglycine (PAG), the inhibitor of endogenous H2S production, on the endometrium of diabetic rats. A total of 40 female Wistar rats were separated into control group, diabetic group, diabetic group treated with NaHS and diabetic group treated with PAG. Serum levels of insulin, glucose, total cholesterol (TC) and triglycerides (TG) were assessed. Uterine tissue markers of oxidative stress, inflammation, apoptosis and cell proliferation were analysed. Diabetes-induced endometrial overgrowth associated with oxidative stress, inflammation and inhibition of apoptosis. NaHS administration reversed the previous conditions while PAG administration got them worse. We concluded that H2S prevented endometrial overgrowth in a rat model of type 1 diabetes through modulation of PPARγ/mTOR and Nrf-2/NF-κB pathways.

糖尿病是导致女性子宫内膜疾病的主要原因之一。目前还没有研究探讨硫化氢(H2S)供体对 1 型糖尿病子宫内膜损伤的影响。本研究旨在研究 H2S 供体硫化氢钠(NaHS)或内源性 H2S 生成抑制剂 DL-丙炔基甘氨酸(PAG)对糖尿病大鼠子宫内膜的影响。将 40 只雌性 Wistar 大鼠分为对照组、糖尿病组、NaHS 治疗糖尿病组和 PAG 治疗糖尿病组。对血清中的胰岛素、葡萄糖、总胆固醇(TC)和甘油三酯(TG)水平进行了评估。分析了子宫组织氧化应激、炎症、细胞凋亡和细胞增殖的标志物。糖尿病诱发的子宫内膜增生与氧化应激、炎症和细胞凋亡抑制有关。服用 NaHS 可逆转之前的情况,而服用 PAG 则会使情况恶化。我们的结论是,H2S 通过调节 PPARγ/mTOR 和 Nrf-2/NF-κB 通路,防止了 1 型糖尿病大鼠模型中的子宫内膜过度增生。
{"title":"Hydrogen sulfide protects the endometrium in a rat model of type 1 diabetes via modulation of PPARγ/mTOR and Nrf-2/NF-κb pathways.","authors":"Heba A Abdel-Hamid, Heba Marey, Manar Fouli Gaber Ibrahim","doi":"10.1080/13813455.2024.2347239","DOIUrl":"10.1080/13813455.2024.2347239","url":null,"abstract":"<p><p>Diabetes is one of the leading causes of endometrial diseases in women. No study has addressed the influence of hydrogen sulphide (H<sub>2</sub>S) donors on endometrial injury on top of type 1 diabetes. This research was conducted to study either the effect of sodium hydrosulphide (NaHS), the H<sub>2</sub>S donor, or DL-propargylglycine (PAG), the inhibitor of endogenous H<sub>2</sub>S production, on the endometrium of diabetic rats. A total of 40 female Wistar rats were separated into control group, diabetic group, diabetic group treated with NaHS and diabetic group treated with PAG. Serum levels of insulin, glucose, total cholesterol (TC) and triglycerides (TG) were assessed. Uterine tissue markers of oxidative stress, inflammation, apoptosis and cell proliferation were analysed. Diabetes-induced endometrial overgrowth associated with oxidative stress, inflammation and inhibition of apoptosis. NaHS administration reversed the previous conditions while PAG administration got them worse. We concluded that H<sub>2</sub>S prevented endometrial overgrowth in a rat model of type 1 diabetes through modulation of PPARγ/mTOR and Nrf-2/NF-κB pathways.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"909-920"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140847372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Omentin-1 and diabetes: more evidence but far from enough. Omentin-1和糖尿病:更多证据,但还远远不够。
IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-12-01 Epub Date: 2023-07-03 DOI: 10.1080/13813455.2023.2230380
Jing Xu, Min Li, Xinli Jiang, Yuling Wang, Huijie Ma, Yaru Zhou, Meimei Tian, Yan Liu

Aims and background: Omentin-1 (oment-1) is a type of adipokines that is mainly expressed in visceral fat tissue. Based on accumulating evidence, oment-1 is closely related to diabetes and its complications. However, so far data about oment-1 and diabetes is fragmented. In this review, we focus on the role of oment-1 on diabetes, including its possible signalling pathways, the correlation of circulating omens-1 levels with diabetes and its complications.

Methods: The web of PubMed was searched for articles of relevant studies published until February, 2023.

Results and conclusions: Oment-1 might exert its effects by inhibiting the NF-κB pathway and activating the Akt and AMPK-dependent pathways. The level of circulating oment-1 is negatively correlated with the occurrence of type 2 diabetes and some complications, including diabetic vascular disease, cardiomyopathy, and retinopathy, which can be affected by anti-diabetic therapies. Oment-1 could be a promising marker for screening and targeted therapy for diabetes and its complications; however, more studies are still needed.

目的与背景:Omentin-1 (Omentin-1)是一种主要表达于内脏脂肪组织的脂肪因子。越来越多的证据表明,comment -1与糖尿病及其并发症密切相关。然而,到目前为止,关于评论-1和糖尿病的数据是碎片化的。在这篇综述中,我们将重点介绍omen -1在糖尿病中的作用,包括其可能的信号通路,循环中omen -1水平与糖尿病及其并发症的相关性。方法:检索PubMed网站至2023年2月发表的相关研究文章。结果和结论:omt -1可能通过抑制NF-κB通路,激活Akt和ampk依赖性通路发挥作用。2型糖尿病及糖尿病血管病、心肌病、视网膜病变等并发症的发生与循环中网膜-1的水平呈负相关,这些并发症可受抗糖尿病治疗的影响。comment -1可能成为糖尿病及其并发症筛查和靶向治疗的有前景的标志物;然而,还需要更多的研究。
{"title":"Omentin-1 and diabetes: more evidence but far from enough.","authors":"Jing Xu, Min Li, Xinli Jiang, Yuling Wang, Huijie Ma, Yaru Zhou, Meimei Tian, Yan Liu","doi":"10.1080/13813455.2023.2230380","DOIUrl":"10.1080/13813455.2023.2230380","url":null,"abstract":"<p><strong>Aims and background: </strong>Omentin-1 (oment-1) is a type of adipokines that is mainly expressed in visceral fat tissue. Based on accumulating evidence, oment-1 is closely related to diabetes and its complications. However, so far data about oment-1 and diabetes is fragmented. In this review, we focus on the role of oment-1 on diabetes, including its possible signalling pathways, the correlation of circulating omens-1 levels with diabetes and its complications.</p><p><strong>Methods: </strong>The web of PubMed was searched for articles of relevant studies published until February, 2023.</p><p><strong>Results and conclusions: </strong>Oment-1 might exert its effects by inhibiting the NF-κB pathway and activating the Akt and AMPK-dependent pathways. The level of circulating oment-1 is negatively correlated with the occurrence of type 2 diabetes and some complications, including diabetic vascular disease, cardiomyopathy, and retinopathy, which can be affected by anti-diabetic therapies. Oment-1 could be a promising marker for screening and targeted therapy for diabetes and its complications; however, more studies are still needed.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"599-605"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9740475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Intermittent fasting in health and disease. 健康和疾病方面的间歇性禁食。
IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-12-01 Epub Date: 2023-10-13 DOI: 10.1080/13813455.2023.2268301
Anubhav Mishra, Devika Sobha, Dimple Patel, Padmanaban S Suresh

Context: Intermittent fasting, a new-age dietary concept derived from an age-old tradition, involves repetitive cycles of fasting/calorie restriction and eating.

Objective: We aim to take a deep dive into the biological responses to intermittent fasting, delineate the disease-modifying and cognitive effects of intermittent fasting, and also shed light on the possible side effects.

Methods: Numerous in vitro and in vivo studies were reviewed, followed by an in-depth analysis, and compilation of their implications in health and disease.

Results: Intermittent fasting improves the body's stress tolerance, which is further amplified with exercise. It impacts various pathological conditions like cancer, obesity, diabetes, cardiovascular disease, and neurodegenerative diseases.

Conclusion: During dietary restriction, the human body experiences a metabolic switch due to the depletion of liver glycogen, which promotes a shift towards utilising fatty acids and ketones in the system, thereby significantly impacting adiposity, ageing and the immune response to various diseases.

背景:间歇性禁食是一种源自古老传统的新时代饮食概念,涉及禁食/热量限制和饮食的重复循环。目的:我们旨在深入研究间歇性禁食的生物学反应,描述间歇性禁食对疾病的改善和认知影响,并阐明可能的副作用。方法:回顾了大量的体外和体内研究,然后对其在健康和疾病中的意义进行了深入分析和汇编。结果:间歇性禁食可以提高身体的应激耐受能力,而运动会进一步增强这种能力。它影响各种病理状况,如癌症、肥胖、糖尿病、心血管疾病和神经退行性疾病。结论:在饮食限制期间,由于肝糖原的消耗,人体经历了代谢转换,这促进了系统中脂肪酸和酮的利用,从而显著影响肥胖、衰老和对各种疾病的免疫反应。
{"title":"Intermittent fasting in health and disease.","authors":"Anubhav Mishra, Devika Sobha, Dimple Patel, Padmanaban S Suresh","doi":"10.1080/13813455.2023.2268301","DOIUrl":"10.1080/13813455.2023.2268301","url":null,"abstract":"<p><strong>Context: </strong>Intermittent fasting, a new-age dietary concept derived from an age-old tradition, involves repetitive cycles of fasting/calorie restriction and eating.</p><p><strong>Objective: </strong>We aim to take a deep dive into the biological responses to intermittent fasting, delineate the disease-modifying and cognitive effects of intermittent fasting, and also shed light on the possible side effects.</p><p><strong>Methods: </strong>Numerous <i>in vitro</i> and <i>in vivo</i> studies were reviewed, followed by an in-depth analysis, and compilation of their implications in health and disease.</p><p><strong>Results: </strong>Intermittent fasting improves the body's stress tolerance, which is further amplified with exercise. It impacts various pathological conditions like cancer, obesity, diabetes, cardiovascular disease, and neurodegenerative diseases.</p><p><strong>Conclusion: </strong>During dietary restriction, the human body experiences a metabolic switch due to the depletion of liver glycogen, which promotes a shift towards utilising fatty acids and ketones in the system, thereby significantly impacting adiposity, ageing and the immune response to various diseases.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"755-767"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41189552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Correction. 更正。
IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-11-23 DOI: 10.1080/13813455.2024.2432763
{"title":"Correction.","authors":"","doi":"10.1080/13813455.2024.2432763","DOIUrl":"https://doi.org/10.1080/13813455.2024.2432763","url":null,"abstract":"","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1"},"PeriodicalIF":2.5,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
期刊
Archives of Physiology and Biochemistry
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1