Naunyn-Schmiedeberg's archives of pharmacology最新文献_第3页

Diacerein ameliorates amiodarone-induced pulmonary fibrosis via targeting the TGFβ1/α-SMA/Smad3 pathway. 双醋瑞因通过靶向 TGFβ1/α-SMA/Smad3 通路改善胺碘酮诱导的肺纤维化。

IF 3.1 4区医学

Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-04-01 Epub Date: 2024-10-17 DOI: 10.1007/s00210-024-03450-8

Hadir Farouk, Passant E Moustafa, Marwa S Khattab, Salma A El-Marasy

{"title":"Diacerein ameliorates amiodarone-induced pulmonary fibrosis via targeting the TGFβ1/α-SMA/Smad3 pathway.","authors":"Hadir Farouk, Passant E Moustafa, Marwa S Khattab, Salma A El-Marasy","doi":"10.1007/s00210-024-03450-8","DOIUrl":"10.1007/s00210-024-03450-8","url":null,"abstract":"This study is aimed at investigating the possible protective effect of diacerein (DIA) against AMD-induced pulmonary fibrosis in rats. Rats were classified into 4 groups: a normal group that received distilled water, control group that received AMD (100 mg/kg, p.o.) for 21 days to induce pulmonary fibrosis, and 2 treatment groups that received diacerein, in 2 dose levels (50 and 100 mg/kg, p.o., respectively) in addition to AMD (100 mg/kg, p.o.), for 21 days. Lung function test was assessed using a spirometer; serum and tissue were collected. Biochemical, real-time PCR, histopathological, and immunohistopathological analyses were carried out. AMD reduced tidal volume (TV), peripheral expiratory rate (PER), forced vital capacity (FVC), serum reduced glutathione (GSH) levels, Beclin, and LCII, while it elevated transform growth factor (TGF-β1) gene expression, serum malondialdehyde (MDA) level, alpha-smooth muscle actin (α-SMA), Smad3, phosphorylated signal transducer and activator of transcription (p-STAT3), and p62 lung content. Also, AMD elevated tumor necrosis factor-alpha (TNF-α) and caspase-3 protein expression. DIA elevated TV, PER, FVC, serum GSH level, Beclin, and LCII, while it reduced TGF-β1 gene expression, serum MDA level, α-SMA, Smad3, p-STAT-3, and p62 lung content. Moreover, DIA reduced TNF-α and caspase-3 protein expression. DIA attenuated AMD-induced pulmonary fibrosis via alleviating the TGF1/α-SMA/Smad3 pathway, reducing STAT-3 activation, and combating oxidative stress and inflammation in addition to promoting autophagy and abrogating apoptosis.","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"4111-4122"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470321","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

Pirfenidone mitigates demyelination and electrophysiological alterations in multiple sclerosis: Targeting NF-κB, sirt1, and neurotrophic genes. 吡非尼酮可减轻多发性硬化症的脱髓鞘和电生理改变：靶向 NF-κB、sirt1 和神经营养基因

IF 3.1 4区医学

Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-04-01 Epub Date: 2024-10-15 DOI: 10.1007/s00210-024-03496-8

Reda A A Abo-Elsoud, Eman A Ali, Marwa A Al-Gholam, Mohamed S Rizk, Rasha S A Elseadawy, Omnia Ameen

{"title":"Pirfenidone mitigates demyelination and electrophysiological alterations in multiple sclerosis: Targeting NF-κB, sirt1, and neurotrophic genes.","authors":"Reda A A Abo-Elsoud, Eman A Ali, Marwa A Al-Gholam, Mohamed S Rizk, Rasha S A Elseadawy, Omnia Ameen","doi":"10.1007/s00210-024-03496-8","DOIUrl":"10.1007/s00210-024-03496-8","url":null,"abstract":"Multiple sclerosis (MS) is a demyelinating disease affecting the central nervous system associated with progressive neurodegeneration. Pirfenidone (Pir) is a well-known antifibrotic agent; however, Pir's function in MS is little explored. We evaluated the neuroprotective effects of Pir in MS and its possible underlying mechanisms. Forty male Swiss mice were divided equally into control, cuprizone (CPZ), Pir, and CPZ + Pir groups. Assessment of motor function was conducted using neurobehavioral tests, EMG, and nerve conduction velocity (NCV). Mice's brains were extracted to measure oxidative stress, neuroinflammatory markers, and the expression of neurotrophic genes. The corpus callosum and the sciatic nerve were subjected to histopathological and immunohistochemical studies. The CPZ group was associated with significant reductions in muscle power, frequency of contraction, sciatic NCV, SOD, IL-10, SIRT1, NGF, and neuregulin-1. Significant increases in MDA, TNF-α, INF-γ, IL-17, TGF-β, and NF-κB were also detected. Multiple areas of partially demyelinated nerve fibers in the corpus callosum, the loss of oligodendrocyte nuclei, and increased microglia and astrocytes were also observed. The sciatic nerve revealed partial demyelination with significantly reduced myelin basic protein (MBP) expression. Pir significantly restored motor function, demyelination, and neurodegenerative changes induced by CPZ. Besides the antifibrotic action of Pir, we concluded that it improves motor function in MS by alleviating the demyelinating process and neurodegeneration. Its potential anti-inflammatory, antioxidant, and antifibrotic properties could be contributing factors. These effects could be mediated by modulating the NF-κB, SIRT1, NGF, and neuregulin-1 pathways. Pir is a promising agent for treating MS.","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"4019-4036"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470332","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

Enhancing sensitivity to oxaliplatin in tongue squamous cell carcinoma: mechanistic insights and therapeutic potential of DHA combination therapy. 提高舌鳞状细胞癌对奥沙利铂的敏感性：DHA联合疗法的机理认识和治疗潜力。

IF 3.1 4区医学

Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-04-01 Epub Date: 2024-10-30 DOI: 10.1007/s00210-024-03548-z

Hailan Mo, Hongyan Fang, Lifeng Jia, Shitong Zhou, Menglong Feng, Xiaolu Wu, Wei Yuan

{"title":"Enhancing sensitivity to oxaliplatin in tongue squamous cell carcinoma: mechanistic insights and therapeutic potential of DHA combination therapy.","authors":"Hailan Mo, Hongyan Fang, Lifeng Jia, Shitong Zhou, Menglong Feng, Xiaolu Wu, Wei Yuan","doi":"10.1007/s00210-024-03548-z","DOIUrl":"10.1007/s00210-024-03548-z","url":null,"abstract":"Squamous cell carcinoma of the tongue, a common and aggressive malignancy, poses a substantial threat to health and well-being. Despite the promising results of combination therapy with dihydroartemisinin (DHA) and oxaliplatin (Oxa) in various cancers, its effectiveness in treating tongue squamous cell carcinoma had not been explored prior to this study. Our research found that DHA significantly enhances the sensitivity of tongue squamous cell carcinoma cells to Oxa, even at very low concentrations. The combination treatment was observed to modulate the activity of CDK1 and Cyclin B1, arresting the cell cycle in the G2 phase. Additionally, it reduces mitochondrial membrane potential, prompting the release of cytochrome c and activating cleaved caspase-3, which promotes apoptosis. Notably, surface plasmon resonance and immunoprecipitation experiments revealed that DHA targets and attenuates CDK1 modification, weakening its interaction with STAT3 protein. This leads to reduced expression of anti-apoptotic genes and facilitates programmed cell death in CAL-27 cells. The findings underscore the potential of DHA and Oxa as a potent therapeutic strategy for tongue squamous cell carcinoma, opening avenues for clinical application and further exploration into its mechanistic pathways.","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"4393-4407"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142546456","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

Unveiling the interaction, cytotoxicity and antibacterial potential of pyridine derivatives: an experimental and theoretical approach with bovine serum albumin. 揭示吡啶衍生物的相互作用、细胞毒性和抗菌潜力：与牛血清白蛋白的实验和理论方法。

IF 3.1 4区医学

Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-04-01 Epub Date: 2024-11-01 DOI: 10.1007/s00210-024-03541-6

Rosalin Das, Patitapaban Mohanty, Pragyan P Dash, Swagatika Mishra, Ajit K Bishoyi, Lokanath Mishra, Laxmipriya Prusty, Devi P Behera, Debasmita Dubey, Monalisa Mishra, Harekrushna Sahoo, Mohd S Khan, Santosh K Sethi, Bigyan R Jali

{"title":"Unveiling the interaction, cytotoxicity and antibacterial potential of pyridine derivatives: an experimental and theoretical approach with bovine serum albumin.","authors":"Rosalin Das, Patitapaban Mohanty, Pragyan P Dash, Swagatika Mishra, Ajit K Bishoyi, Lokanath Mishra, Laxmipriya Prusty, Devi P Behera, Debasmita Dubey, Monalisa Mishra, Harekrushna Sahoo, Mohd S Khan, Santosh K Sethi, Bigyan R Jali","doi":"10.1007/s00210-024-03541-6","DOIUrl":"10.1007/s00210-024-03541-6","url":null,"abstract":"The binding interactions between bovine serum albumin (BSA) and three pyridine derivatives, i.e., 2-(5-bromopyridin-3-yl) acetic acid (L1), 3-bromo-5-nitropyridine (L2) and 2-chloro-4-nitropyridine (L3), have been carried out using UV-Vis and fluorescence spectroscopic methods. Fluorescence intensity quenching is observed by adding L2 and L3 to the BSA solution. The quenched fluorescence emission is due to the static nature. An isothermal titration calorimetry (ITC) experiment shows the binding ability of L1 with BSA. The binding constants are found to be 7.23 ± 0.32 × 105 M-1 for L1. The thermodynamic parameters were calculated from ITC measurements (i.e., ∆H = -2.78 ± 0.08 kcal/mol, ∆G = -5.65 ± 0.25 kcal/mol, and -T∆S = -2.87 ± 0.11 kcal/mol), which indicated that the protein-ligand complex formation between L1 and BSA is mainly due to the hydrogen bonds and van der Waals interactions. Cyclic voltammetry (CV) and structure activity and relationship (SAR) studies have been carried out to establish the relationship between ligands and proteins. Additionally, we conducted an antibacterial assay with gram-positive Staphylococcus aureus, Enterococcus faecalis, and negative bacterial strains Acinetobacter baumannii and Escherichia coli against L1, L2, and L3, aiming to address the challenges posed by the co-existence of multidrug-resistant bacteria. Finally, drosophila is used to test the cytotoxicity of ligands L1, L2, and L3's in vitro.","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"4449-4466"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142562460","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

Sarecycline for moderate to severe acne: a promising narrow-spectrum antibacterial drug. 治疗中重度痤疮的沙瑞霉素：一种前景看好的窄谱抗菌药物。

IF 3.1 4区医学

Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-04-01 Epub Date: 2024-11-04 DOI: 10.1007/s00210-024-03557-y

Amr Elrosasy, Mohamed Abo Zeid, Esraa M AlEdani, Amira A Aboali, Aya M Fayoud, Kareem Ibraheem, Maha Abdullah Alwaili, Samy Selim, Ahmed Hamdy Zabady

引用次数: 0

Study on the mechanism of OSM participating in myocardial fibrosis by inhibiting TGFβ-induced EndMT of cardiac microvascular endothelial cells through SPARC/SMAD signaling. 研究 OSM 通过 SPARC/SMAD 信号转导抑制 TGFβ 诱导的心脏微血管内皮细胞 EndMT 参与心肌纤维化的机制

IF 3.1 4区医学

Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-04-01 Epub Date: 2024-11-04 DOI: 10.1007/s00210-024-03472-2

Ying Zhu, Zhuo Xu, Min Chen

{"title":"Study on the mechanism of OSM participating in myocardial fibrosis by inhibiting TGFβ-induced EndMT of cardiac microvascular endothelial cells through SPARC/SMAD signaling.","authors":"Ying Zhu, Zhuo Xu, Min Chen","doi":"10.1007/s00210-024-03472-2","DOIUrl":"10.1007/s00210-024-03472-2","url":null,"abstract":"Cardiac fibrosis constitutes a crucial element in the progression of diverse chronic cardiac conditions. Notably, a significant correlation has been observed between the endothelial-to-mesenchymal transition (EndMT) and the emergence of cardiac fibrosis. To investigate mechanisms, we employed immunofluorescence for α-SMA and CD31 analysis, Western blotting for CD34, vimentin, and SPARC overexpression. CCK8, wound healing, and transwell assay-assessed cell viability, invasion, and migration. SPARC overexpression plasmid was constructed and validated by Western blotting. Fibrosis levels were quantified via Masson staining, and collagen 1 and 3 expressions were measured using ELISA assays. Notably, in TGF-β-induced H5V cells, the downregulation of CD31 and CD34 expression, along with the upregulation of α-SMA and vimentin, suggests the induction of EndMT in cardiac fibrosis. Interestingly, OSM treatment mitigated EndMT progression, cell invasion, migration, and the expression of p-SMAD2, p-SMAD3, and SPARC in TGF-β-treated H5V cells. Further analysis revealed that OSM alleviated TGFβ-induced EndMT, invasion, and migration of cardiac microvascular endothelial cells by suppressing SPARC/SMAD signaling. Moreover, OSM therapy notably mitigated myocardial tissue fibrosis, along with a reduction in the expression of collagen 1, collagen 3, α-SMA, and CD34, while augmenting CD31 and vimentin expression in ISO-induced myocardial tissue. Additionally, OSM exhibited the ability to suppress myocardial tissue fibrosis and the expression of EndMT markers as well as SPARC/SMAD signals in ISO-induced myocardial tissue. Our comprehensive analysis unveiled that OSM contributes significantly to myocardial fibrosis modulation by inhibiting TGFβ-mediated EndMT in myocardial microvascular endothelial cells via SPARC/SMAD signaling.","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"4479-4489"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569112","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

The effect of adipose-derived mesenchymal stem cells against high fructose diet induced liver dysfunction and dysbiosis. 脂肪间充质干细胞对高果糖饮食引起的肝功能紊乱和菌群失调的影响

IF 3.1 4区医学

Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-04-01 Epub Date: 2024-11-05 DOI: 10.1007/s00210-024-03518-5

Marwa Abdeltawab Mohammed, Nesma Hussein Abel Hay, Maha Tarek Mohammed, Hoda Sayed Mahmoud, Manar Yehia Ahmed, Ahmed Abdelmenem, Dina Sayed Abdelrahim

{"title":"The effect of adipose-derived mesenchymal stem cells against high fructose diet induced liver dysfunction and dysbiosis.","authors":"Marwa Abdeltawab Mohammed, Nesma Hussein Abel Hay, Maha Tarek Mohammed, Hoda Sayed Mahmoud, Manar Yehia Ahmed, Ahmed Abdelmenem, Dina Sayed Abdelrahim","doi":"10.1007/s00210-024-03518-5","DOIUrl":"10.1007/s00210-024-03518-5","url":null,"abstract":"High fructose diet (HFrD) has been approved to be involved in the pathogenesis of insulin resistance. Mesenchymal stem cells have a vital role in the treatment of various diseases including metabolic disturbances. We investigated the effect of Adipose-derived mesenchymal stem cells (ADMSCs) against HFrD-induced metabolic disorders and the molecular mechanisms for this effect. Rats were divided into 3 groups; control, HFrD, and combined HFrD with ADMSCs. We assessed liver functions, gut microbiota activity, oxidative stress, adiponectin, and IL10 levels. Also, we measured SREBP-1, IRS-1 expression using Western blot, and Malat1 expression using rt-PCR. ADMSCs antagonized metabolic abnormalities induced by HFrD in the form of improvement of liver functions and alleviation of oxidative stress. In addition, ADMSCs ameliorated gut microbiota activity besides the elevation of adiponectin and IL10 levels. ADMSCs attenuated insulin resistance through upregulation of IRS1 and downregulation of SREBP-1 and Malat1. ADMSCs can protect against HFrD-induced metabolic hazards.","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"4525-4537"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583718","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

Ameliorative effects of osthole on acrylamide-induced neurotoxicity in PC12 cells: Role of oxidative stress, apoptosis and ERK pathways. 奥斯特孔对丙烯酰胺诱导的 PC12 细胞神经毒性的改善作用：氧化应激、细胞凋亡和ERK通路的作用

IF 3.1 4区医学

Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-04-01 Epub Date: 2024-10-29 DOI: 10.1007/s00210-024-03560-3

Leili Kachranlouei, Hossein Hosseinzadeh, Gholamreza Karimi, Fatemeh Rajabian, Soghra Mehri

{"title":"Ameliorative effects of osthole on acrylamide-induced neurotoxicity in PC12 cells: Role of oxidative stress, apoptosis and ERK pathways.","authors":"Leili Kachranlouei, Hossein Hosseinzadeh, Gholamreza Karimi, Fatemeh Rajabian, Soghra Mehri","doi":"10.1007/s00210-024-03560-3","DOIUrl":"10.1007/s00210-024-03560-3","url":null,"abstract":"The possible protective effects of osthole on acrylamide-induced neurotoxicity in PC12 cells. Cells were pretreated with different concentrations of osthole (1- 25 μM) for 24 h and then the IC50 value of acrylamide (5 mM) was added. After 24 h, cell viability and intracellular ROS content were detected by MTT assay and DCF-DA methods, respectively. Also, DNA fragmentation in apoptotic cells was determined by propidium iodide assay, and apoptosis (Caspase-3, Bax, Bcl-2, ERK, and P-ERK) was measured by the western blot method. Exposing PC12 cells to acrylamide diminished cell viability, and enhanced the intracellular ROS generation and the percentage of apoptotic cells. Furthermore, acrylamide elevated the P-ERK/ERK and Bax/Bcl-2 ratio, and the level of cleaved caspase-3 protein in PC12 cells. Pretreating cells with osthole enhanced cell viability and reduced ROS generation. Also, osthole (10 μM) significantly reduced P-ERK/ERK and Bax/Bcl-2 ratio, the level of cleaved caspase-3 protein, and the percentage of apoptotic cells in comparison to the acrylamide group. Osthole can exhibit a protective effect on the neurotoxicity of acrylamide through the inhibition of oxidative stress and apoptosis in PC12 cells.","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"4361-4372"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142546386","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

The potential role of targeting the leptin receptor as a treatment for breast cancer in the context of hyperleptinemia: a literature review. 针对高瘦素血症的瘦素受体治疗乳腺癌的潜在作用：文献综述。

IF 3.1 4区医学

Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-04-01 Epub Date: 2024-11-20 DOI: 10.1007/s00210-024-03592-9

Abbas S Neamah, Al-Hassan Soliman Wadan, Fadhel M Lafta, Doha El-Sayed Elakwa

{"title":"The potential role of targeting the leptin receptor as a treatment for breast cancer in the context of hyperleptinemia: a literature review.","authors":"Abbas S Neamah, Al-Hassan Soliman Wadan, Fadhel M Lafta, Doha El-Sayed Elakwa","doi":"10.1007/s00210-024-03592-9","DOIUrl":"10.1007/s00210-024-03592-9","url":null,"abstract":"Since cancer is becoming a leading cause of death worldwide, efforts should be concentrated on understanding its underlying biological alterations that would be utilized in disease management, especially prevention strategies. Within this context, multiple bodies of evidence have highlighted leptin's practical and promising role, a peptide hormone extracted from adipose and fatty tissues with other adipokines, in promoting the proliferation, migration, and metastatic invasion of breast carcinoma cells. Excessive blood leptin levels and hyperleptinemia increase body fat content and stimulate appetite. Also, high leptin level is believed to be associated with several conditions, including overeating, emotional stress, inflammation, obesity, and gestational diabetes. It has been noted that when leptin has impaired signaling in CNS, causing the lack of its normal function in energy balance, it results in leptin resistance, leading to a rise in its concentration in peripheral tissues. Our research paper will shed highlighting on potentially targeting the leptin receptor and its cellular signaling in suppressing breast cancer progression.","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3451-3466"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142676262","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

Pathological role of RAGE underlying progression of various diseases: its potential as biomarker and therapeutic target. RAGE 在各种疾病进展中的病理作用：作为生物标记物和治疗靶点的潜力。

IF 3.1 4区医学

Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-04-01 Epub Date: 2024-11-26 DOI: 10.1007/s00210-024-03595-6

Sinjini Sarkar

引用次数: 0