Current molecular pharmacology最新文献

Positive Regulation of Osteoblast Proliferation and Differentiation in MC3T3- E1 Cells by 7,3′,4′-Trimethoxyflavone 7,3′,4′-三甲氧基黄酮对 MC3T3- E1 细胞成骨细胞增殖和分化的正向调节作用

IF 2.7 4区生物学

Current molecular pharmacology Pub Date : 2024-07-31 DOI: 10.2174/0118761429305367240725112731

Sharmeen Fayyaz, Atia tul-Wahab, Bushra Taj, M. Iqbal Choudhary

{"title":"Positive Regulation of Osteoblast Proliferation and Differentiation in MC3T3- E1 Cells by 7,3′,4′-Trimethoxyflavone","authors":"Sharmeen Fayyaz, Atia tul-Wahab, Bushra Taj, M. Iqbal Choudhary","doi":"10.2174/0118761429305367240725112731","DOIUrl":"https://doi.org/10.2174/0118761429305367240725112731","url":null,"abstract":"Objectives: Increasing ratio of bone fragility, and susceptibility to fractures constitutes a major health problem worldwide. Therefore, we aimed to identify new compounds with a potential to increase proliferation and differentiation of osteoblasts. Methods: Cellular and molecular assays, such as ALP activity, alizarin staining, and flow cytometry were employed to check the effect of TMF on osteogenesis. Moreover, gene expression analysis of certain important genes and transcriptional factors was also performed. Results: Our findings report for the first time that 7,3′,4′-trimethoxyflavone is capable of enhancing proliferation, and differentiation in osteoblast cells. Results from flow cytometry analysis also indicated that TMF increases the number of cells in S-phase. Furthermore, treatment with TMF altered the expression of osteogenic genes, OCN and Axin-2 indicating possible activation of Wnt signaling pathway. Conclusion: Taken together, this study identified that 7,3′,4′-trimethoxyflavone has the potential to enhance osteoblast proliferation and differentiation, possibly due to the activation of Wnt/β-catenin pathway. Thus, demonstrating TMF as naturally occurring agent to promote osteogenesis and prevention of bone fragility, and related disorders.","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"30 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141866240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to: IMPDH2 Positively Impacts the Proliferation Potential of Hepatoblastoma Cells by Activating JunB Signaling Pathway 更正： IMPDH2 通过激活 JunB 信号通路积极影响肝母细胞瘤细胞的增殖潜力IMPDH2 通过激活 JunB 信号通路积极影响肝母细胞瘤细胞的增殖潜力

IF 2.7 4区生物学

Current molecular pharmacology Pub Date : 2024-05-03 DOI: 10.2174/187446721701240419165931

Li Yuan, Liang Zeng, Feng Ye, Kai Chen, Zhengrong Chen, Liping Li

引用次数: 0

RNA Interference-based Therapies for the Reduction of Cardiovascular Risk 基于 RNA 干扰的降低心血管风险疗法

IF 2.7 4区生物学

Current molecular pharmacology Pub Date : 2024-03-05 DOI: 10.2174/0118761429264553231204115314

Natalia Nazarenko, Jiyoung Seo, Sanjana Nagraj, Leonidas Palaiodimos, Damianos G. Kokkinidis

引用次数: 0

IMPDH2 Positively Impacts the Proliferation Potential of Hepatoblastoma Cells by Activating JunB Signaling Pathway IMPDH2 通过激活 JunB 信号通路积极影响肝母细胞瘤细胞的增殖潜力

IF 2.7 4区生物学

Current molecular pharmacology Pub Date : 2024-02-22 DOI: 10.2174/0118761429257350231212093136

Li Yuan, Liang Zeng, Feng Ye, Kai Chen, Zhengrong Chen, Liping Li

{"title":"IMPDH2 Positively Impacts the Proliferation Potential of Hepatoblastoma Cells by Activating JunB Signaling Pathway","authors":"Li Yuan, Liang Zeng, Feng Ye, Kai Chen, Zhengrong Chen, Liping Li","doi":"10.2174/0118761429257350231212093136","DOIUrl":"https://doi.org/10.2174/0118761429257350231212093136","url":null,"abstract":"Background: Amplification of inosine monophosphate dehydrogenase II, EC 1,1,1,205 (IMPDH2) has been reported in various cancers, which results in transformation and tumorigenicity. In our current work, we have explored the oncogenic properties and the underlying pathophysiology of IMPDH2 in hepatoblastoma (HB). Methods: To investigate IMPDH2 expression in HB tissues and prognostic significance in HB patients, gene expression profiling interactive analysis (GEPIA) has been adopted. Immunohistochemistry has also helped to validate the protein expression of IMPDH2 in HB tissues. The effect of IMPDH2 overexpression or depletion on the proliferation of Hepatoblastoma cells in vitro has been evaluated by CCK8 assays and colony formation assays. Xenograft tumor growth of mice has been detected. Luciferase reporter assays have been conducted to determine the interaction of IMPDH2 and JunB, which was further asserted by pharmacological inhibition of JunB. Results: IMPDH2 was highly expressed in HB tissues. Experimentally, the proliferation and colony formation of HuH6 cells were increased by IMPDH2 overexpression. Conversely, genetic inactivation of IMPDH2 impaired the proliferative efficiency and colony-forming rate of HepG2 cells. Besides, the luciferase reporter assay validated IMPDH2 overexpression to be associated with enhanced JunB transcriptional activity, while its activity was diminished in the case of IMPDH2 depletion. JunB inhibitor neutralized the IMPDH2-mediated increased phosphorylation of JunB. Conclusion: Our findings, thus, suggest that IMPDH2 exhibits its oncogenic role in HB partially via JunB-dependent proliferation.","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"1 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139949549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sanguinarine Attenuates Lung Cancer Progression via Oxidative Stress-induced Cell Apoptosis 山金车花碱通过氧化应激诱导的细胞凋亡减缓肺癌进展

IF 2.7 4区生物学

Current molecular pharmacology Pub Date : 2024-02-07 DOI: 10.2174/0118761429269383231119062233

Asmat Ullah, Anum Razzaq, Mohammad Y. Alfaifi, Serag Eldin I. Elbehairi, Farid Menaa, Najeeb Ullah, Somia Shehzadi, Touseef Nawaz, Haroon Iqbal

{"title":"Sanguinarine Attenuates Lung Cancer Progression via Oxidative Stress-induced Cell Apoptosis","authors":"Asmat Ullah, Anum Razzaq, Mohammad Y. Alfaifi, Serag Eldin I. Elbehairi, Farid Menaa, Najeeb Ullah, Somia Shehzadi, Touseef Nawaz, Haroon Iqbal","doi":"10.2174/0118761429269383231119062233","DOIUrl":"https://doi.org/10.2174/0118761429269383231119062233","url":null,"abstract":"Background:: Lung cancer (LC) incidence is rising globally and is reflected as a leading cause of cancer-associated deaths. Lung cancer leads to multistage carcinogenesis with gradually increasing genetic and epigenetic changes. Aims:: Sanguinarine (sang) mediated the anticancer effect in LCC lines by involving the stimulation of reactive oxygen species (ROS), impeding Bcl2, and enhancing Bax and other apoptosis-associated protein Caspase-3, -9, and -PARP, subsequently inhibiting the LC invasion and migration. Objective:: This study was conducted to investigate the apoptotic rate and mechanism of Sang in human LC cells (LCC) H522 and H1299. Methods:: MTT assay to determine the IC50, cell morphology, and colony formation assay were carried out to show the sanguinarine effect on the LC cell line. Moreover, scratch assay and transwell assay were performed to check the migration. Western blotting and qPCR were done to show its effects on targeted proteins and genes. ELISA was performed to show the VEGF effect after Sanguinarine treatment. Immunofluorescence was done to check the interlocution of the targeted protein. Results:: Sang significantly inhibited the growth of LCC lines in both time- and dose-dependent fashions. Flow cytometry examination and Annexin-V labeling determined that Sang increased the apoptotic cell percentage. H522 and H1299 LCC lines treated with Sang showed distinctive characteristics of apoptosis, including morphological changes and DNA fragmentation. Conclusion:: Sang exhibited anticancer potential in LCC lines and could induce apoptosis and impede the invasion and migration of LCC, emerging as a promising anticancer natural agent in lung cancer management.","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"4 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139763862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Impact of Nicosulfuron on Sperm Quality: Insights into Testicular Cell Apoptosis and NF-κB Signaling Pathway in Mice Testes 烟嘧磺隆对精子质量的影响：洞察小鼠睾丸细胞凋亡和 NF-κB 信号通路

IF 2.7 4区生物学

Current molecular pharmacology Pub Date : 2024-02-07 DOI: 10.2174/0118761429282063231119180457

Jianqiu Han, Chen Zhao, Qing Shen, Yalei Qi, Yanjia Zhang, Faisal Raza, Yongmei Li, Hajra Zafar, Tengfei Liu, Juan Tan, Honghui Han, Xueyun Ma

{"title":"Impact of Nicosulfuron on Sperm Quality: Insights into Testicular Cell Apoptosis and NF-κB Signaling Pathway in Mice Testes","authors":"Jianqiu Han, Chen Zhao, Qing Shen, Yalei Qi, Yanjia Zhang, Faisal Raza, Yongmei Li, Hajra Zafar, Tengfei Liu, Juan Tan, Honghui Han, Xueyun Ma","doi":"10.2174/0118761429282063231119180457","DOIUrl":"https://doi.org/10.2174/0118761429282063231119180457","url":null,"abstract":"Background:: Nicosulfuron, a widely used herbicide in crops, has raised concerns due to its escalating presence as an environmental pollutant, particularly in soil and water. The potential adverse effects of nicosulfuron on animals, including reproductive toxicity, have garnered attention. Objective:: The study aimed to evaluate the reproductive toxicity of nicosulfuron in male mice. Methods:: Male mice were orally administrated with three different concentration gradients (350, 700, and 1400 mg/kg) of nicosulfuron for 35 days. The investigation delved into sperm quality, testicular structures, and expression of cleaved caspase-3 and NF-κB p65 of the testes. Results:: The finding unveiled a correlation between nicosulfuron exposure and detrimental effects on sperm quality and alteration of testicular structure. Notably, parameters, such as sperm survival rate (SUR) and sperm motility (MOT), exhibited a decline in relation to increasing nicosulfuron dosages. Moreover, in the mice subjected to higher doses of nicosulfuron, elevated expression of cleaved caspase-3 and NF-κB p65 was observed in the testes. Interestingly, we also observed an increase of NF-κB p65 expression in the mice exposed to the nicosulfuron. Conclusion:: Our research revealed that exposure to nicosulfuron resulted in compromised sperm quality and alterations in testicular structure. The correlation between nicosulfuron and apoptosis, especially via the NF-κB pathway, provided significant insights into the mechanisms underpinning these detrimental effects. These findings significantly enhance our comprehension of the potential hazards associated with nicosulfuron exposure and its impacts on the reproductive health of animals.","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"22 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139763953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nrf2 Mediates Effect of Resveratrol in Ischemia-reperfusion Injury Nrf2介导白藜芦醇对缺血再灌注损伤的影响

IF 2.7 4区生物学

Current molecular pharmacology Pub Date : 2024-02-07 DOI: 10.2174/0118761429246578231130064830

Ali Mohammad Pourbagher-Shahri, Tahereh Farkhondeh, Amir Masoud Jafari-Nozad, Majid Darroudi, Kobra Naseri, Masoumeh Amirian, Saeed Samarghandian

{"title":"Nrf2 Mediates Effect of Resveratrol in Ischemia-reperfusion Injury","authors":"Ali Mohammad Pourbagher-Shahri, Tahereh Farkhondeh, Amir Masoud Jafari-Nozad, Majid Darroudi, Kobra Naseri, Masoumeh Amirian, Saeed Samarghandian","doi":"10.2174/0118761429246578231130064830","DOIUrl":"https://doi.org/10.2174/0118761429246578231130064830","url":null,"abstract":":: Ischemia-Reperfusion Injury (IRI) is a paradoxical phenomenon where removing the source of injury can cause additional damage. Ischemia reduces ATP production and intracellular pH, reducing oxidative reactions, increasing lactic acid release, and activating anaerobic metabolism. Reperfusion restores aerobic respiration and increases ROS production, leading to malfunction of transmembrane transport, activation of proteases, DNA dissolution, and protein denaturation, leading to apoptotic cell death. Nrf2 is a transcription factor that regulates cellular inflammation and oxidative responses. It is activated by oxidants and electrophiles and enhances detoxifying enzyme expression, maintaining redox homeostasis. It also activates ARE, which activates several ARE-regulated genes that favor cell survival by exhibiting resistance to oxidants and electrophiles. Nrf2 regulates the antioxidant defense system by producing phase II and antioxidant defense enzymes, including HO-1, NQO-1, gglutamylcysteine synthetase, and rate-limiting enzymes for glutathione synthesis. Nrf2 protects mitochondria from damage and supports mitochondrial function in stress conditions. Resveratrol is a stilbene-based compound with a wide variety of health benefits for humans, including antioxidant, anticarcinogenic, antitumor, and estrogenic/antiestrogenic. Resveratrol protects against IRI through several signaling pathways, including the Nrf2/ARE pathway. Here, we review the studies that investigated the mechanisms of resveratrol protection against IRI through modulation of the Nrf2 signaling pathway.","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"20 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139763786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Advancements in the Research of GEF-H1: Biological Functions and Tumor Associations GEF-H1 的研究进展：生物功能与肿瘤关系

IF 2.7 4区生物学

Current molecular pharmacology Pub Date : 2024-02-07 DOI: 10.2174/0118761429274883231129103220

Liqi Li, Yunyun Li, Xiaoshu Zhou

引用次数: 0

A Review of the Dual Role of MicroRNA-21 in Cardiovascular Diseases: Risk Factor or a Potential Therapeutic Target MicroRNA-21 在心血管疾病中的双重作用综述：风险因素或潜在治疗靶点

IF 2.7 4区生物学

Current molecular pharmacology Pub Date : 2024-01-29 DOI: 10.2174/0118761429287057240116040703

Amir Masoud Jafari-Nozad, Negin Rostami, Melika Esmaeili, Haniye Vahdati, Serajoddin Hosseini, Tahereh Farkhondeh, Saeed Samarghandian

{"title":"A Review of the Dual Role of MicroRNA-21 in Cardiovascular Diseases: Risk Factor or a Potential Therapeutic Target","authors":"Amir Masoud Jafari-Nozad, Negin Rostami, Melika Esmaeili, Haniye Vahdati, Serajoddin Hosseini, Tahereh Farkhondeh, Saeed Samarghandian","doi":"10.2174/0118761429287057240116040703","DOIUrl":"https://doi.org/10.2174/0118761429287057240116040703","url":null,"abstract":": Cardiovascular diseases [CVD] are the number one reason for morbidity and mortality in the modern world, and their incidence is increasing at an incredible pace. Increasing evidence has shown the significant functions of microRNAs in the cardiovascular system and has highlighted their potential application as a new era of diagnostic and therapeutic targets for CVD that can improve the prognosis and life expectancy of patients. Among more than 2,000 microRNAs, microRNA-21 [miR-21] is highly expressed in human hearts and has earned the interest of researchers as a potential biomarker in a wide range of common heart conditions. Here, we summarized recent research progress regarding the significant role of miR-21 in CVD, focusing on cardiotoxicity, heart arrhythmias, cardiomyopathies, and hypertension. Several signaling pathways [TGF-β1/Smad2 signaling, FGFR1/FGF21/PPARγ, NF-κB/miR-21/SMAD7, miR-21/SPRY1/ERK/mTOR …] and molecular targets [BTG2, PDCD4, PTEN, STAT3…] were reported to be controlled, at least partially, by miR-21 and are linked to CVD pathogenesis. Most investigations highlighted miR-21 cardioprotective functions in heart injury, while some other studies showed that this miR is elevated in the serum/tissue of patients, promoting fibrosis and cardiac dysfunction. This dual role can be explained by the fact that miR-21 has multiple regulatory functions depending on the microenvironment, downstream signaling, and target genes, which indicates that cell-type-specific investigations should receive more attention. With further investigations, miR-21 can be considered a novel tailored therapy with favorable outcomes.","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"12 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139588056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular Insight into the Apoptotic Mechanism of Cancer Cells: An Explicative Review 癌细胞凋亡机制的分子洞察力：说明性综述

IF 2.7 4区生物学

Current molecular pharmacology Pub Date : 2024-01-19 DOI: 10.2174/0118761429273223231124072223

Dipanjan Karati, Dileep Kumar

{"title":"Molecular Insight into the Apoptotic Mechanism of Cancer Cells: An Explicative Review","authors":"Dipanjan Karati, Dileep Kumar","doi":"10.2174/0118761429273223231124072223","DOIUrl":"https://doi.org/10.2174/0118761429273223231124072223","url":null,"abstract":":: Mitosis of somatic cells produces a daughter cell. Apoptosis, a naturally programmed cellular death mechanism, kills abnormal cells produced by mitosis. Cancer can develop when this equilibrium is disrupted, either by an upsurge in cell propagation or a reduction in tissue demise. Cancer therapy aims to cause cancer cells to die while inflicting little harm to healthy cells. This review of apoptotic mechanism processes improves our understanding of how certain malignancies begin and develop. The current cancer treatments can operate either by inducing apoptosis or causing direct cell damage. An insight into the resistance to apoptosis may explicate why malignancy treatments fail in some situations. New therapies grounded on our understanding of apoptotic processes are being developed to induce apoptosis of cancer cells while limiting the simultaneous death of normal cells. Various biological activities require redox equilibrium to function properly. : Antineoplastic medications that cause oxidative stress by raising ROS and blocking antioxidant mechanisms have recently attracted much interest. The rapid accumulation of ROS impairs redox balance and damages cancer cells severely. Here, we discuss ROS-instigating malignancy therapy and the antineoplastic mechanism used by prooxidative drugs.","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"40 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139506448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0