Korean Journal of Physiology & Pharmacology最新文献_第3页

Effects of in vivo treatment with K_v7.4 activator, URO-K10, on the impaired relaxation of pulmonary arteries in the monocrotaline-induced pulmonary hypertensive rats. Kv7.4激活剂URO-K10在体内治疗对单苦参碱诱导的肺动脉舒张受损大鼠的影响

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-07-01 DOI: 10.4196/kjpp.25.122

Seung Beom Oh, Young Keul Jeon, Nari Choi, Hae Young Yoo, Sung Joon Kim

{"title":"Effects of in vivo treatment with Kv7.4 activator, URO-K10, on the impaired relaxation of pulmonary arteries in the monocrotaline-induced pulmonary hypertensive rats.","authors":"Seung Beom Oh, Young Keul Jeon, Nari Choi, Hae Young Yoo, Sung Joon Kim","doi":"10.4196/kjpp.25.122","DOIUrl":"10.4196/kjpp.25.122","url":null,"abstract":"Pulmonary arterial hypertension (PAH) is a fatal disease marked by increased pulmonary vascular resistance and right ventricular (RV) failure. Impaired vascular relaxation and vasoconstrictive signaling, including Rho-associated kinase (ROCK2) upregulation and myosin phosphatase target subunit 1 (MYPT1) downregulation, contribute to disease progression. We investigated the therapeutic effects of URO-K10, a novel Kv7.4 channel activator, in a monocrotaline-induced rat model of PAH (PAH-MCT). In PAH-MCT rats, chronic URO-K10 administration improved body weight gain, and significantly reduced RV hypertrophy. Functional studies revealed enhanced pulmonary artery relaxation, while relaxation after high K+-induced contraction showed only partial recovery. Immunoblot analysis demonstrated that ROCK2 upregulation was reversed by URO-K10, but MYPT1 remained downregulated and MLC2 diphosphorylation persisted. Interestingly, treatment with 8-Br-cGMP restored delayed relaxation and reduced MLC2 phosphorylation in URO-K10-treated PAH-MCT while not in the untreated PAH-MCT rats, suggesting that cGMP supplementation can compensate for the recovery from impaired endogenous signaling by the URO-K10 application. These findings suggest that URO-K10 improves pulmonary hemodynamics and RV remodeling via Kv7.4 activation and downregulation of ROCK2. However, incomplete recovery of MYPT1 and MLC2 phosphorylation highlights the complexity of contractile regulation in PAH. Kv7.4 activation represents a promising therapeutic approach but may require combination strategies to fully restore vascular function in PAH.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"29 4","pages":"475-485"},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198454/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144477863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Atypical antipsychotic drug olanzapine inhibits 5-HT₃ receptor-mediated currents by allosteric and non-competitive mechanisms. 非典型抗精神病药物奥氮平通过异位和非竞争机制抑制 5-HT3 受体介导的电流。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-07-01 Epub Date: 2024-12-18 DOI: 10.4196/kjpp.24.340

Yong Soo Park, Gyu Min Kim, Ho Jun Sung, Ju Yeong Yu, Ki-Wug Sung

{"title":"Atypical antipsychotic drug olanzapine inhibits 5-HT3 receptor-mediated currents by allosteric and non-competitive mechanisms.","authors":"Yong Soo Park, Gyu Min Kim, Ho Jun Sung, Ju Yeong Yu, Ki-Wug Sung","doi":"10.4196/kjpp.24.340","DOIUrl":"10.4196/kjpp.24.340","url":null,"abstract":"Olanzapine, an atypical antipsychotic, is widely used in the treatment of schizophrenia and bipolar disorder due to its modulation of dopamine and serotonin receptor systems. While its primary action involves antagonism of dopamine D2 and serotonin 5-HT (5-hydroxytryptamine)2A receptors, recent evidence suggests that olanzapine also inhibits 5-HT3 receptors, which are ligand-gated ion channels involved in synaptic transmission in central and peripheral nervous systems. The present study aimed to investigate the action of olanzapine on 5-HT3 receptor-mediated currents using whole-cell voltage-clamp recordings in NCB-20 neuroblastoma cells. Results of this study indicated that olanzapine could act as a non-competitive antagonist of the 5-HT3 receptor, exhibiting concentration-dependent inhibition of ion currents. Moreover, olanzapine facilitated both deactivation and desensitization kinetics, accelerating decay of 5-HT3 receptor-mediated currents. Recovery from desensitization was significantly delayed by olanzapine, whereas recovery from deactivation was largely unaffected by it. Current-voltage relationship analysis revealed that olanzapine reduced the amplitude of 5-HT3 receptor-mediated currents across all holding potentials without altering reversal potential, suggesting a voltage-independent inhibition. Furthermore, olanzapine exhibited use-dependent inhibition, with a greater reduction in current observed during more frequent 5-HT application. These findings provide novel insights into a non-competitive and allosteric inhibition of 5-HT3 receptors by olanzapine, contributing to a deeper understanding of its pharmacological profile in neuropsychiatric and gastrointestinal conditions where serotonergic neurotransmission is implicated.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"431-442"},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142848222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Chelidonine inhibits melanoma cell malignancy by inactivating TLR4/NF-κB and PI3K/AKT signaling pathways. Chelidonine通过灭活TLR4/NF-κB和PI3K/AKT信号通路抑制黑色素瘤细胞恶性。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-07-01 Epub Date: 2025-04-11 DOI: 10.4196/kjpp.24.383

Yu Zhou, Han Han, Peng Li, Wei Wei

{"title":"Chelidonine inhibits melanoma cell malignancy by inactivating TLR4/NF-κB and PI3K/AKT signaling pathways.","authors":"Yu Zhou, Han Han, Peng Li, Wei Wei","doi":"10.4196/kjpp.24.383","DOIUrl":"10.4196/kjpp.24.383","url":null,"abstract":"Melanoma is a common and aggressive tumor, characterized by a high incidence rate and extensive metastasis. Chelidonine exhibits a broad range of biological properties including anti-inflammatory, antimicrobial, and anticancer effects. Our study is intended to explore the effects chelidonine of on melanoma cells. In detail, CCK-8 assay was used for detection of cell viability. The colony formation assay was carried out to measure cell proliferation. Wound healing assay and Transwell assay were employed to evaluate cell migration and invasion, respectively. Cell apoptosis was determined by flow cytometry analysis, and protein level was measured by Western blotting. The experimental results demonstrated that chelidonine treatment inhibited cell viability and cell proliferation but facilitated cell apoptosis of melanoma cells. Besides, chelidonine suppressed melanoma cancer cell migration and invasion by attenuating epithelial-mesenchymal transition process. Moreover, chelidonine inhibited the activation of TLR4/NF-κB and PI3K/AKT pathways by downregulation of the protein level of TLR4, phosphorylated p65, phosphorylated PI3K, and phosphorylated AKT in melanoma cells. Furthermore, TAK-242 or LY294002 further enhanced the inhibitory effects chelidonine of on malignant cell behavior. In conclusion, our findings demonstrate that chelidonine effectively suppresses the malignancy of melanoma cells through the inhibition of TLR4/NF-κB and PI3K/AKT signaling pathways, suggesting its potential as a promising therapeutic agent for melanoma treatment.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"509-5159"},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 inhibits MPP⁺-induced HT22 cell death by suppressing Bax activation and improving mitochondrial function. 蜂毒素通过抑制Bax激活和改善线粒体功能抑制MPP+诱导的HT22细胞死亡。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-07-01 Epub Date: 2025-01-06 DOI: 10.4196/kjpp.24.293

Tingting Yu, Zirui Yuan, Jiaona Yu, Lu Chen, Wei Hao, Xiaohui Xu

{"title":"Melittin inhibits MPP+-induced HT22 cell death by suppressing Bax activation and improving mitochondrial function.","authors":"Tingting Yu, Zirui Yuan, Jiaona Yu, Lu Chen, Wei Hao, Xiaohui Xu","doi":"10.4196/kjpp.24.293","DOIUrl":"10.4196/kjpp.24.293","url":null,"abstract":"Melittin (MEL) is the main bioactive component of bee venom and has been reported to have various pharmacological effects. This study investigates the protective effect of MEL on MPP+-injured HT22 cells and the possible mechanisms involved. We treated the cells with 4 mM MPP+ for 24 h to induce a cellular injury model. HT22 cells were pretreated with 0.1 μM MEL for 6 h and then exposed to 4 mM MPP+ for 24 h. We measured cell viability, the expression of Bax, the indicators and protein levels associated with apoptosis and parthanatos, and the co-localisation of MEL and mitochondria, and mitochondrial function-related indices such as the mitochondrial membrane potential (MMP) and mito-SOX. We show that PAR protein expression was significantly increased in the MPP+-treated cell model and that the parthanatos inhibitor DPQ significantly reduced MPP+-induced cell death, suggesting that MPP+ can cause PARP1-dependent cell death. MEL significantly inhibited cell death, increased cell viability as well as NAD+ and ATP levels, increased the expression of Bcl-2 and suppressed the activation of Bax, cleaved-caspase3, and cleaved-PARP1. Moreover, MEL was found to be localised on the mitochondria of HT22 cells and to improve mitochondrial functions including increased MMP and decreased mitochondrial reactive oxygen species. We speculate that MEL may protect neurons against MPP+-induced HT22 cell injury by inhibiting Bax activation, suppressing changes in mitochondrial permeability, and improving mitochondrial function, thereby preventing cell parthanatos and apoptosis.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"487-496"},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198447/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Wogonin inhibits radiation-induced DNA damage repair in hepatocellular carcinoma cells by upregulating p21. Wogonin通过上调p21抑制辐射诱导的肝癌细胞DNA损伤修复。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-07-01 Epub Date: 2025-02-06 DOI: 10.4196/kjpp.24.213

Xiao Xu, Yonghong Qian, Shusheng Zhu, Hu Tian, Pingping Zhai, Shimin Zhu, Jingjing Wang, Lei Xie, Songbing Qin

{"title":"Wogonin inhibits radiation-induced DNA damage repair in hepatocellular carcinoma cells by upregulating p21.","authors":"Xiao Xu, Yonghong Qian, Shusheng Zhu, Hu Tian, Pingping Zhai, Shimin Zhu, Jingjing Wang, Lei Xie, Songbing Qin","doi":"10.4196/kjpp.24.213","DOIUrl":"10.4196/kjpp.24.213","url":null,"abstract":"Wogonin has been shown to exhibit anti-tumor effects by regulating the growth and inducing cell death in hepatocellular carcinoma (HCC) cells. However, its impact on radiotherapy for HCC remains unclear. This study aimed to elucidate the mechanisms and effects of wogonin in enhancing radiotherapy for HCC. The viability and cell cycle of HCC cells were assessed using CCK-8, trypan blue dye exclusion, and flow cytometry. RNA sequencing was performed to explore the genomic effects of wogonin on HCC cells. Immunofluorescence staining was employed to detect γ-H2AX distribution, and Western blot was used to evaluate the expression of γ-H2AX and p21. Wogonin induced cell cycle arrest and inhibited DNA damage repair in SMMC-7721 and HCC-LM3 cells following irradiation. RNA sequencing analysis of wogonin-and radiation-treated cells revealed significant enrichment of genes related to cell cycle progression, with notable changes in CDK inhibitor expression. Furthermore, wogonin in combination with irradiation increased the expression of γ-H2AX and p21 in HCC cells. Notably, p21 interference partially abrogated the anti-tumor effects of wogonin and radiation. Wogonin enhances the efficacy of radiotherapy in HCC by promoting cell cycle arrest and inhibiting DNA damage repair through upregulation of p21.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"419-429"},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143256067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Tricyclic antidepressants dose-dependently modulate the biphasic activity of the TRPC5 channel through opioid receptors. 三环抗抑郁药通过阿片受体剂量依赖性调节TRPC5通道的双相活性。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-07-01 DOI: 10.4196/kjpp.25.121

Byeongseok Jeong, Ji Yeon Chung, Jae Yeoul Jun, Chansik Hong

{"title":"Tricyclic antidepressants dose-dependently modulate the biphasic activity of the TRPC5 channel through opioid receptors.","authors":"Byeongseok Jeong, Ji Yeon Chung, Jae Yeoul Jun, Chansik Hong","doi":"10.4196/kjpp.25.121","DOIUrl":"10.4196/kjpp.25.121","url":null,"abstract":"Tricyclic antidepressants (TCAs) have been widely used for the treatment of major depressive disorder and other psychiatric conditions. However, their clinical application has declined due to adverse side effects and the availability of newer antidepressants with improved safety profiles. TCAs primarily target serotonin and norepinephrine receptors but also interact with a variety of other receptors and ion channels, contributing to both their therapeutic and adverse effects. We previously reported that TCAs regulate transient receptor potential canonical type 4 (TRPC4) channels. In this study, we investigated whether TCAs similarly modulate TRPC5 channels. Using HEK293 cells overexpressing TRPC5, we measured TRPC5 currents and intracellular calcium levels. Without altering TRPC5 expression levels, TCAs (amitriptyline, desipramine, and imipramine) dose-dependently reduced inward currents through TRPC5, with IC₅₀ values of 2.9, 10.3, and 11.7 μM, respectively. Given that TCAs can act as off-target agonists at opioid receptors (ORs), we co-expressed TRPC5 with various OR subtypes (μ-, δ-, and κ-ORs). Our results revealed that at low concentrations, TCAs enhanced TRPC5 activation through OR stimulation, whereas at higher concentrations, competitive inhibition of TRPC5 activity predominated. The biphasic modulation of TRPC5 by TCAs may contribute to a wide spectrum of cardiovascular and neurological manifestations, depending on the dosage and clinical application. Overall, these findings enhance the pharmacological understanding of the molecular mechanisms underlying the actions of TCAs and emphasize the need for more targeted therapeutic approaches.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"29 4","pages":"455-464"},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144477864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Syringetin relieves bone cancer pain in rats induced by breast cancer cells through the ESR1/PRDM2 axis. 紫丁香素通过ESR1/PRDM2轴缓解乳腺癌细胞诱导的大鼠骨癌疼痛。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-07-01 Epub Date: 2025-04-11 DOI: 10.4196/kjpp.24.303

Yueping Chen, Xianhong Zhang, Jinfeng Yang, Junjun Li, Chunhui Huang

引用次数: 0

Activation of transient receptor potential vanilloid 3 is required for keratinocyte differentiation and epidermal barrier formation. 瞬时受体电位香草样蛋白3的激活是角化细胞分化和表皮屏障形成所必需的。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-07-01 Epub Date: 2025-04-28 DOI: 10.4196/kjpp.24.324

Elina Da Sol Chung, Yu Ran Nam, Hyun Jong Kim, Young Keul Jeon, Kyung Sun Park, Woo Kyung Kim, Sung Joon Kim, Joo Hyun Nam

{"title":"Activation of transient receptor potential vanilloid 3 is required for keratinocyte differentiation and epidermal barrier formation.","authors":"Elina Da Sol Chung, Yu Ran Nam, Hyun Jong Kim, Young Keul Jeon, Kyung Sun Park, Woo Kyung Kim, Sung Joon Kim, Joo Hyun Nam","doi":"10.4196/kjpp.24.324","DOIUrl":"10.4196/kjpp.24.324","url":null,"abstract":"Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca²+ signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and triggers the release of pro-inflammatory cytokines, causing inflammation and itching. However, the regulation of skin barrier recovery by TRPV3 and its expression during keratinocyte differentiation remain unexplored. This study aimed to investigate the role and expression levels of TRPV3 in keratinocyte differentiation and skin barrier recovery, focusing on the effects of varying TRPV3 activation using pharmacological agents. Differentiation of primary human keratinocytes was induced in high-calcium media, and TRPV3 activity and expression were assessed using patch-clamp, fura-2 fluorimetry, and immunoblotting. The effects of TRPV3 agonists on skin barrier recovery following tape stripping were evaluated by measuring transepidermal water loss in mice. Results showed that TRPV3 expression, current density, and agonist-induced [Ca2+]i changes increased with keratinocyte differentiation. The TRPV3 antagonist, ruthenium red, inhibited both keratinocyte differentiation and TRPV3 upregulation. TRPV3 agonists (2-APB/carvacrol) facilitated early differentiation but paradoxically downregulated TRPV3 expression at higher concentrations. Moderate TRPV3 activation by lower agonist concentrations enhanced skin barrier recovery, while higher concentrations hindered recovery and induced immune cell infiltration. These findings highlight the dual role of TRPV3 in skin homeostasis and suggest that targeted modulation of TRPV3 could be a promising strategy for treating skin disorders.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"409-418"},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144058061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Deciphering the role of nicotinamide metabolism and melanin-related genes in acute myocardial infarction: a machine learning approach integrating bioinformatics analysis. 解析烟酰胺代谢和黑色素相关基因在急性心肌梗死中的作用：一种整合生物信息学分析的机器学习方法。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-07-01 Epub Date: 2025-05-26 DOI: 10.4196/kjpp.24.431

Jun Li, Chao Li, Tao Qian

{"title":"Deciphering the role of nicotinamide metabolism and melanin-related genes in acute myocardial infarction: a machine learning approach integrating bioinformatics analysis.","authors":"Jun Li, Chao Li, Tao Qian","doi":"10.4196/kjpp.24.431","DOIUrl":"10.4196/kjpp.24.431","url":null,"abstract":"Acute myocardial infarction (AMI) represents a significant global mortality factor. Alterations in nicotinamide metabolism within the myocardium post-AMI can influence the progression of the condition. Additionally, melanin plays a crucial role in nicotinamide metabolism and exhibits anti-inflammatory properties. Nevertheless, the diagnostic biomarkers for AMI that are based on nicotinamide metabolism and melanin-associated genes remain poorly defined. In this study, the AMI transcriptomic data from the Gene Expression Omnibus were analyzed to identify differentially expressed genes (DEGs) intersecting with nicotinamide metabolism and melatonin-related genes. Machine learning algorithms, including RandomForest, least absolute shrinkage and selection operator, and support vector machine-recursive feature elimination, were applied to select feature genes. Diagnostic markers were further evaluated based on area under the curve from receiver operating characteristic analysis. We identified 14 candidate genes, refined to 4 key genes, with NAMPT and BST1 ultimately selected as diagnostic biomarkers. These were used to classify AMI into two molecular subtypes. Immune landscape analysis revealed increased infiltration of monocytes, neutrophils, macrophages, and parainflammation in AMI. Enrichment analyses showed DEGs were mainly involved in innate immune response and cytokine production. Additionally, hsa-miR-34a-5p and hsa-miR-181b-5p were identified as potential regulators of NAMPT and BST1. In summary, NAMPT and BST1 are promising diagnostic biomarkers associated with nicotinamide metabolism and melatonin in AMI. The molecular subtyping based on these genes will enhance the management and hierarchical treatment of AMI, offering significant implications for clinical diagnosis and therapeutic strategies.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"521-532"},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Cholestyramine in hemodialysis: a new approach for hyperphosphatemia management. 血液透析中的胆甾胺：治疗高磷血症的新方法。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-07-01 Epub Date: 2025-02-06 DOI: 10.4196/kjpp.24.269

Ahmed Essam Abd El Hady Ali Ghanem, Radwa Maher El Borolossy, Tamer Wahid El Said, Sara Mahmoud Zaki Shaheen

{"title":"Cholestyramine in hemodialysis: a new approach for hyperphosphatemia management.","authors":"Ahmed Essam Abd El Hady Ali Ghanem, Radwa Maher El Borolossy, Tamer Wahid El Said, Sara Mahmoud Zaki Shaheen","doi":"10.4196/kjpp.24.269","DOIUrl":"10.4196/kjpp.24.269","url":null,"abstract":"Hyperphosphatemia is a potentially life altering condition in end-stage renal disease patients who are on regular hemodialysis that can lead to cardiovascular calcification, metabolic bone disease and secondary hyperparathyroidism. Bile acid sequestrants are anion exchange resins bind to bile acids and phosphate in the intestine resulting in preventing intestinal absorption of dietary phosphate, interruption of bile acid homeostasis and reduction in low-density lipoprotein cholesterol levels. Cholestyramine is chosen for study in hemodialysis patients based on the effectiveness and safety of bile acid sequestrants such colestilan and colestipol in the treatment of hyperphosphatemia and hypercholesterolemia in hemodialysis patients. A prospective, interventional, randomized, double blinded, placebo-controlled two arm study was carried out to assess the efficacy of oral cholestyramine on reduction of serum phosphate level in adult hemodialysis patients. 76 eligible patients were randomly assigned to either a drug group or a placebo group for the 2-month study period. The protocol was approved by the institutional review board of the faculty of pharmacy Ain Shams University Ethical committee and has been registered on ClinicalTrials.gov: NCT05577507. Over the 2-month treatment period, patients in cholestyramine group showed a significant decline in serum phosphorus levels versus placebo group (4.6 mg/dl vs. 6.6 mg/dl; p < 0.001) and serum calcium-phosphorus product (40 mg2/dl2 vs. 59.8 mg2/dl2; p < 0.001). Median serum triglyceride and low-density lipoprotein cholesterol levels had decreased significantly versus baseline values in the cholestyramine group. Cholestyramine used with phosphate binders effectively lowers phosphorus levels, improves the lipid profile, and has mild adverse effects.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"465-473"},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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