Journal of pharmacological sciences最新文献_第2页

Microtubule-dependent regulation of TMEM16A-mediated Ca2+-activated Cl− currents in vascular smooth muscle cells 血管平滑肌细胞中tmem16a介导的Ca2+激活Cl -电流的微管依赖性调节

IF 2.9 3区医学

Journal of pharmacological sciences Pub Date : 2025-09-06 DOI: 10.1016/j.jphs.2025.09.001

Ryosuke Hemmi , Akane Suzukawa , Moe Fujiwara , Rubii Kondo , Yoshiaki Suzuki , Aya Yamamura , Hisao Yamamura

引用次数: 0

Protective role of orphan G protein-coupled receptor GPR35 in the pathogenesis of colitis through regulating epithelial barrier function and immune responses 孤儿G蛋白偶联受体GPR35通过调节上皮屏障功能和免疫应答在结肠炎发病中的保护作用

IF 2.9 3区医学

Journal of pharmacological sciences Pub Date : 2025-08-27 DOI: 10.1016/j.jphs.2025.08.009

Koga Tokuyama , Hiroyuki Yasuda , Michiko Saito , Shusaku Hayashi , Shinichi Kato

{"title":"Protective role of orphan G protein-coupled receptor GPR35 in the pathogenesis of colitis through regulating epithelial barrier function and immune responses","authors":"Koga Tokuyama , Hiroyuki Yasuda , Michiko Saito , Shusaku Hayashi , Shinichi Kato","doi":"10.1016/j.jphs.2025.08.009","DOIUrl":"10.1016/j.jphs.2025.08.009","url":null,"abstract":"<div><h3>Background and objective</h3><div>GPR35 is involved in the pathogenesis of colitis. However, because GPR35 is expressed in colonic epithelial and inflammatory/immune cells, its precise protective mechanisms remain unclear. We investigated the role of GPR35 in colitis, especially its relation to epithelial barrier function and inflammatory/immune responses.</div></div><div><h3>Methods</h3><div>We performed GPR35 knockout (KO) in a dextran sodium sulfate (DSS)-induced murine colitis model and elucidated the role of GPR35 through various experiments, including histological analysis, intestinal permeability, immunohistochemical staining, RT-qPCR, and western blotting.</div></div><div><h3>Results</h3><div>GPR35KO mice exhibited significantly exacerbated DSS-induced colitis, accompanied by upregulation of cytokines, compared with wild-type (WT) mice. An investigation using bone marrow (BM)-chimeric mice revealed that GPR35KO, which is expressed in both hematopoietic and non-hematopoietic cells, contributed to this exacerbation. GPR35KO mice showed significantly increased intestinal permeability compared with WT mice under normal conditions. Although no differences were observed in goblet cell number or epithelial proliferation between WT and GPR35KO mice, the expression levels of intercellular junction proteins were significantly lower in the normal colons of GPR35KO mice. Lipopolysaccharide-stimulated cytokine expression was significantly enhanced in BM-derived macrophages obtained from GPR35KO mice compared with WT mice.</div></div><div><h3>Conclusions</h3><div>GPR35 contributes to colonic protection by regulating epithelial barrier function and inflammatory/immune responses.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"159 3","pages":"Pages 191-201"},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145026570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aprepitant attenuates cutaneous mast cell migration in oxaliplatin-treated mice 阿瑞吡坦减轻奥沙利铂治疗小鼠皮肤肥大细胞的迁移

IF 2.9 3区医学

Journal of pharmacological sciences Pub Date : 2025-08-25 DOI: 10.1016/j.jphs.2025.08.008

Tsugunobu Andoh

引用次数: 0

TRPV1 antagonist AMG9810 suppresses focal epileptiform discharges and seizures by decreasing extracellular glutamate concentrations in mice TRPV1拮抗剂AMG9810通过降低小鼠细胞外谷氨酸浓度抑制局灶性癫痫样放电和癫痫发作

IF 2.9 3区医学

Journal of pharmacological sciences Pub Date : 2025-08-22 DOI: 10.1016/j.jphs.2025.08.007

Hiroshi Moriyama , Hirochika Imoto , Sadahiro Nomura , Naomasa Mori , Yuichi Maruta , Natsumi Fujii , Shunsuke Fujitsuku , Hideyuki Ishihara

{"title":"TRPV1 antagonist AMG9810 suppresses focal epileptiform discharges and seizures by decreasing extracellular glutamate concentrations in mice","authors":"Hiroshi Moriyama , Hirochika Imoto , Sadahiro Nomura , Naomasa Mori , Yuichi Maruta , Natsumi Fujii , Shunsuke Fujitsuku , Hideyuki Ishihara","doi":"10.1016/j.jphs.2025.08.007","DOIUrl":"10.1016/j.jphs.2025.08.007","url":null,"abstract":"<div><div>The development of targeted anti-epilepsy drugs is crucial, as 30 % of patients with epilepsy are resistant to current therapeutics. Transient receptor potential vanilloid 1 (TRPV1) channel antagonists have been demonstrated to suppress drug-induced epileptiform discharges (EDs) and seizures (ESs). Here, we investigated the correlation between the anti-epileptiform efficacy of AMG9810 and extracellular glutamate levels. The somatosensory cortices of male C57BL/6N mice were intracortically injected with penicillin G (PG: 200 IU, 1 μL/10 min), a seizure inducer that inhibits the GABA<sub>A</sub> receptor. The mice were intracortically injected with AMG9810 (3 μM, 1 μL/10 min) either before or after PG administration. EDs, ESs, and glutamate levels were subsequently evaluated. The results of each experiment were compared between the vehicle and AMG9810-injected groups. AMG9810 injected after PG reduced glutamate levels and ED power, and there was a positive correlation between AMG9810 efficacy and these parameters. Injecting AMG9810 before PG injection decreased the increase in glutamate levels and development of EDs and ESs, with positive correlations observed among the three parameters. These findings suggest that TRPV1 antagonists suppress the development of EDs and ESs by decreasing extracellular glutamate levels, indicating that TRPV1 channels may represent a promising treatment option for epilepsy.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"159 3","pages":"Pages 163-171"},"PeriodicalIF":2.9,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144903646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Subacute intranasal oxytocin improves neurological recovery after ischemic stroke 亚急性鼻内催产素促进缺血性脑卒中后神经系统恢复

IF 2.9 3区医学

Journal of pharmacological sciences Pub Date : 2025-08-22 DOI: 10.1016/j.jphs.2025.08.006

Yusuke Morishita , Youichirou Higashi , Daichi Tani , Mio Togo , Takahiro Shimizu , Mikiya Fujieda , Motoaki Saito

{"title":"Subacute intranasal oxytocin improves neurological recovery after ischemic stroke","authors":"Yusuke Morishita , Youichirou Higashi , Daichi Tani , Mio Togo , Takahiro Shimizu , Mikiya Fujieda , Motoaki Saito","doi":"10.1016/j.jphs.2025.08.006","DOIUrl":"10.1016/j.jphs.2025.08.006","url":null,"abstract":"<div><div>Oxytocin (OXT) is a neuropeptide known for its anti-inflammatory and neuroprotective properties; however, its role in post-stroke recovery remains poorly defined. In this study, we investigated whether intranasal OXT administration during the subacute phase of stroke improves neurological outcomes and modulates microglial responses. Male mice underwent permanent middle cerebral artery occlusion and received intranasal OXT (300 ng/g) or saline on days 3 and 5 post-stroke. Neurological function was assessed using the modified neurological severity score; infarct volume was evaluated through hematoxylin-eosin (HE) staining, and survival rates were monitored until day 7. Immunofluorescence was used to assess microglial polarization in the peri-infarct region. OXT-treated mice showed significantly greater functional improvement and higher survival rates than saline-treated controls. Infarct volume was significantly reduced, and microglial polarization was altered by OXT, with a decrease in pro-inflammatory M1-type markers and an increase in anti-inflammatory M2-type markers. These findings demonstrate that OXT promotes neurological recovery through anti-inflammatory and neuroprotective mechanisms. Given its feasibility as a non-invasive delivery method, intranasal OXT may offer a promising therapeutic approach to enhance post-stroke neurorepair.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"159 3","pages":"Pages 151-158"},"PeriodicalIF":2.9,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144903632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sulfasalazine disrupts the interaction between TNFα and TNFR1 thus inhibiting NF-kB signaling activation to promote bone fracture healing 磺胺吡啶破坏TNFα和TNFR1之间的相互作用，从而抑制NF-kB信号激活，促进骨折愈合

IF 2.9 3区医学

Journal of pharmacological sciences Pub Date : 2025-08-21 DOI: 10.1016/j.jphs.2025.08.005

Jingwei Liu , Cheng Qiu , Xiaoxiong Wang , Ziqian Xiang , Junyuan Sun , Mingzheng Chang , Qingliang Ma , Yan Zhuang , Yunpeng Zhao , Qiang Yang , Lianlei Wang , Xinyu Liu

{"title":"Sulfasalazine disrupts the interaction between TNFα and TNFR1 thus inhibiting NF-kB signaling activation to promote bone fracture healing","authors":"Jingwei Liu , Cheng Qiu , Xiaoxiong Wang , Ziqian Xiang , Junyuan Sun , Mingzheng Chang , Qingliang Ma , Yan Zhuang , Yunpeng Zhao , Qiang Yang , Lianlei Wang , Xinyu Liu","doi":"10.1016/j.jphs.2025.08.005","DOIUrl":"10.1016/j.jphs.2025.08.005","url":null,"abstract":"<div><div>Fracture is a common type of traumas and alternative therapies to boost bone fracture healing is necessary. The aim of this study is to elucidate the role of sulfasalazine in bone fracture healing by using MC3T3-E1 cells in vitro and murine femoral fracture model in vivo. Western blotting, flow cytometry, RNA sequencing, Calcein AM/PI staining, Alizarin-Red-S staining, ALP activity assay, transmission electron microscope, histological staining, immunohistochemistry, immunofluorescence and Surface plasmon resonance analysis were performed in this study. Sulfasalazine failed to elicit ferroptosis in osteoblasts within acceptable dose manner while promoted osteogenic differentiation. Furthermore, sulfasalazine was identified to inhibit inflammation by declination of inflammatory biomarkers. Besides, TNFα was verified as a potential downstream target for sulfasalazine and the adverse effect of TNFα on osteogenic differentiation could be largely salvaged by sulfasalazine due to direct binding between these two molecules. RNA-seq further implied decreased transcription of genes related to NF-κB pathway. Murine study showed sulfasalazine promotes fracture healing as evidenced by increased bone remodeling both histologically and radiologically. Overall, sulfasalazine accelerates osteogenic differentiation and promotes bone healing by direct binding to and thus inhibiting TNFα, which subsequently suppresses NF-κB signaling. Therefore, sulfasalazine shows a promising outcome for the treatment of bone fracture.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"159 3","pages":"Pages 139-150"},"PeriodicalIF":2.9,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144902645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Protocatechuic aldehyde restrains NLRP3 inflammasome activation to alleviate inflammatory response in sepsis 原儿茶醛抑制NLRP3炎性体激活以减轻脓毒症的炎症反应

IF 2.9 3区医学

Journal of pharmacological sciences Pub Date : 2025-08-21 DOI: 10.1016/j.jphs.2025.08.003

Yu-fei Li , Ao Sun , Yang Miao , Hong-xia Wang , Lin-lin Zhang

{"title":"Protocatechuic aldehyde restrains NLRP3 inflammasome activation to alleviate inflammatory response in sepsis","authors":"Yu-fei Li , Ao Sun , Yang Miao , Hong-xia Wang , Lin-lin Zhang","doi":"10.1016/j.jphs.2025.08.003","DOIUrl":"10.1016/j.jphs.2025.08.003","url":null,"abstract":"<div><div>Sepsis, a life-threatening organ dysfunction syndrome triggered by infection, is characterized by complex pathophysiology involving dysregulated inflammation, coagulation abnormalities, and mitochondrial dysfunction. Excessive activation of the NLRP3 inflammasome plays a pivotal role in sepsis progression. This study investigated the therapeutic effects and underlying mechanisms of protocatechuic aldehyde (PCA) in sepsis. Seventy-five potential PCA targets for sepsis were identified, with KEGG enrichment highlighting involvement in inflammatory and apoptotic pathways. PPI network analysis pinpointed TNF, IL-6, and IL-1β as key inflammatory targets. PCA dose-dependently suppressed IL-1β and TNF-α release in LPS/ATP-stimulated macrophages, reduced ASC speck formation and NLRP3-ASC interaction, and decreased mt-ROS production and TXNIP-NLRP3 co-localization. PCA also preserved mitochondrial network integrity by interacting with mitochondrial dynamics proteins DRP1 and MFN2, improving mitochondrial membrane potential and morphology. In LPS-induced septic mice, PCA significantly reduced serum IL-1β and TNF-α levels, improved survival rates, and downregulated NLRP3, pro-IL-1β, and cleaved-IL-1β expression in peritoneal macrophages. PCA alleviates inflammatory responses and organ damage in septic mice by inhibiting the mt-ROS/TXNIP/NLRP3 signaling axis and maintaining mitochondrial function, offering a promising natural therapeutic candidate for sepsis.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"159 3","pages":"Pages 172-183"},"PeriodicalIF":2.9,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144908020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

(2R,6R)-hydroxynorketamine reverses mechanical and thermal pain hypersensitivity produced by the chemotherapeutic agent oxaliplatin in rats （2R,6R）-羟诺氯胺酮逆转大鼠化疗药物奥沙利铂产生的机械和热痛超敏反应

IF 2.9 3区医学

Journal of pharmacological sciences Pub Date : 2025-08-20 DOI: 10.1016/j.jphs.2025.08.004

Maria Campanile , Kaitlin Castell , Justin O. Pampalone , Bruno Carabelli , Irwin Lucki , Caroline A. Browne

{"title":"(2R,6R)-hydroxynorketamine reverses mechanical and thermal pain hypersensitivity produced by the chemotherapeutic agent oxaliplatin in rats","authors":"Maria Campanile , Kaitlin Castell , Justin O. Pampalone , Bruno Carabelli , Irwin Lucki , Caroline A. Browne","doi":"10.1016/j.jphs.2025.08.004","DOIUrl":"10.1016/j.jphs.2025.08.004","url":null,"abstract":"<div><div>Chemotherapy-induced peripheral neuropathy (CIPN) is a common and debilitating side effect of a number of anticancer drugs, like oxaliplatin, leading to chronic sensory hypersensitivity and neuropathic pain. This study investigated the efficacy of (2R,6R)-hydroxynorketamine ((2R,6R)-HNK), a metabolite of ketamine, in a rat model of CIPN induced by oxaliplatin. Rats treated with oxaliplatin developed long-lasting mechanical and thermal hypersensitivity, as assessed by the Von Frey test and the hot plate test, respectively. A single injection of (2R,6R)-HNK (30 mg/kg, s.c.) significantly reversed both mechanical and thermal hypersensitivity for up to 24 h. Furthermore, repeated treatment with (2R,6R)-HNK (30 mg/kg/day) for 7 days produced sustained analgesia on mechanical hypersensitivity that persisted up to 14 days after treatment cessation. In comparison, repeated duloxetine (15 mg/kg/day, s.c.) showed only a short-lasting reduction of thermal hypersensitivity and no effect on mechanical hypersensitivity. Locomotor activity was not affected by (2R,6R)-HNK treatment, although duloxetine caused a transient decrease. This is the first demonstration that (2R,6R)-HNK produced analgesia in a rat model of CIPN. The persistence of analgesia with repeated treatment and sustained effects following treatment cessation suggests that (2R,6R)-HNK may represent a promising new therapeutic strategy for the rapid and sustained relief of pain associated with CIPN.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"159 3","pages":"Pages 184-190"},"PeriodicalIF":2.9,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144917546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Theanine boosts frontal theta and hippocampal beta and gamma oscillations for familiarity in object recognition 茶氨酸促进额叶θ波和海马β波和γ波的振荡，以熟悉物体识别

IF 2.9 3区医学

Journal of pharmacological sciences Pub Date : 2025-08-13 DOI: 10.1016/j.jphs.2025.08.002

Kisa Watanabe , Kinjiro Takeda , Takeshi Nagahiro , Sena Iijima , Yuji Ikegaya , Nobuyoshi Matsumoto

{"title":"Theanine boosts frontal theta and hippocampal beta and gamma oscillations for familiarity in object recognition","authors":"Kisa Watanabe , Kinjiro Takeda , Takeshi Nagahiro , Sena Iijima , Yuji Ikegaya , Nobuyoshi Matsumoto","doi":"10.1016/j.jphs.2025.08.002","DOIUrl":"10.1016/j.jphs.2025.08.002","url":null,"abstract":"<div><div>Object recognition memory encourages animals to distinguish between new and known objects, supported by neural activity in the hippocampus, prefrontal cortex, and perirhinal cortex. Theanine, a non-proteinogenic amino acid derivative from green tea leaves, enhances object recognition memory in rats through facilitated neurogenesis. Although the cellular mechanism for the theanine-enhanced object recognition memory has been elucidated to some extent, physiological evidence still remains unclear. To tackle this issue, we chronically fed mice with theanine (or tap water) for three weeks, implanted electrodes into the hippocampus and frontal cortex, both of which are responsible for object recognition memory. We then recorded the local field potentials from the two regions during the novel object recognition task, evaluated the memory performance, and broke down the neural signals in the hippocampus and frontal cortex into delta, theta, beta, low gamma, and high gamma frequency bands. The memory performance of theanine-treated mice was higher than that of vehicle-treated mice. We also found that theta oscillations in the frontal cortex and beta and low gamma oscillations in the hippocampus in theanine-treated mice were simultaneously enhanced for familiar objects. These results shed light on the new physiological underpinnings of object recognition memory enhanced by exogenous substances.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"159 3","pages":"Pages 129-138"},"PeriodicalIF":2.9,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lactucin alleviates lipid accumulation via AMPK-mediated autophagy and fatty acid β-oxidation in FFA-induced HepG2 cells 乳酸素通过ampk介导的自噬和脂肪酸β-氧化在ffa诱导的HepG2细胞中减轻脂质积累

IF 2.9 3区医学

Journal of pharmacological sciences Pub Date : 2025-08-08 DOI: 10.1016/j.jphs.2025.08.001

Xiaoyan Ma , Yilizere Aibaidula , Chunzi Zhang , Shuwen Qi , Tuxia Pang , Juan Zhang , Wenhui Hou , Xiaoli Ma

{"title":"Lactucin alleviates lipid accumulation via AMPK-mediated autophagy and fatty acid β-oxidation in FFA-induced HepG2 cells","authors":"Xiaoyan Ma , Yilizere Aibaidula , Chunzi Zhang , Shuwen Qi , Tuxia Pang , Juan Zhang , Wenhui Hou , Xiaoli Ma","doi":"10.1016/j.jphs.2025.08.001","DOIUrl":"10.1016/j.jphs.2025.08.001","url":null,"abstract":"<div><div>Lactucin is a natural sesquiterpene lactone isolated from <em>Cichorium glandulosum</em> Boiss. et Huet (CG) has unique biological and pharmaceutical properties. This study was designed to investigate the mechanisms by which Lactucin inhibits lipid accumulation in free fatty acid (FFA)-treated HepG2 cells. We demonstrated that Lactucin exerts a protective effect against hepatic steatosis in vitro. In FFA-induced HepG2 cells, Lactucin effectively ameliorated lipid accumulation, oxidative stress, and mitochondrial dysfunction. Mechanistically, we showed that activation of AMP-activated protein kinase (AMPK) and hormone-sensitive lipase (HSL) by Lactucin promoted lipolysis and further enhanced fatty acid β-oxidation (FAβO) by increasing the activity of FAβO-related enzymes, thereby contributing to the reduction of lipid accumulation. Moreover, Lactucin activated autophagy and modulated the AMPK/mammalian target of rapamycin (mTOR) signaling pathway. Notably, we found that Lactucin-induced autophagy played a significant role in decreasing lipid droplet accumulation, suggesting it may be a key underlying mechanism. These findings, for the first time, provide new insights into the pharmaceutical mechanism of Lactucin in protecting against nonalcoholic fatty liver disease (NAFLD).</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"159 2","pages":"Pages 116-127"},"PeriodicalIF":2.9,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144826763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0