Journal of pharmacological sciences最新文献

{"title":"Specnuezhenide and ecliptasaponin A from Ligustrum lucidum Ait and Ecliptae Herba improved premature ovarian failure by targeting the ESR1","authors":"Jia Xu ,&nbsp;Lei Lei ,&nbsp;Ping Li ,&nbsp;Zi-Chun Huang ,&nbsp;Ying Meng ,&nbsp;Bing He ,&nbsp;Ji-Lin Kuang","doi":"10.1016/j.jphs.2025.02.011","DOIUrl":"10.1016/j.jphs.2025.02.011","url":null,"abstract":"<div><div>This study was designed to investigate the role of <em>Ligustrum lucidum Ait</em> and <em>Ecliptae Herba</em> on premature ovarian failure (POF) and the underlying mechanisms. In the POF mouse model constructed using cyclophosphamide (CTX), <em>Ligustrum lucidum Ait</em> and <em>Ecliptae Herba</em> increased ovarian index and estradiol (E2) levels and curtailed motility and follicle-stimulating hormone (FSH). <em>Ligustrum lucidum Ait</em> and <em>Ecliptae Herba</em> alleviated ovarian pathological damage in POF mice and promoted the expression of ovarian CD31 and Vascular Endothelial Growth Factor A (VEGFA). Through high-performance liquid chromatography-mass spectrometry (HPLC-MS) and network pharmacology, Specnuezhenide and ecliptasaponin A were identified as the key components of <em>Ligustrum lucidum Ait</em> and <em>Ecliptae Herba</em> in anti-POF action. The important target associated with these components is Estrogen Receptor (ESR) 1. Molecular docking and <em>in vitro</em> experiments showed that Specnuezhenide and ecliptasaponin A can both bind to the ESR protein; knocking down ESR1 inhibited the anti-apoptotic effect of Specnuezhenide and ecliptasaponin A on CTX-induced POF cells. In conclusion, the key components of <em>Ligustrum lucidum Ait</em> and <em>Ecliptae Herba</em> that alleviate POF are Specnuezhenide and ecliptasaponin A, which improve the condition by upregulating ESR1.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 1","pages":"Pages 13-26"},"PeriodicalIF":3.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143578354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Possible involvement of α, β-unsaturated carbonyl compounds in ferroptosis induced by the cigarette smoke extract of heated tobacco products in vascular smooth muscle cells","authors":"Takahiro Horinouchi ,&nbsp;Yuichi Mazaki ,&nbsp;Soichi Miwa","doi":"10.1016/j.jphs.2025.02.010","DOIUrl":"10.1016/j.jphs.2025.02.010","url":null,"abstract":"<div><div>In this study, we aimed to determine the cytotoxic factors involved in ferroptosis induced by nicotine- and tar-free cigarette smoke extract (CSE) from heated tobacco products (HTPs) in vascular smooth muscle cells. CSE decreased mitochondrial metabolic activity and increased lactate dehydrogenase leakage. These cytotoxic effects completely disappeared after removing the carbonyls from the mainstream smoke. α, β-Unsaturated carbonyl compounds (acrolein, methyl vinyl ketone, crotonaldehyde, and methacrolein) in the mainstream smoke of HTPs and CSE caused cell damage, which was inhibited by a ferroptosis inhibitor, UAMC-3203. These results suggest that α, β-unsaturated carbonyl compounds might be involved in CSE-induced ferroptosis.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 1","pages":"Pages 8-12"},"PeriodicalIF":3.0,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143550935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Senescent cardiac fibroblasts-derived extracellular vesicles induced autophagy in cardiac fibroblasts via suppression of ras homolog enriched in brain like 1","authors":"Yusei Fujioka,&nbsp;Kosuke Otani,&nbsp;Muneyoshi Okada,&nbsp;Hideyuki Yamawaki","doi":"10.1016/j.jphs.2025.02.007","DOIUrl":"10.1016/j.jphs.2025.02.007","url":null,"abstract":"<div><div>Cardiac fibroblasts (CFs) play roles in the maintenance of myocardial tissue structure. Cellular senescence is a state of stable cell cycle arrest. We previously reported that extracellular vesicles (EV) secreted by doxorubicin (DOX, 1000 nM)-induced senescent CFs (D10³-EV) caused autophagy in CFs. EV mediate cell-to-cell communication through the transfer of microRNA (miRNA). In this study, we focused on miRNA contained in EV and aimed to elucidate mechanisms underlying the autophagy induction by D10³-EV in CFs. Neonatal rat CFs (NRCFs) were treated with DOX for the induction of cellular senescence. EV were isolated from culture media of NRCFs. miRNA was extracted from the EV and miRNA profiles were analyzed using miRNA-seq. Seven miRNAs were significantly decreased, whereas 14 miRNAs were significantly increased in D10³-EV compared with the vehicle-treated NRCFs-derived EV. Among the target genes of 14 miRNAs, <em>Rhebl1</em> was identified. D10³-EV significantly increased microtubule-associated protein 1 light chain 3 (LC3)-II/LC3-I and decreased protein expression of Ras homolog enriched in brain like 1 (RHEBL1) in NRCFs. Small interfering RNA against <em>Rhebl1</em> tended to increase LC3-II/LC3-I. In conclusion, we for the first time revealed that the senescent NRCFs-derived EV induced autophagy in NRCFs via the suppression of RHEBL1 protein.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"158 1","pages":"Pages 1-7"},"PeriodicalIF":3.0,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143529791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Midnolin gene expression is enhanced by Gq-coupled muscarinic acetylcholine receptor stimulation in SH-SY5Y human neuroblastoma cells","authors":"Ikuo Norota ,&nbsp;Yusuke Zuiki ,&nbsp;Ayano Chiba ,&nbsp;Mikako Nagashima ,&nbsp;Jiro Ogura ,&nbsp;Hiroaki Yamaguchi ,&nbsp;Kuniaki Ishii ,&nbsp;Yutaro Obara","doi":"10.1016/j.jphs.2025.02.006","DOIUrl":"10.1016/j.jphs.2025.02.006","url":null,"abstract":"<div><div>We previously demonstrated that the midnolin gene (<em>MIDN</em>) is a risk factor for Parkinson's disease (PD) in Yamagata and British cohorts, and that neurite outgrowth is abolished by <em>MIDN</em> knockout in PC12 cells. Therefore, drugs that upregulate <em>MIDN</em> may have neurotrophic effects. In this study, acetylcholine increased <em>MIDN</em> promoter activity and gene expression in a concentration-dependent manner in SH-SY5Y cells. These effects were suppressed by atropine and a G_q inhibitor, YM254890, indicating that muscarinic receptor/G_q signaling is required for the induction of <em>MIDN</em> by acetylcholine. Our findings suggest that drugs that upregulate <em>MIDN</em> may have therapeutic potential for PD.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"157 4","pages":"Pages 229-232"},"PeriodicalIF":3.0,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of netrin-1/DCC signaling pathway by Jiawei Kongsheng Zhenzhong Pill improves synaptic structural plasticity in PSD rats","authors":"Yue Zhao ,&nbsp;Aizhen Song ,&nbsp;Guowei Liu ,&nbsp;Qiuyue Chen ,&nbsp;Qiaolan Wu ,&nbsp;Zu Gao ,&nbsp;Zifa Li ,&nbsp;Huayun Yu ,&nbsp;Zhichun Wu","doi":"10.1016/j.jphs.2025.02.004","DOIUrl":"10.1016/j.jphs.2025.02.004","url":null,"abstract":"<div><div>Jiawei Kongsheng Zhenzhong Pill(JKZP) is based on Kongsheng Zhenzhong Pill contained in the Tang Dynasty's “<em>Thousand Golden Prescriptions</em>,” which exhibited good anti-ischemic and antidepressant effects in the previous study. However, its specific effects on post-stroke depression (PSD) and the mechanism are not clear. This study aimed to investigate the effects of JKZP in the treatment of PSD and related mechanisms. The decoction of JKZP was first analyzed for its medicinal chemical composition and screened for representative components of JKZP. The Middle cerebral artery occlusion (MCAO) method combined with solitary rearing and chronic unpredictable mild stress (CUMS) was used to establish a rat model of PSD, and to observe the effects of JKZP on the behavior and synaptic plasticity of PSD rats, and to investigate the mechanism of JKZP in the treatment of PSD by detecting the mRNA level, protein expression and activity of Netrin-1/DCC signaling pathway-related proteins. The results showed that the JKZP decoction contained loganin, β-asarone and other pharmaceutical ingredients, which have been reported to protect against cerebral ischemic injury and antidepressant effects. JKZP significantly improved the depression-like behavior of PSD rats and improved the damage to pyramidal neurons in the medial prefrontal cortex (mPFC) of PSD rats. Moreover, JKZP increased the density of dendritic spines in the mPFC of PSD rats, improved synaptic gap width and thickness of the post-synaptic density, and increased the number of synaptic vesicles. The results of Real-Time quantitative reverse transcription PCR (qRT-PCR), Western blotting, and pull-down assays revealed that JKZP increased netrin-1, deleted in colorectal cancer (DCC), and focal adhesion kinase (FAK) mRNA and protein expression, elevated the <em>p</em>-FAK/FAK ratio, and decreased myosin II protein expression and Ras homolog gene family member A (RhoA-GTP) activity in the mPFC of PSD rats. Taken together, JKZP can affect synaptic structural remodeling and improve depressive manifestations and neuronal damage in PSD rats by regulating the expression and activity of signaling molecules related to the netrin-1/DCC signaling pathway.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"157 4","pages":"Pages 242-252"},"PeriodicalIF":3.0,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143511865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YAP activation in Müller cells alleviates oxidative stress in the rat retina after intravitreal injection with methylglyoxal","authors":"Toshihide Kashihara,&nbsp;Mayuko Yasaki,&nbsp;Yumi Okuyama,&nbsp;Aki Murayama,&nbsp;Akane Morita,&nbsp;Tsutomu Nakahara","doi":"10.1016/j.jphs.2025.02.005","DOIUrl":"10.1016/j.jphs.2025.02.005","url":null,"abstract":"<div><div>Methylglyoxal (MGO), a highly reactive dicarbonyl compound produced via the glycolytic pathway, plays a key role in the pathogenesis of various diabetic complications, such as diabetic retinopathy. Müller cells provide neurotrophic support and maintain retinal homeostasis, including the redox balance. This dysfunction leads to retinal disease. Yes-associated protein (YAP), a major downstream effector of the Hippo pathway, plays a crucial role in regulating cell survival. In this study, we investigated the roles of Müller cell YAP during MGO-induced retinal injury using normal rats intravitreally injected with MGO and a rat Müller cell line (rMC-1). Immunohistochemistry revealed that MGO injection increased the glial fibrillary acidic protein immunoreactivity in Müller cells. The alignment of Müller cell nuclei was disrupted in MGO-treated retinas. YAP increased and activated in Müller cells two days after MGO injection. This increase in YAP levels was independent of the Hippo pathway and partially attributed to the upregulation of <em>YAP</em> mRNA levels. YAP inhibition by verteporfin exacerbated MGO-induced cell damage and decreased Bcl-xL levels in rMC-1 cells. Intravitreal verteporfin injection also enhanced MGO-induced retinal oxidative stress. Overall, our findings suggest that YAP activation in Müller cells alleviates oxidative stress in the retina following MGO-induced retinal injury.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"157 4","pages":"Pages 219-228"},"PeriodicalIF":3.0,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spinal dorsal horn neurons involved in the alleviating effects of cannabinoid receptor agonists on neuropathic allodynia-like behaviors in rats","authors":"Daichi Sueto ,&nbsp;Eriko I ,&nbsp;Akihisa Onishi ,&nbsp;Makoto Tsuda","doi":"10.1016/j.jphs.2025.02.008","DOIUrl":"10.1016/j.jphs.2025.02.008","url":null,"abstract":"<div><div>Mechanical allodynia, the pain caused by innocuous tactile stimuli, is a hallmark symptom of neuropathic pain that is often resistant to currently available treatments. Cannabinoids are widely used for pain management; however, their therapeutic mechanisms for neuropathic mechanical allodynia remain unclear. Using transgenic rats that enable to optogenetically stimulate touch-sensing Aβ fibers in the skin, we found that the intrathecal administration of the synthetic cannabinoid, WIN 55,212-2, alleviated the Aβ fiber-derived neuropathic allodynia. Furthermore, we injected adeno-associated virus vectors incorporating the rat cannabinoid receptor 1 (CB₁ receptor) (encoded by <em>Cnr1</em>) promoter and tdTomato or short hairpin RNA targeting the CB₁ receptor into the spinal dorsal horn (SDH) and demonstrated that the conditional knockdown of CB₁ receptors in <em>Cnr1</em>⁺ SDH neurons attenuates the anti-allodynic effects of intrathecally administered WIN 55,212-2. Electrophysiological analysis revealed that <em>Cnr1</em>⁺ SDH neurons received excitatory synaptic inputs from the primary afferent Aβ fibers. Collectively, our results suggest that the CB₁ receptors in <em>Cnr1</em>⁺ SDH neurons are molecular and cellular targets of intrathecal WIN 55,212-2 to alleviate neuropathic allodynia.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"157 4","pages":"Pages 253-260"},"PeriodicalIF":3.0,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143511866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Japanese black vinegar Kurozu promotes lifespan and healthspan extension in Caenorhabditis elegans","authors":"Yutaro Fukushima ,&nbsp;Asuka Kagami ,&nbsp;Hirotaka Sonoda ,&nbsp;Kotomi Shimokawa ,&nbsp;Sota Nishikawa ,&nbsp;Mary Ann Suico ,&nbsp;Hirofumi Kai ,&nbsp;Marina Miyazaki ,&nbsp;Kanta Torigoe ,&nbsp;Yuki Yoshinaga ,&nbsp;Yoshiyuki Matsumoto ,&nbsp;Tsuyoshi Shuto","doi":"10.1016/j.jphs.2025.02.003","DOIUrl":"10.1016/j.jphs.2025.02.003","url":null,"abstract":"<div><div>Kurozu, a traditional Japanese black vinegar (JBV), is produced from steamed unpolished rice, koji, and water through saccharification, alcoholic fermentation, and acetic fermentation. These processes result in a vinegar rich in amino acids, vitamins, organic acids, and proteins. While Kurozu has demonstrated benefits, including anti-oxidative and anti-adipogenic activities, its effects on health at the organismal level remain poorly understood. This study aimed to evaluate the impact of Kurozu on healthspan of <em>Caenorhabditis elegans</em> (<em>C. elegans</em>) using the <em>C. elegans</em> Health lifespan Auto-monitoring System (C-HAS). Kurozu concentrated liquid (KCL) was tested at concentrations ranging from 0.005% to 0.5%. Results showed that 0.5% KCL significantly extended lifespan and healthspan, particularly when heat-killed (HK) <em>E. coli</em> OP50 was provided as the food source. In contrast, the lifespan- and healthspan-extending effects at 0.5% KCL were abolished when live <em>E. coli</em> was used as the food source. This suggests that active components in KCL may be metabolized by live bacteria, diminishing their beneficial effects. Further reproducibility tests at 0.5% and 1% KCL concentrations confirmed the healthspan-extending effects under conditions of dead bacterial feeding. This study highlights the health-promoting impact of KCL and provides new insights into its role as a functional food ingredient.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"157 4","pages":"Pages 233-241"},"PeriodicalIF":3.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143508143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective effects of compounds interacting with carrier-mediated amantadine transport across the blood–retinal barrier in rats","authors":"Yusuke Shinozaki,&nbsp;Shin-ichi Akanuma,&nbsp;Yuma Tega,&nbsp;Ken-ichi Hosoya","doi":"10.1016/j.jphs.2025.02.002","DOIUrl":"10.1016/j.jphs.2025.02.002","url":null,"abstract":"<div><div>Retinal drug delivery via peripheral administration enhances the safety and efficacy of retinal pharmacotherapy. As retinal drug distribution from the circulating blood is limited by the blood–retinal barrier (BRB), BRB-permeable retinal drugs with potent pharmacological effects are needed for peripheral administration. Our previous research indicated carrier-mediated retinal transport of amantadine, which has neuroprotective effects by inhibiting N-methyl-<span>d</span>-aspartate receptors, across the BRB. As several amantadine derivatives are also suggestive to strongly interact with the carrier-mediated amantadine transport at the BRB, these compounds are proposed as candidates for the treatment of retinal diseases after peripheral administration. To find the appropriate retinal drug candidate, neuroprotective effects of compounds interacting with carrier-mediated amantadine transport across the BRB were firstly evaluated using primary-cultured rat cortical neurons. As a result, N'-(1-adamantyl)ethane-1,2-diamine (test compound) exerted the most potent neuroprotective effects. In addition, this test compound indicated neuroprotective effects against retinal damage after intraperitoneal administration in retinal damage rats. Our findings suggest the test compound, which interacts with carrier-mediated amantadine transport across the BRB and protected neurons from excitotoxicity <em>in vitro</em>, is a key agent to develop the pharmacotherapy with peripheral administration of medicines for retinal diseases.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"157 4","pages":"Pages 212-218"},"PeriodicalIF":3.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intraoral treatment of persimmon tannin, a polyphenol extracted from persimmon, significantly ameliorates gingivitis, plaque and halitosis via directly influence the periodontal bacteria Porphyromonas gulae","authors":"Megu Toyooka ,&nbsp;Mao Kaneki ,&nbsp;Chiharu Ohira ,&nbsp;Azusa Hachiya ,&nbsp;Tomoki Fukuyama","doi":"10.1016/j.jphs.2025.02.001","DOIUrl":"10.1016/j.jphs.2025.02.001","url":null,"abstract":"<div><h3>Background</h3><div>As periodontal disease (PD) is an irreversible disorder, preventive dentistry in human and veterinary medicine has become pertinent. This study focused on <em>persimmon tannin</em> (PT) and examined its bactericidal, anti-halitosis, and anti-inflammatory effects by focusing on <em>Porphyromonas gulae</em> (<em>P. gulae</em>).</div></div><div><h3>Methods</h3><div>The direct effects of PT on <em>P. gulae</em> were evaluated <em>in vitro.</em> Pro-inflammatory cytokines secretion induced by <em>P. gulae</em> in the macrophage cell lines were determined. A clinical study in dogs with <em>P. gulae</em>-associated PD was performed by one-month intraoral treatment with 0.1% PT-containing gel.</div></div><div><h3>Results</h3><div>PT exhibited a significant bactericidal effect to <em>P. gulae</em>. The biofilm formation and methyl mercaptan generated by <em>P. gulae</em> was significantly decreased by PT even after a short exposure period. <em>P. gulae</em>-induced proinflammatory cytokine production in macrophage cell lines was inhibited by PT treatment in a dose-dependent manner. In a clinical study of dogs, intraoral treatment with 0.1% PT did not significantly influence the gingivitis and plaque scores, however, the concentrations of hydrogen sulfide and methyl mercaptan were also significantly decreased by the PT treatment. Although there was no anti-bacterial <em>in vitro</em>, <em>P. gulae</em> activity and DNA detection decreased with PT treatment.</div></div><div><h3>Conclusions</h3><div>These findings suggest that intraoral administration of PT can prevent PD.</div></div>","PeriodicalId":16786,"journal":{"name":"Journal of pharmacological sciences","volume":"157 4","pages":"Pages 203-211"},"PeriodicalIF":3.0,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}