Korean Journal of Physiology & Pharmacology最新文献_第2页

Microglial galectin-3 increases with aging in the mouse hippocampus. 小鼠海马小胶质半凝集素-3随着年龄的增长而增加。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-03-01 Epub Date: 2025-01-14 DOI: 10.4196/kjpp.24.196

Hyun Joo Shin, So Jeong Lee, Hyeong Seok An, Ha Nyeoung Choi, Eun Ae Jeong, Jaewoong Lee, Kyung Eun Kim, Bong-Hoi Choi, Seung Pil Yun, Dawon Kang, Sang Soo Kang, Gu Seob Roh

{"title":"Microglial galectin-3 increases with aging in the mouse hippocampus.","authors":"Hyun Joo Shin, So Jeong Lee, Hyeong Seok An, Ha Nyeoung Choi, Eun Ae Jeong, Jaewoong Lee, Kyung Eun Kim, Bong-Hoi Choi, Seung Pil Yun, Dawon Kang, Sang Soo Kang, Gu Seob Roh","doi":"10.4196/kjpp.24.196","DOIUrl":"10.4196/kjpp.24.196","url":null,"abstract":"Microglial activation during aging is associated with neuroinflammation and cognitive impairment. Galectin-3 plays a crucial role in microglial activation and phagocytosis. However, the role of galectin-3 in the aged brain is not completely understood. In the present study, we investigated aging-related mechanisms and microglial galectin-3 expression in the mouse hippocampus using female 6-, 12-, and 24-month-old C57BL/6 mice. Western blot analysis revealed neurodegeneration, blood-brain barrier leakage, and increased levels of neuroinflammation-related proteins in 24-month-old mice compared to 6- and 12-month-old mice. Immunohistochemistry revealed an increase in activated microglia in the hippocampus of 24-month-old mice compared to 6- and 12-month-old mice. Furthermore, we found more galectin-3 and triggering receptor expressed on myeloid cells-2-positive microglia in 24-month-old mice compared to 6- and 12-month-old mice. Using primary mouse microglial cells, galectin -3 was also increased by lipopolysaccharide treatment. These findings suggest that galectin-3 may play an important role in microglial activation and neuroinflammation during brain aging.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"215-225"},"PeriodicalIF":1.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142980688","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

Monotropein resists atherosclerosis by reducing inflammation, oxidative stress, and abnormal proliferation and migration of vascular smooth muscle cells.

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-03-01 DOI: 10.4196/kjpp.24.352

Hongliang Li, Bingqian Ye, Jiping Tian, Bofan Wang, Yiwen Zha, Shuying Zheng, Tan Ma, Wenwen Zhuang, Won Sun Park, Jingyan Liang

{"title":"Monotropein resists atherosclerosis by reducing inflammation, oxidative stress, and abnormal proliferation and migration of vascular smooth muscle cells.","authors":"Hongliang Li, Bingqian Ye, Jiping Tian, Bofan Wang, Yiwen Zha, Shuying Zheng, Tan Ma, Wenwen Zhuang, Won Sun Park, Jingyan Liang","doi":"10.4196/kjpp.24.352","DOIUrl":"10.4196/kjpp.24.352","url":null,"abstract":"Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR-/- mice given high-fat diet to investigate the effects of monotropein on atherosclerosis. Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"29 2","pages":"245-255"},"PeriodicalIF":1.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460811","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

Toxicity and efficacy study of a combination of two retinoic acids in an ApoE knockout mouse model of atherosclerosis. 两种维甲酸复方制剂在载脂蛋白E基因敲除小鼠动脉粥样硬化模型中的毒性和疗效研究。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-03-01 Epub Date: 2024-11-14 DOI: 10.4196/kjpp.24.165

Da Som Jeong, Ji-Young Lee, Hyo-Jeong Han, Soo Min Ko, Dong Hyun Lee, Yerin Lee, Young-Sik Park, Byong-Cheol Shin, Woo-Chan Son

{"title":"Toxicity and efficacy study of a combination of two retinoic acids in an ApoE knockout mouse model of atherosclerosis.","authors":"Da Som Jeong, Ji-Young Lee, Hyo-Jeong Han, Soo Min Ko, Dong Hyun Lee, Yerin Lee, Young-Sik Park, Byong-Cheol Shin, Woo-Chan Son","doi":"10.4196/kjpp.24.165","DOIUrl":"10.4196/kjpp.24.165","url":null,"abstract":"Atherosclerosis is a major contributor to cardiovascular disease, characterized by inflammation and lipid accumulation in arterial walls, leading to plaque formation. Elevated low-density lipoprotein cholesterol is a primary risk factor for atherosclerosis. All-trans retinoic acid (ATRA), a metabolite of vitamin A, has demonstrated anti-inflammatory effects and potential in regulating vascular injury. 9-cisretinoic acid (9cRA) is an active metabolite of vitamin A and activates the retinoid X receptor. This study investigates whether potassium retinoate (PA9RA), a synthetic combination of ATRA and 9cRA, offers superior efficacy in treating atherosclerosis compared to established treatments such as clopidogrel and atorvastatin. Male ApoE-/- mice were fed a Western-type diet and treated with PA9RA, clopidogrel, or atorvastatin for 10 weeks. The body weight, organ weight, serum biochemistry, and histopathology, including atherosclerotic lesion area and liver steatosis were assessed. PA9RA treatment led to a significant reduction in body weight and inguinal fat, with the 45 mg/kg/day dose showing marked efficacy in decreasing atherosclerotic lesion size and ameliorating liver steatosis. Histopathological evaluation revealed decreased foam cell formation and improved liver histology in PA9RA-treated groups compared to controls. Notable side effects included epidermal hyperplasia and gastric hyperplasia at high doses of PA9RA. PA9RA exhibits superior efficacy over clopidogrel and atorvastatin in ameliorating atherosclerosis and fatty liver in ApoE-/- mice. This study highlights PA9RA's potential as a promising therapeutic agent for atherosclerosis. Further research is needed to elucidate its mechanisms of action and assess long-term safety and efficacy.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"179-189"},"PeriodicalIF":1.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142632840","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

Human induced pluripotent stem cell-cardiomyocytes for cardiotoxicity assessment: a comparative study of arrhythmiainducing drugs with multi-electrode array analysis.

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-03-01 DOI: 10.4196/kjpp.24.413

Na Kyeong Park, Yun-Gwi Park, Ji-Hee Choi, Hyung Kyu Choi, Sung-Hwan Moon, Soon-Jung Park, Seong Woo Choi

{"title":"Human induced pluripotent stem cell-cardiomyocytes for cardiotoxicity assessment: a comparative study of arrhythmiainducing drugs with multi-electrode array analysis.","authors":"Na Kyeong Park, Yun-Gwi Park, Ji-Hee Choi, Hyung Kyu Choi, Sung-Hwan Moon, Soon-Jung Park, Seong Woo Choi","doi":"10.4196/kjpp.24.413","DOIUrl":"10.4196/kjpp.24.413","url":null,"abstract":"Reliable preclinical models for assessing drug-induced cardiotoxicity are essential to reduce the high rate of drug withdrawals during development. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have emerged as a promising platform for such assessments due to their expression of cardiacspecific ion channels and electrophysiological properties. In this study, we investigated the effects of eight arrhythmogenic drugs-E4031, nifedipine, mexiletine, JNJ303, flecainide, moxifloxacin, quinidine, and ranolazine-on hiPSC-CMs derived from both healthy individuals and a long QT syndrome (LQTS) patient using multielectrode array systems. The results demonstrated dose-dependent changes in field potential duration and arrhythmogenic risk, with LQTS-derived hiPSC-CMs showing increased sensitivity to hERG channel blockers such as E4031. Furthermore, the study highlights the potential of hiPSC-CMs to model disease-specific cardiac responses, providing insights into genetic predispositions and personalized drug responses. Despite challenges related to the immaturity of hiPSC-CMs, their ability to recapitulate human cardiac electrophysiology makes them a valuable tool for preclinical cardiotoxicity assessments. This study underscores the utility of integrating patientderived hiPSC-CMs with advanced analytical platforms, such as multi-electrode array systems, to evaluate drug-induced electrophysiological changes. These findings reinforce the role of hiPSC-CMs in drug development, facilitating safer and more efficient screening methods while supporting precision medicine applications.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"29 2","pages":"257-269"},"PeriodicalIF":1.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460810","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.

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub 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":"https://doi.org/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 wogoninand 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":""},"PeriodicalIF":1.6,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","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.

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub 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":"https://doi.org/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":"128"},"PeriodicalIF":1.6,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","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 : 2025-01-06 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":"https://doi.org/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":""},"PeriodicalIF":1.6,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differential expression of ORAI channels and STIM proteins in renal cell carcinoma subtypes: implications for metastasis and therapeutic targeting. 肾细胞癌亚型中 ORAI 通道和 STIM 蛋白的差异表达：对转移和靶向治疗的影响。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-01-01 Epub Date: 2024-10-31 DOI: 10.4196/kjpp.24.126

Ji-Hee Kim, Kyu-Hee Hwang, Jiyeon Oh, Sung-Eun Kim, Mi-Young Lee, Tae Sic Lee, Seung-Kuy Cha

{"title":"Differential expression of ORAI channels and STIM proteins in renal cell carcinoma subtypes: implications for metastasis and therapeutic targeting.","authors":"Ji-Hee Kim, Kyu-Hee Hwang, Jiyeon Oh, Sung-Eun Kim, Mi-Young Lee, Tae Sic Lee, Seung-Kuy Cha","doi":"10.4196/kjpp.24.126","DOIUrl":"10.4196/kjpp.24.126","url":null,"abstract":"Renal cell carcinoma (RCC) presents significant clinical challenges, highlighting the importance of understanding its molecular mechanisms. While store-operated Ca2+ entry (SOCE) is known to play an essential role in tumorigenesis and metastasis, its specific implications across various RCC subtypes remain underexplored. This study analyzed SOCE-related mRNA profiles from the KIRC and KIRP projects in The Cancer Genome Atlas (TCGA) database, focusing on differential gene expression and overall survival outcomes. Functional studies in clear cell RCC (Caki-1) and papillary RCC cell lines (pRCC, Caki-2) revealed increased expression of Orai1 and Orai3, along with STIM1, exhibited in both subtypes, with decreased STIM2 and increased Orai2 expression in pRCC. Notably, Orai3 expression had a gender-specific impact on survival, particularly in females with pRCC, where it inversely correlated with STIM2 expression. Functional assays showed Orai3 dominance in Caki-2 and Orai1 in Caki- 1. Interestingly, 2-APB inhibited SOCE in Caki-1 but enhanced it in Caki-2, suggesting Orai3 as the primary SOCE channel in pRCC. Knockdown of Orai1 and Orai3 reduced cell migration and proliferation via regulating focal adhesion kinase (FAK) and Cyclin D1 in both cell lines. These findings highlight the critical roles of Orai1 and Orai3 in RCC metastasis, with Orai3 linked to poorer prognosis in females with pRCC. This study offers valuable insights into RCC diagnostics and potential therapeutic strategies targeting ORAI channels and STIM proteins.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"33-43"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142559472","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

Fine particulate matter induces osteoclast-mediated bone loss in mice. 细颗粒物会诱发小鼠破骨细胞介导的骨质流失。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-01-01 Epub Date: 2024-10-31 DOI: 10.4196/kjpp.24.115

Hye Young Mun, Septika Prismasari, Jeong Hee Hong, Hana Lee, Doyong Kim, Han Sung Kim, Dong Min Shin, Jung Yun Kang

{"title":"Fine particulate matter induces osteoclast-mediated bone loss in mice.","authors":"Hye Young Mun, Septika Prismasari, Jeong Hee Hong, Hana Lee, Doyong Kim, Han Sung Kim, Dong Min Shin, Jung Yun Kang","doi":"10.4196/kjpp.24.115","DOIUrl":"10.4196/kjpp.24.115","url":null,"abstract":"Fine particulate matter (FPM) is a major component of air pollution and has emerged as a significant global health concern owing to its adverse health effects. Previous studies have investigated the correlation between bone health and FPM through cohort or review studies. However, the effects of FPM exposure on bone health are poorly understood. This study aimed to investigate the effects of FPM on bone health and elucidate these effects in vitro and in vivo using mice. Micro-CT analysis in vivo revealed FPM exposure decreased bone mineral density, trabecular bone volume/total volume ratio, and trabecular number in the femurs of mice, while increasing trabecular separation. Histological analysis showed that the FPM-treated group had a reduced trabecular area and an increased number of osteoclasts in the bone tissue. Moreover, in vitro studies revealed that low concentrations of FPM significantly enhanced osteoclast differentiation. These findings further support the notion that short-term FPM exposure negatively impacts bone health, providing a foundation for further research on this topic.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"9-19"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142559473","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

Astragalus polysaccharide ameliorates diabetic retinopathy by inhibiting the SHH-Gli1-AQP1 signaling pathway in streptozotocin-induced type 2 diabetic rats. 黄芪多糖通过抑制链脲佐菌素诱导的2型糖尿病大鼠的SHH-Gli1-AQP1信号通路改善糖尿病视网膜病变

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2025-01-01 Epub Date: 2024-11-14 DOI: 10.4196/kjpp.23.251

Jingrong Qu, Bo Wang, Yulong Wang, Hao Li, Xiaomei An

{"title":"Astragalus polysaccharide ameliorates diabetic retinopathy by inhibiting the SHH-Gli1-AQP1 signaling pathway in streptozotocin-induced type 2 diabetic rats.","authors":"Jingrong Qu, Bo Wang, Yulong Wang, Hao Li, Xiaomei An","doi":"10.4196/kjpp.23.251","DOIUrl":"10.4196/kjpp.23.251","url":null,"abstract":"This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses. Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1- AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZ-induced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"21-32"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142632817","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