Korean Journal of Physiology & Pharmacology最新文献_第7页

The NADPH oxidase inhibitor diphenyleneiodonium suppresses Ca²⁺ signaling and contraction in rat cardiac myocytes. NADPH 氧化酶抑制剂二苯基碘抑制大鼠心肌细胞的 Ca2+ 信号传导和收缩。

IF 1.6 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2024-07-01 DOI: 10.4196/kjpp.2024.28.4.335

Qui Anh Le, Tran Nguyet Trinh, Phuong Kim Luong, Vu Thi Van Anh, Ha Nam Tran, Joon-Chul Kim, Sun-Hee Woo

{"title":"The NADPH oxidase inhibitor diphenyleneiodonium suppresses Ca2+ signaling and contraction in rat cardiac myocytes.","authors":"Qui Anh Le, Tran Nguyet Trinh, Phuong Kim Luong, Vu Thi Van Anh, Ha Nam Tran, Joon-Chul Kim, Sun-Hee Woo","doi":"10.4196/kjpp.2024.28.4.335","DOIUrl":"10.4196/kjpp.2024.28.4.335","url":null,"abstract":"Diphenyleneiodonium (DPI) has been widely used as an inhibitor of NADPH oxidase (Nox) to discover its function in cardiac myocytes under various stimuli. However, the effects of DPI itself on Ca2+ signaling and contraction in cardiac myocytes under control conditions have not been understood. We investigated the effects of DPI on contraction and Ca2+ signaling and their underlying mechanisms using video edge detection, confocal imaging, and whole-cell patch clamp technique in isolated rat cardiac myocytes. Application of DPI suppressed cell shortenings in a concentration-dependent manner (IC50 of ≅0.17 µM) with a maximal inhibition of ~70% at ~100 µM. DPI decreased the magnitude of Ca2+ transient and sarcoplasmic reticulum Ca2+ content by 20%-30% at 3 µM that is usually used to remove the Nox activity, with no effect on fractional release. There was no significant change in the half-decay time of Ca2+ transients by DPI. The L-type Ca2+ current (ICa) was decreased concentration-dependently by DPI (IC50 of ≅40.3 µM) with ≅13.1%-inhibition at 3 µM. The frequency of Ca2+ sparks was reduced by 3 µM DPI (by ~25%), which was resistant to a brief removal of external Ca2+ and Na+. Mitochondrial superoxide level was reduced by DPI at 3-100 µM. Our data suggest that DPI may suppress L-type Ca2+ channel and RyR, thereby attenuating Ca2+-induced Ca2+ release and contractility in cardiac myocytes, and that such DPI effects may be related to mitochondrial metabolic suppression.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"28 4","pages":"335-344"},"PeriodicalIF":1.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11211754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141460720","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

Novel artesunate-metformin conjugate inhibits bladder cancer cell growth associated with Clusterin/SREBP1/FASN signaling pathway. 新型青蒿琥酯-二甲双胍共轭物可抑制与 Clusterin/SREBP1/FASN 信号通路相关的膀胱癌细胞生长。

IF 2 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2024-05-01 DOI: 10.4196/kjpp.2024.28.3.219

Peiyu Lin, Xiyue Yang, Linghui Wang, Xin Zou, Lingli Mu, Cangcang Xu, Xiaoping Yang

{"title":"Novel artesunate-metformin conjugate inhibits bladder cancer cell growth associated with Clusterin/SREBP1/FASN signaling pathway.","authors":"Peiyu Lin, Xiyue Yang, Linghui Wang, Xin Zou, Lingli Mu, Cangcang Xu, Xiaoping Yang","doi":"10.4196/kjpp.2024.28.3.219","DOIUrl":"https://doi.org/10.4196/kjpp.2024.28.3.219","url":null,"abstract":"Bladder cancer remains the 10th most common cancer worldwide. In recent years, metformin has been found to have potential anti-bladder cancer activity while high concentration of IC50 at millimolar level is needed, which could not be reached by regular oral administration route. Thus, higher efficient agent is urgently demanded for clinically treating bladder cancer. Here, by conjugating artesunate to metformin, a novel artesunate-metformin dimer triazine derivative AM2 was designed and synthesized. The inhibitory effect of AM2 on bladder cancer cell line T24 and the mechanism underlying was determined. Anti-tumor activity of AM2 was assessed by MTT, cloning formation and wound healing assays. Decreasing effect of AM2 on lipogenesis was determined by oil red O staining. The protein expressions of Clusterin, SREBP1 and FASN in T24 cells were evaluated by Western blotting. The results show that AM2 significantly inhibited cell proliferation and migration at micromolar level, much higher than parental metformin. AM2 reduced lipogenesis and down-regulated the expressions of Clusterin, SREBP1 and FASN. These results suggest that AM2 inhibits the growth of bladder cancer cells T24 by inhibiting cellular lipogenesis associated with the Clusterin/SREBP1/FASN signaling pathway.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"28 3","pages":"219-227"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140874180","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

Development and assessment of nano drug delivery systems for combined delivery of rosuvastatin and ezetimibe. 开发和评估联合给药罗伐他汀和依折麦布的纳米给药系统。

IF 2 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2024-05-01 DOI: 10.4196/kjpp.2024.28.3.275

Mohamed Ali Metwally, El-Yamani Ibrahim El-Zawahry, Maher Amer Ali, Diaa Farrag Ibrahim, Shereen Ahmed Sabry, Omnia Mohamed Sarhan

{"title":"Development and assessment of nano drug delivery systems for combined delivery of rosuvastatin and ezetimibe.","authors":"Mohamed Ali Metwally, El-Yamani Ibrahim El-Zawahry, Maher Amer Ali, Diaa Farrag Ibrahim, Shereen Ahmed Sabry, Omnia Mohamed Sarhan","doi":"10.4196/kjpp.2024.28.3.275","DOIUrl":"https://doi.org/10.4196/kjpp.2024.28.3.275","url":null,"abstract":"Worldwide, cardiovascular disease is the main cause of death, which accordingly increased by hyperlipidemia. Hyperlipidemia therapy can include lifestyle changes and medications to control cholesterol levels. Statins are the medications of the first choice for dealing with lipid abnormalities. Rosuvastatin founds to control high lipid levels by hindering liver production of cholesterol and to achieve the targeted levels of low-density lipoprotein cholesterol, another lipid lowering agents named ezetimibe may be used as an added therapy. Both rosuvastatin and ezetimibe have low bioavailability which will stand as barrier to decrease cholesterol levels, because of such depictions, formulations of this combined therapy in nanotechnology will be of a great assistance. Our study demonstrated preparations of nanoparticles of this combined therapy, showing their physical characterizations, and examined their behavior in laboratory conditions and vivo habitation. The mean particle size was uniform, polydispersity index and zeta potential of formulations were found to be in the ranges of (0.181-0.72) and (-13.4 to -6.24), respectively. Acceptable limits of entrapment efficiency were affirmed with appearance of spherical and uniform nanoparticles. In vitro testing showed a sustained release of drug exceeded 90% over 24 h. In vivo study revealed an enhanced dissolution and bioavailability from loaded nanoparticles, which was evidenced by calculated pharmacokinetic parameters using triton for hyperlipidemia induction. Stability studies were performed and assured that the formulations are kept the same up to one month. Therefore, nano formulations is a suitable transporter for combined therapy of rosuvastatin and ezetimibe with improvement in their dissolution and bioavailability.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"28 3","pages":"275-284"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140868283","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

Tivozanib-induced activation of the mitochondrial apoptotic pathway and suppression of epithelial-to-mesenchymal transition in oral squamous cell carcinoma. Tivozanib诱导激活线粒体凋亡途径并抑制口腔鳞状细胞癌的上皮细胞向间质转化。

IF 2 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2024-05-01 DOI: 10.4196/kjpp.2024.28.3.197

Nak-Eun Choi, Si-Chan Park, In-Ryoung Kim

{"title":"Tivozanib-induced activation of the mitochondrial apoptotic pathway and suppression of epithelial-to-mesenchymal transition in oral squamous cell carcinoma.","authors":"Nak-Eun Choi, Si-Chan Park, In-Ryoung Kim","doi":"10.4196/kjpp.2024.28.3.197","DOIUrl":"https://doi.org/10.4196/kjpp.2024.28.3.197","url":null,"abstract":"The potential of tivozanib as a treatment for oral squamous cell carcinoma (OSCC) was explored in this study. We investigated the effects of tivozanib on OSCC using the Ca9-22 and CAL27 cell lines. OSCC is a highly prevalent cancer type with a significant risk of lymphatic metastasis and recurrence, which necessitates the development of innovative treatment approaches. Tivozanib, a vascular endothelial growth factor receptor inhibitor, has shown efficacy in inhibiting neovascularization in various cancer types but has not been thoroughly studied in OSCC. Our comprehensive assessment revealed that tivozanib effectively inhibited OSCC cells. This was accompanied by the suppression of Bcl-2, a reduction in matrix metalloproteinase levels, and the induction of intrinsic pathway-mediated apoptosis. Furthermore, tivozanib contributed to epithelial-to-mesenchymal transition (EMT) inhibition by increasing E-cadherin levels while decreasing N-cadherin levels. These findings highlight the substantial anticancer potential of tivozanib in OSCC and thus its promise as a therapeutic option. Beyond reducing cell viability and inducing apoptosis, the capacity of tivozanib to inhibit EMT and modulate key proteins presents the possibility of a paradigm shift in OSCC treatment.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"28 3","pages":"197-207"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140875039","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

Pectolinarigenin ameliorated airway inflammation and airway remodeling to exhibit antitussive effect. 果胶苷元可改善气道炎症和气道重塑，从而发挥止咳作用。

IF 2 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2024-05-01 DOI: 10.4196/kjpp.2024.28.3.229

Quan He, Weihua Liu, Xiaomei Ma, Hongxiu Li, Weiqi Feng, Xuzhi Lu, Ying Li, Zi Chen

{"title":"Pectolinarigenin ameliorated airway inflammation and airway remodeling to exhibit antitussive effect.","authors":"Quan He, Weihua Liu, Xiaomei Ma, Hongxiu Li, Weiqi Feng, Xuzhi Lu, Ying Li, Zi Chen","doi":"10.4196/kjpp.2024.28.3.229","DOIUrl":"https://doi.org/10.4196/kjpp.2024.28.3.229","url":null,"abstract":"Cough is a common symptom of several respiratory diseases. However, frequent coughing from acute to chronic often causes great pain to patients. It may turn into cough variant asthma, which seriously affects people's quality of life. For cough treatment, it is dominated by over-the-counter antitussive drugs, such as asmeton, but most currently available antitussive drugs have serious side effects. Thus, there is a great need for the development of new drugs with potent cough suppressant. BALB/c mice were used to construct mice model with cough to investigate the pharmacological effects of pectolinarigenin (PEC). Hematoxylin-eosin and Masson staining were used to assess lung injury and airway remodeling, and ELISA was used to assess the level of inflammatory factor release. In addition, inflammatory cell counts were measured to assess airway inflammation. Airway hyperresponsiveness assay was used to assess respiratory resistance in mice. Finally, we used Western blotting to explore the potential mechanisms of PEC. We found that PEC could alleviate lung tissue injury and reduce the release of inflammatory factors, inhibit of cough frequency and airway wall collagen deposition in mice model with cough. Meanwhile, PEC inhibited the Ras/ERK/c-Fos pathway to exhibit antitussive effect. Therefore, PEC may be a potential drug for cough suppression.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"28 3","pages":"229-237"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140862742","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

Ferroptosis and its role in gastric and colorectal cancers. 铁蛋白沉积及其在胃癌和结肠直肠癌中的作用

IF 2 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2024-05-01 DOI: 10.4196/kjpp.2024.28.3.183

Jinxiu Hou, Bo Wang, Jing Li, Wenbo Liu

{"title":"Ferroptosis and its role in gastric and colorectal cancers.","authors":"Jinxiu Hou, Bo Wang, Jing Li, Wenbo Liu","doi":"10.4196/kjpp.2024.28.3.183","DOIUrl":"https://doi.org/10.4196/kjpp.2024.28.3.183","url":null,"abstract":"Ferroptosis is a novel mechanism of programmed cell death, characterized by intracellular iron overload, intensified lipid peroxidation, and abnormal accumulation of reactive oxygen species, which ultimately resulting in cell membrane impairment and demise. Research has revealed that cancer cells exhibit a greater demand for iron compared to normal cells, indicating a potential susceptibility of cancer cells to ferroptosis. Stomach and colorectal cancers are common gastrointestinal malignancies, and their elevated occurrence and mortality rates render them a global health concern. Despite significant advancements in medical treatments, certain unfavorable consequences and drug resistance persist. Consequently, directing attention towards the phenomenon of ferroptosis in gastric and colorectal cancers holds promise for enhancing therapeutic efficacy. This review aims to elucidate the intricate cellular metabolism associated with ferroptosis, encompassing lipid and amino acid metabolism, as well as iron metabolic processes. Furthermore, the significance of ferroptosis in the context of gastric and colorectal cancer is thoroughly examined and discussed.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"28 3","pages":"183-196"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140866099","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

Relation between heart rate variability and spectral analysis of electroencephalogram in chronic neuropathic pain patients. 慢性神经病理性疼痛患者心率变异性与脑电图频谱分析之间的关系

IF 2 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2024-05-01 DOI: 10.4196/kjpp.2024.28.3.253

John Rajan, Girwar Singh Gaur, Karthik Shanmugavel, Adinarayanan S

{"title":"Relation between heart rate variability and spectral analysis of electroencephalogram in chronic neuropathic pain patients.","authors":"John Rajan, Girwar Singh Gaur, Karthik Shanmugavel, Adinarayanan S","doi":"10.4196/kjpp.2024.28.3.253","DOIUrl":"https://doi.org/10.4196/kjpp.2024.28.3.253","url":null,"abstract":"Chronic neuropathic pain (CNP) is a complex condition often arising from neural maladaptation after nerve injury. Understanding CNP complications involves the intricate interplay between brain-heart dynamics, assessed through quantitative electroencephalogram (qEEG) and heart rate variability (HRV). However, insights into their interaction in chronic pain are limited. Resting EEG and simultaneous electrocardiogram (lead II) of the participants were recorded for qEEG and HRV analysis. Correlations between HRV and qEEG parameters were calculated and compared with age, sex, and body mass index (BMI)-matched controls. CNP patients showed reduced HRV and significant increases in qEEG power spectral densities within delta, theta, and beta frequency ranges. A positive correlation was found between low frequency/ high frequency (LF/HF) ratio in HRV analysis and theta, alpha, and beta frequency bands in qEEG among CNP patients. However, no significant correlation was observed between parasympathetic indices and theta, beta bands in qEEG within CNP group, unlike age, sex, and BMI-matched healthy controls. CNP patients display significant HRV reductions and distinctive qEEG patterns. While healthy controls exhibit significant correlations between parasympathetic HRV parameters and qEEG spectral densities, these relationships are diminished or absent in CNP individuals. LF/HF ratio, reflecting sympathovagal balance, correlates significantly with qEEG frequency bands (theta, alpha, beta), illuminating autonomic dysregulation in CNP. These findings emphasize the intricate brain-heart interplay in chronic pain, warranting further exploration.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"28 3","pages":"253-264"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140873145","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

RNA polymerase I subunit D activated by Yin Yang 1 transcription promote cell proliferation and angiogenesis of colorectal cancer cells. 阴阳 1 转录激活的 RNA 聚合酶 I 亚基 D 促进结直肠癌细胞的增殖和血管生成。

IF 2 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2024-05-01 DOI: 10.4196/kjpp.2024.28.3.265

Jianfeng Shan, Yuanxiao Liang, Zhili Yang, Wenshan Chen, Yun Chen, Ke Sun

{"title":"RNA polymerase I subunit D activated by Yin Yang 1 transcription promote cell proliferation and angiogenesis of colorectal cancer cells.","authors":"Jianfeng Shan, Yuanxiao Liang, Zhili Yang, Wenshan Chen, Yun Chen, Ke Sun","doi":"10.4196/kjpp.2024.28.3.265","DOIUrl":"https://doi.org/10.4196/kjpp.2024.28.3.265","url":null,"abstract":"This study aims to explore possible effect of RNA polymerase I subunit D (POLR1D) on proliferation and angiogenesis ability of colorectal cancer (CRC) cells and mechanism herein. The correlation of POLR1D and Yin Yang 1 (YY1) expressions with prognosis of CRC patients in TCGA database was analyzed. Quantitative realtime polymerase chain reaction (qRT-PCR) and Western blot were applied to detect expression levels of POLR1D and YY1 in CRC cell lines and CRC tissues. SW480 and HT- 29 cells were transfected with si-POLR1D or pcDNA3.1-POLR1D to achieve POLR1D suppression or overexpression before cell migration, angiogenesis of human umbilical vein endothelial cells were assessed. Western blot was used to detect expressions of p38 MAPK signal pathway related proteins and interaction of YY1 with POLR1D was confirmed by dual luciferase reporter gene assay and chromatin immunoprecipitation (ChIP). TCGA data showed that both POLR1D and YY1 expressions were up-regulated in CRC patients. High expression of POLR1D was associated with poor prognosis of CRC patients. The results showed that POLR1D and YY1 were highly expressed in CRC cell lines. Inhibition or overexpression of POLR1D can respectively suppress or enhance proliferation and angiogenesis of CRC cells. YY1 inhibition can suppress CRC progression and deactivate p38 MAPK signal pathway, which can be counteracted by POLR1D overexpression. JASPAR predicted YY1 can bind with POLR1D promoter, which was confirmed by dual luciferase reporter gene assay and ChIP. YY1 transcription can up-regulate POLR1D expression to activate p38 MAPK signal pathway, thus promoting proliferation and angiogenesis ability of CRC cells.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"28 3","pages":"265-273"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140863307","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

Cardioprotection via mitochondrial transplantation supports fatty acid metabolism in ischemia-reperfusion injured rat heart. 通过线粒体移植保护心脏，支持缺血再灌注损伤大鼠心脏的脂肪酸代谢。

IF 2 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2024-05-01 DOI: 10.4196/kjpp.2024.28.3.209

Jehee Jang, Ki-Woon Kang, Young-Won Kim, Seohyun Jeong, Jaeyoon Park, Jihoon Park, Jisung Moon, Junghyun Jang, Seohyeon Kim, Sunghun Kim, Sungjoo Cho, Yurim Lee, Hyoung Kyu Kim, Jin Han, Eun-A Ko, Sung-Cherl Jung, Jung-Ha Kim, Jae-Hong Ko

{"title":"Cardioprotection via mitochondrial transplantation supports fatty acid metabolism in ischemia-reperfusion injured rat heart.","authors":"Jehee Jang, Ki-Woon Kang, Young-Won Kim, Seohyun Jeong, Jaeyoon Park, Jihoon Park, Jisung Moon, Junghyun Jang, Seohyeon Kim, Sunghun Kim, Sungjoo Cho, Yurim Lee, Hyoung Kyu Kim, Jin Han, Eun-A Ko, Sung-Cherl Jung, Jung-Ha Kim, Jae-Hong Ko","doi":"10.4196/kjpp.2024.28.3.209","DOIUrl":"https://doi.org/10.4196/kjpp.2024.28.3.209","url":null,"abstract":"In addition to cellular damage, ischemia-reperfusion (IR) injury induces substantial damage to the mitochondria and endoplasmic reticulum. In this study, we sought to determine whether impaired mitochondrial function owing to IR could be restored by transplanting mitochondria into the heart under ex vivo IR states. Additionally, we aimed to provide preliminary results to inform therapeutic options for ischemic heart disease (IHD). Healthy mitochondria isolated from autologous gluteus maximus muscle were transplanted into the hearts of Sprague-Dawley rats damaged by IR using the Langendorff system, and the heart rate and oxygen consumption capacity of the mitochondria were measured to confirm whether heart function was restored. In addition, relative expression levels were measured to identify the genes related to IR injury. Mitochondrial oxygen consumption capacity was found to be lower in the IR group than in the group that underwent mitochondrial transplantation after IR injury (p < 0.05), and the control group showed a tendency toward increased oxygen consumption capacity compared with the IR group. Among the genes related to fatty acid metabolism, Cpt1b (p < 0.05) and Fads1 (p < 0.01) showed significant expression in the following order: IR group, IR + transplantation group, and control group. These results suggest that mitochondrial transplantation protects the heart from IR damage and may be feasible as a therapeutic option for IHD.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"28 3","pages":"209-217"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140855976","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

Fibroblast-derived interleukin-6 exacerbates adverse cardiac remodeling after myocardial infarction. 成纤维细胞衍生的白细胞介素-6会加剧心肌梗死后的不良心脏重塑。

IF 2 4区医学

Korean Journal of Physiology & Pharmacology Pub Date : 2024-05-01 DOI: 10.4196/kjpp.2024.28.3.285

Hongkun Li, Yunfei Bian

{"title":"Fibroblast-derived interleukin-6 exacerbates adverse cardiac remodeling after myocardial infarction.","authors":"Hongkun Li, Yunfei Bian","doi":"10.4196/kjpp.2024.28.3.285","DOIUrl":"https://doi.org/10.4196/kjpp.2024.28.3.285","url":null,"abstract":"Myocardial infarction is one of the leading causes of mortality globally. Currently, the pleiotropic inflammatory cytokine interleukin-6 (IL-6) is considered to be intimately related to the severity of myocardial injury during myocardial infarction. Interventions targeting IL-6 are a promising therapeutic option for myocardial infarction, but the underlying molecular mechanisms are not well understood. Here, we report the novel role of IL-6 in regulating adverse cardiac remodeling mediated by fibroblasts in a mouse model of myocardial infarction. It was found that the elevated expression of IL-6 in myocardium and cardiac fibroblasts was observed after myocardial infarction. Further, fibroblast-specific knockdown of Il6 significantly attenuated cardiac fibrosis and adverse cardiac remodeling and preserved cardiac function induced by myocardial infarction. Mechanistically, the role of Il6 contributing to cardiac fibrosis depends on signal transduction and activation of transcription (STAT)3 signaling activation. Additionally, Stat3 binds to the Il11 promoter region and contributes to the increased expression of Il11, which exacerbates cardiac fibrosis. In conclusion, these results suggest a novel role for IL-6 derived from fibroblasts in mediating Stat3 activation and substantially augmented Il11 expression in promoting cardiac fibrosis, highlighting its potential as a therapeutic target for cardiac fibrosis.","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"28 3","pages":"285-294"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140867336","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