Journal of Clinical Biochemistry and Nutrition最新文献_第8页

Regulation of type I IFN responses by deubiquitinating enzyme A in inflammatory bowel diseases. 去泛素化酶A在炎性肠病中对I型IFN反应的调节

IF 2.4 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.23-24

Yasuhiro Masuta, Yasuo Otsuka, Kosuke Minaga, Hajime Honjo, Masatoshi Kudo, Tomohiro Watanabe

{"title":"Regulation of type I IFN responses by deubiquitinating enzyme A in inflammatory bowel diseases.","authors":"Yasuhiro Masuta, Yasuo Otsuka, Kosuke Minaga, Hajime Honjo, Masatoshi Kudo, Tomohiro Watanabe","doi":"10.3164/jcbn.23-24","DOIUrl":"https://doi.org/10.3164/jcbn.23-24","url":null,"abstract":"The development of Inflammatory bowel disease (IBD) is driven by excessive production of pro-inflammatory cytokines including TNF-α, IL-12, and IL-23. This notion is supported by the remarkable clinical success of biologics targeting these cytokines. Recognition of cell wall components derived from intestinal bacteria by Toll-like receptors (TLRs) induces the production of these pro-inflammatory cytokines by macrophages and dendritic cells in human IBD and experimental colitis model. Although sensing of bacterial nucleic acids by endosomal TLRs, specifically TLR3, TLR7, and TLR9 leads to robust production of type I IFNs, it remains debatable whether TLR-mediated type I IFN responses are pathogenic or protective in IBD patients. Additionally, recent studies identified deubiquitinating enzyme A (DUBA) as a novel negative regulator of TLR-mediated type I IFN responses. In light of these observations and their potential applications, in this review, we summarize recent findings on the roles of type I IFN responses and DUBA-mediated negative regulation of these responses in human IBD and experimental colitis model.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"103-107"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/72/07/jcbn23-24.PMC10493212.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10240625","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

TMEM189 as a target gene of MiR-499a-5p regulates breast cancer progression through the ferroptosis pathway. TMEM189作为MiR-499a-5p的靶基因通过铁下垂途径调控乳腺癌的进展。

IF 2.4 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.22-130

Dong Fan, Yue Ma, Yujuan Qi, Xiaozhou Yang, Huadong Zhao

{"title":"TMEM189 as a target gene of MiR-499a-5p regulates breast cancer progression through the ferroptosis pathway.","authors":"Dong Fan, Yue Ma, Yujuan Qi, Xiaozhou Yang, Huadong Zhao","doi":"10.3164/jcbn.22-130","DOIUrl":"https://doi.org/10.3164/jcbn.22-130","url":null,"abstract":"MicroRNA (miR)-499a-5p has been reported to regulate the progression of various tumours. However, the role of miR-499a-5p in breast cancer is unclear. The purpose of this study was to investigate the role and mechanism of miR-499a-5p in breast cancer. The growth effect of miR-499a-5p on breast cancer cells was investigated by the CCK-8 assay, wound healing assay and Transwell invasion assay. The luciferase activity assay was used to verify the downstream targets of miR-499a-5p. The levels of GSH, MDA, and ROS were detected by kits. Quantitative real-time PCR and Western blot were used to determine the expression levels of TMEM189, COX-2, GPX4, and other related genes in cells. miR-499a-5p was down-regulated in MDA-MB-231 cells and was shown to reduced the viability, migration and invasion of MDA-MB-231 cells. Further studies revealed that TMEM189 is a target of miR-499a-5p. miR-499a-5p inhibited breast cancer cell growth by downregulating TMEM189. Furthermore, the down-regulation of TMEM189 promotes ferroptosis in breast cancer cells. The low expression of TMEM189 inhibited the development of breast cancer through the ferroptosis pathway. We have demonstrated for the first time that miR-499a-5p inhibits breast cancer progression by targeting the TMEM189-mediated ferroptosis pathway.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"154-160"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d2/79/jcbn22-130.PMC10493215.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10240629","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

Metabolomics analysis of amino acid and fatty acids in colorectal cancer patients based on tandem mass spectrometry. 基于串联质谱法的结直肠癌患者氨基酸和脂肪酸代谢组学分析。

IF 2.4 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.22-110

Zhuo Zhao, Jing Bai, Chang Liu, Yansong Wang, Shuang Wang, Furong Zhao, Qiufang Gu

{"title":"Metabolomics analysis of amino acid and fatty acids in colorectal cancer patients based on tandem mass spectrometry.","authors":"Zhuo Zhao, Jing Bai, Chang Liu, Yansong Wang, Shuang Wang, Furong Zhao, Qiufang Gu","doi":"10.3164/jcbn.22-110","DOIUrl":"https://doi.org/10.3164/jcbn.22-110","url":null,"abstract":"Metabolic differences between colorectal cancer (CRC) and NI (NI) play an important role in early diagnoses and in-time treatments. We investigated the metabolic alterations between CRC patients and NI, and identified some potential biomarkers, and these biomarkers might be used as indicators for diagnosis of CRC. In this study, there were 79 NI, 50 CRC I patients, 52 CRC II patients, 56 CRC III patients, and 52 CRC IV patients. MS-MS was used to measure the metabolic alterations. Univariate and multivariate data analysis and metabolic pathway analysis were applied to analyze metabolic data and determine differential metabolites. These indicators revealed that amino acid and fatty acids could separate these groups. Several metabolites indicated an excellent variables capability in the separation of CRC patients and NI. Ornithine, arginine, octadecanoyl carnitine, palmitoyl carnitine, adipoyl carnitine, and butyryl carnitine/propanoyl carnitine were selected to distinguish the CRC patients and NI. And methionine and propanoyl carnitine, were directly linked to different stages of CRC. Receiver operating characteristics curves and variables importance in projection both represented an excellent performance of these metabolites. In conclusion, we assessed the difference between CRC patients and NI, which supports guidelines for an early diagnosis and effective treatment.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"161-171"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/30/9a/jcbn22-110.PMC10493213.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10232123","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

Quality analysis of the clinical laboratory literature and its effectiveness on clinical quality improvement: a systematic review. 临床实验室文献的质量分析及其对提高临床质量的作用:系统综述。

IF 2.4 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.23-22

Ahmed Shabbir Chaudhry, Yu Inata, Etsuko Nakagami-Yamaguchi

{"title":"Quality analysis of the clinical laboratory literature and its effectiveness on clinical quality improvement: a systematic review.","authors":"Ahmed Shabbir Chaudhry, Yu Inata, Etsuko Nakagami-Yamaguchi","doi":"10.3164/jcbn.23-22","DOIUrl":"https://doi.org/10.3164/jcbn.23-22","url":null,"abstract":"Quality improvement in clinical laboratories is crucial to ensure accurate and reliable test results. With increasing awareness of the potential adverse effects of errors in laboratory practice on patient outcomes, the need for continual improvement of laboratory services cannot be overemphasized. A literature search was conducted on PubMed and a web of science core collection between October and February 2021 to evaluate the scientific literature quality of clinical laboratory quality improvement; only peer-reviewed articles written in English that met quality improvement criteria were included. A structured template was used to extract data, and the papers were rated on a scale of 0-16 using the Quality Improvement Minimum Quality Criteria Set (QI-MQCS). Out of 776 studies, 726 were evaluated for clinical laboratory literature quality analysis. Studies were analyzed according to the quality improvement and control methods and interventions, such as training, education, task force, and observation. Results showed that the average score of QI-MQCS for quality improvement papers from 1981-2000 was 2.5, while from 2001-2020, it was 6.8, indicating continuous high-quality improvement in the clinical laboratory sector. However, there is still room to establish a proper system to judge the quality of clinical laboratory literature and improve accreditation programs within the sector.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"108-115"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4e/27/jcbn23-22.PMC10493209.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10232118","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

NEK7 inhibition attenuates Aβ₄₂-induced cognitive impairment by regulating TLR4/NF-κB and the NLRP3 inflammasome in mice. 通过调节TLR4/NF-κB和NLRP3炎性体，抑制NEK7可减轻Aβ42诱导的小鼠认知障碍。

IF 2.4 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 Epub Date: 2023-08-11 DOI: 10.3164/jcbn.22-105

Peng Li, Yifan He, Qian Yang, Hena Guo, Nini Li, Dongdong Zhang

{"title":"NEK7 inhibition attenuates Aβ42-induced cognitive impairment by regulating TLR4/NF-κB and the NLRP3 inflammasome in mice.","authors":"Peng Li, Yifan He, Qian Yang, Hena Guo, Nini Li, Dongdong Zhang","doi":"10.3164/jcbn.22-105","DOIUrl":"10.3164/jcbn.22-105","url":null,"abstract":"NEK7 is a serine/threonine kinase that regulates cell mitosis and the activation of the nucleotide-binding oligomerization domain-like (NOD-like) receptor thermal protein domain associated protein 3 (NLRP3) inflammasome, and is related to neuroinflammation and neuronal damage. The purpose of this study was to explore the role and mechanism of NEK7 in cognitive impairment in Alzheimer's disease (AD). BV2 cells, a microglia cell line, was treated with Aβ42. NEK7 expression was measured with reverse transcription-quantitative polymerase chain reaction and Western blotting. An apoptosis kit was used to determine the apoptotic rate. APPswe/PS1dE9 (APP/PS1) transgenic mice were used as an in vivo AD model. The experimental mice were infected with sh-NEK7 lentivirus to downregulate NEK7. The Morris water maze was conducted to explore the effect of NEK7 downregulation on cognitive ability. The results showed that Aβ42 significantly upregulated NEK7 in BV2 cells. Silencing NEK7 suppressed the decrease in BV2 viability and the increase in inflammation, oxidative stress and apoptosis induced by Aβ42. NEK7 mediated it effects through the TLR4/NF-κB signalling pathway and the NLRP3 inflammasome. Finally, inhibition of NEK7 alleviated the cognitive impairment in APP/PS1 mice. In conclusion, Silencing NEK7 suppresses Aβ42-induced cell apoptosis, inflammation and oxidative stress, and improves cognitive performance in AD mice. NEK7 may be a potential target for AD treatment.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"145-153"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e1/bb/jcbn22-105.PMC10493210.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10240630","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

SMOC2 promoted vascular smooth muscle cell proliferation, migration, and extracellular matrix degradation by activating BMP/TGF-β1 signaling pathway. SMOC2通过激活BMP/TGF-β1信号通路，促进血管平滑肌细胞增殖、迁移和细胞外基质降解。

IF 2.4 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.22-100

Xiaowei Wang, Meng Wang, Zhongxiao Zhou, Xin Zou, Guoxin Song, Qingsong Zhang, Haimeng Zhou

{"title":"SMOC2 promoted vascular smooth muscle cell proliferation, migration, and extracellular matrix degradation by activating BMP/TGF-β1 signaling pathway.","authors":"Xiaowei Wang, Meng Wang, Zhongxiao Zhou, Xin Zou, Guoxin Song, Qingsong Zhang, Haimeng Zhou","doi":"10.3164/jcbn.22-100","DOIUrl":"https://doi.org/10.3164/jcbn.22-100","url":null,"abstract":"A widespread degenerative condition of the aorta, abdominal aortic aneurysm (AAA), severely endangers the health of middle-aged and elderly people. SPARC related modular calcium binding2 (SMOC2) is upregulated in the carotid arteries of rats with atherosclerotic lesions, but its function in AAA is still unknown. Therefore, the aim of this research was to evaluate the function of SMOC2 in AAA. The results showed that in the AAA tissues, SMOC2 expression was upregulated compared with healthy controls. Overexpression of SMOC2 promoted vascular smooth muscle cells (VSMCs) proliferation, migration, and extracellular matrix (ECM) degradation. In contrast, silence of SMOC2 inhibited VSMCs proliferation, migration, and ECM degradation. Overexpression of SMOC2 promoted BMP and TGF-β1 expression and silence of SMOC2 had an opposite effect. Besides, inhibition of BMP or TGF-β1 suppressed VSMCs cell proliferation, migration, and ECM degradation. Moreover, inhibition BMP or TGF-β1 reversed the promotive effects of SMOC2 overexpression on VSMCs proliferation, migration, and ECM degradation. SMOC2 may affecte the formation of AAA by upregulating BMP and TGF-β1 to regulate the proliferation, migration, and ECM degradation of VSMCs.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"116-123"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/18/f8/jcbn22-100.PMC10493216.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10232124","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

Cinnamtannin A2, (-)-epicatechin tetramer, attenuates skeletal muscle wasting in disuse atrophy model mice induced by hindlimb suspension. 肉桂酸A2(-)-表儿茶素四聚体减轻后肢悬吊引起的废用性萎缩模型小鼠骨骼肌萎缩。

IF 2.4 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.23-12

Orie Muta, Shiori Oyama, Minayu Odaka, Kenta Shimizu, Sae Katsuragawa, Kenta Suzuki, Taiki Fushimi, Yasuyuki Fujii, Ryota Akagi, Naomi Osakabe

{"title":"Cinnamtannin A2, (-)-epicatechin tetramer, attenuates skeletal muscle wasting in disuse atrophy model mice induced by hindlimb suspension.","authors":"Orie Muta, Shiori Oyama, Minayu Odaka, Kenta Shimizu, Sae Katsuragawa, Kenta Suzuki, Taiki Fushimi, Yasuyuki Fujii, Ryota Akagi, Naomi Osakabe","doi":"10.3164/jcbn.23-12","DOIUrl":"https://doi.org/10.3164/jcbn.23-12","url":null,"abstract":"The impact of repeated administration of cinntamtannin A2 (A2, 25 μg/kg) on skeletal muscle disuse atrophy model mice induced by hindlimb suspension for 14 days was examined. In soleus, weight loss and a reduction in the average myofibre size with shifting to the smaller side of the peak were observed in the suspension-vehicle group, but A2 reduced these changes. Average myofibre size significantly increased in ground-A2 compared to ground-vehicle. A marked increase in the dephosphorylation of forkhead box O (FoxO) 3a by the suspension was reduced by A2. The phosphorylation of protein kinase B (Akt) and eukaryotic translation initiation factor 4E-binding protein (4EBP)-1 were significantly increased by the treatment of A2. In addition, a single dose of A2 increased dramatically in the 24-h excretion of catecholamines in urine. These results suggest that A2 administration results in sympathetic nerve activation and promotes hypertrophy while inhibiting the progress of disuse muscle atrophy.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"124-130"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6c/a6/jcbn23-12.PMC10493217.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10240626","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

Evaluation of cold atmospheric pressure plasma irradiation of water as a method of singlet oxygen generation. 冷常压等离子体辐照水作为单线态氧生成方法的评价。

IF 2.4 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-07-01 DOI: 10.3164/jcbn.22-111

Tokuko Takajo, Hiroki Nagahama, Katsuya Zuinen, Kazunori Tsuchida, Akitoshi Okino, Kazunori Anzai

{"title":"Evaluation of cold atmospheric pressure plasma irradiation of water as a method of singlet oxygen generation.","authors":"Tokuko Takajo, Hiroki Nagahama, Katsuya Zuinen, Kazunori Tsuchida, Akitoshi Okino, Kazunori Anzai","doi":"10.3164/jcbn.22-111","DOIUrl":"https://doi.org/10.3164/jcbn.22-111","url":null,"abstract":"We used cold atmospheric pressure plasma jet to examine in detail 1O2 generation in water. ESR with 2,2,5,5-tetramethyl-3-pyrroline-3-carboxamide, a secondary amine probe, was used for the detection of 1O2. Nitroxide radical formation was detected after cold atmospheric pressure plasma jet irradiation of a 2,2,5,5-tetramethyl-3-pyrroline-3-carboxamide solution. An 1O2 scavenger/quencher inhibited the ESR signal intensity induced by cold atmospheric pressure plasma jet irradiation, but this inhibition was not 100%. As 2,2,5,5-tetramethyl-3-pyrroline-3-carboxamide reacts with oxidizing species other than 1O2, it was assumed that the signal intensity inhibited by NaN3 corresponds to only the nitroxide radical generated by 1O2. The concentration of 1O2 produced by cold atmospheric pressure plasma jet irradiation for 60 s was estimated at 8 μM. When this 1O2 generation was compared to methods of 1O2 generation like rose bengal photoirradiation and 4-methyl-1,4-etheno-2,3-benzodioxin-1(4H)-propanoic acid (endoperoxide) thermal decomposition, 1O2 generation was found to be, in decreasing order, rose bengal photoirradiation ≥ cold atmospheric pressure plasma jet > endoperoxide thermal decomposition. Cold atmospheric pressure plasma jet is presumed to not specifically generate 1O2, but can be used to mimic states of oxidative stress involving multiple ROS.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 1","pages":"9-15"},"PeriodicalIF":2.4,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/cc/a4/jcbn22-111.PMC10390813.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9930372","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

Riboflavin compounds show NAD(P)H dependent quinone oxidoreductase-like quinone reducing activity. 核黄素类化合物具有NAD(P)H依赖的类醌氧化还原酶活性。

IF 2.4 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-07-01 DOI: 10.3164/jcbn.22-140

Midori Nagase, Miku Sakamoto, Sakiko Amekura, Sayaka Akiba, Misato Kashiba, Kenji Yokoyama, Yorihiro Yamamoto, Akio Fujisawa

{"title":"Riboflavin compounds show NAD(P)H dependent quinone oxidoreductase-like quinone reducing activity.","authors":"Midori Nagase, Miku Sakamoto, Sakiko Amekura, Sayaka Akiba, Misato Kashiba, Kenji Yokoyama, Yorihiro Yamamoto, Akio Fujisawa","doi":"10.3164/jcbn.22-140","DOIUrl":"https://doi.org/10.3164/jcbn.22-140","url":null,"abstract":"NAD(P)H-dependent quinone oxidoreductase (NQO) is an essential enzyme in living organisms and cells protecting them from oxidative stress. NQO reduces coenzyme Q (CoQ) using NAD(P)H as an electron donor. In the present study, we searched for coenzyme Q10 reducing activity from fractions of gel filtration-fractionated rat liver homogenate. In addition to the large-molecular-weight fraction containing NQO, CoQ10 reducing activity was also detected in a low-molecular-weight fraction. Furthermore, dicumarol, a conventional inhibitor of NQO1 (DT diaphorase), did not inhibit the reduction but quercetin did, suggesting that the activity was not due to NQO1. After further purification, the NADH-dependent CoQ10-reducing compound was identified as riboflavin. Riboflavin is an active substituent of other flavin compounds such as FAD and FMN. These flavin compounds also reduced not only CoQ homologues but also vitamin K homologues in the presence of NADH. The mechanism was speculated to work as follows: NADH reduces flavin compounds to the corresponding reduced forms, and subsequently, the reduced flavin compounds immediately reduce bio-quinones. Furthermore, the flavin-NADH system reduces CoQ10 bound with saposin B, which is believed to function as a CoQ transfer protein in vivo. This flavin-dependent CoQ10 reduction, therefore, may function in aqueous phases such as the cell cytosol and bodily fluids.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 1","pages":"52-60"},"PeriodicalIF":2.4,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b0/e1/jcbn22-140.PMC10390810.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9924400","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

Factors associated with long-term efficacy of lubiprostone for chronic constipation. 鲁比前列石治疗慢性便秘长期疗效的相关因素。

IF 2.4 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-07-01 DOI: 10.3164/jcbn.22-24

Takashi Morise, Masakatsu Fukuzawa, Mitsushige Sugimoto, Naoyoshi Nagata, Shin Kono, Yoshiya Yamauchi, Akihiko Sugimoto, Kumiko Uchida, Yohei Koyama, Akira Madarame, Hayato Yamaguchi, Taisuke Matsumoto, Yasuyuki Kagawa, Takashi Kawai, Takao Itoi

{"title":"Factors associated with long-term efficacy of lubiprostone for chronic constipation.","authors":"Takashi Morise, Masakatsu Fukuzawa, Mitsushige Sugimoto, Naoyoshi Nagata, Shin Kono, Yoshiya Yamauchi, Akihiko Sugimoto, Kumiko Uchida, Yohei Koyama, Akira Madarame, Hayato Yamaguchi, Taisuke Matsumoto, Yasuyuki Kagawa, Takashi Kawai, Takao Itoi","doi":"10.3164/jcbn.22-24","DOIUrl":"https://doi.org/10.3164/jcbn.22-24","url":null,"abstract":"The prevalence of chronic constipation in Japan is increasing, and is presently almost 1 in 5 people. Because constipation is common, especially in older patients, to avoid adverse events and polypharmacy, simple treatments at low doses are generally desired. Although the chloride channel activator lubiprostone is candidate drug that may solve these problems, factors associated with the long-term efficacy of lubiprostone monotherapy for chronic constipation in treatment-naive patients remain unclear. We here retrospectively investigated the clinical characteristics and factors of patients who achieved long-term constipation improvement with lubiprostone monotherapy. Seventy-four patients with chronic constipation treated with lubiprostone monotherapy (24 or 48 μg/day) from January 2017 to August 2018 were reviewed. Patient characteristics and clinical time-courses were compared between those who sustained improvement for 6 months, and those who became refractory to treatment. In 54 patients (76.1%), constipation improved by lubiprostone administration for 6 months. On multivariate analysis, a significant clinical factor associated with sustained improvement was a starting lubiprostone dose of 24 μg/day (odds ratio: 5.791; 95% confidence interval: 1.032-32.498; p = 0.046). A starting lubiprostone dose of 24 μg/day has efficacy to improve chronic constipation and to prevent adverse events of nausea and diarrhea in Japanese patients.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 1","pages":"91-96"},"PeriodicalIF":2.4,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/59/bc/jcbn22-24.PMC10390812.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9924402","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