预约演示
更新于：2024-12-27
Apocyanin
香草乙酮
更新于：2024-12-27
概要
基本信息
结构/序列
分子式C9H10O3 |
InChIKeyDFYRUELUNQRZTB-UHFFFAOYSA-N |
CAS号498-02-2 |
关联
8
项与 香草乙酮 相关的临床试验CTIS2023-508791-11-00
A placebo-controlled, double-blinded, randomized, dose-finding trial using a combination of apocynin and paeonol (APPA) for the treatment of knee osteoarthritis
EUCTR2020-000249-14-DK
A placebo-controlled, double-blinded, randomized, trial using a combination of apocynin and paeonol (APPA) for the treatment of knee osteoarthritis
IRCT20200418047122N1
Evaluation of the protective effect of a combination drug including Apocynin, Niacin, and Tannin on prevention of cardiovascular and respiratory morbidities and mortality in COVID-19 infection: A Clinical Trial
100 项与 香草乙酮 相关的临床结果
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100 项与 香草乙酮 相关的转化医学
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100 项与 香草乙酮 相关的专利（医药）
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2,193
项与 香草乙酮 相关的文献（医药）2025-02-01FOOD CHEMISTRY
Integrated targeted and untargeted metabolomics profiling of Vanilla species from the Atlantic Forest: Unveiling the bioeconomic potential of Vanilla cribbiana
Article
作者: Koblitz, Maria Gabriela Bello ; da Silva Oliveira, Joana Paula ; Garrett, Rafael ; Macedo, Andrea Furtado
In this study, we employ both targeted and untargeted approaches to explore the metabolomic profiles of Vanilla spp., with a particular focus on V. cribbiana (VCR) and its comparison with V. planifolia (VP). We also examine V. bahiana and V. chamissonis using targeted approaches. Through advanced analytical techniques, our untargeted LC-HRMS approach led to the annotation of 60 metabolites, revealing a complex chemical composition with 34 novel compounds in the Vanilla genus in VCR and VP. These findings highlight significant flavoring compounds and lay the foundation for a subsequent quantitative estimation approach. Our targeted analysis, which measured key molecules, underscores VCR's potential in producing vanillin and acetovanillone at levels comparable to the commercially valuable VP and even higher levels of vanillic acid. This research enriches our understanding of flavor composition in vanilla species and emphasizes the importance of exploring wild relatives of vanilla crop for sustainable production and biodiversity conservation.
2025-01-01CHEMICO-BIOLOGICAL INTERACTIONS
Activation of protein kinase B rescues against thapsigargin-elicited cardiac dysfunction through regulation of NADPH oxidase and ferroptosis
Article
作者: Wang, Xiaohu ; Lin, Ling ; Li, Feng-Juan ; Ren, Jun ; Lin, Jie ; Reiter, Russel J. ; Zhu, Shuyi ; Wang, Guizhen ; Chen, Shuying ; Reiter, Russel J ; Ashrafizadeh, Milad ; Zhang, Yingmei ; Cheng, Yong
Endoplasmic reticulum (ER) stress is a known contributor to cardiac remodeling and contractile dysfunction. Although NADPH oxidase has been implicated in ER stress-induced organ damage, its specific role in myocardial complications resulting from ER stress remains unclear. This study aimed to investigate the possible involvement of NADPH oxidase in ER stress-induced myocardial abnormalities and to evaluate the impact of Akt constitutive activation on these myocardial defects. Mice with cardiac-specific overexpression of active mutant of Akt (Myr-Akt) and their wild-type (WT) littermates were treated with ER stress instigator thapsigargin (1 mg/kg, i. p. 72 hrs) before evaluating myocardial morphology and function. Our results noted that thapsigargin significantly impaired echocardiographic parameters and cell shortening indices, including elevated LVESD, decreased ejection fraction, fractional shortening, peak shortening, electrically-stimulated intracellular Ca2+ release, and cardiomyocyte survival. These functional deteriorations were accompanied by upregulation of NADPH oxidase, O2- production, mitochondrial damage, carbonyl formation, lipid peroxidation, apoptosis, and interstitial fibrosis, with unchanged myocardial size. Constitutive Akt hyperactivation did not generate any response on myocardial morphology and function, although it greatly suppressed or nullified thapsigargin-induced myocardial remodeling and dysfunction. Thapsigargin also triggered dephosphorylation of Akt and its downstream signal GSK3β, along with development of ferroptosis, all of which were nullified by Akt hyperactivation. In vitro studies further revealed that thapsigargin provoked cardiomyocyte mechanical anomalies and lipid peroxidation, similar to in vivo results. These effects were reverted by inhibitors of NADPH oxidase and ferroptosis (apocynin and LIP1). Collectively, our data denote an important protective role for Akt hyperactivation in thapsigargin-evoked myocardial anomalies, likely through NADPH oxidase-mediated regulation of ferroptosis.
2024-12-11JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
Accumulation of Advanced Oxidation Protein Products Promotes Age-Related Decline of Type H Vessels in Bone
Article
作者: Zhu, Guo-Zheng ; Gao, Jia-Wen ; Zhong, Zhao-Ming ; Chen, Xing-Yu ; Li, Hong-Zhou ; Huang, Yu-Sheng ; Wu, Long-Yan ; Han, Dong ; Zhao, Kai ; Tu, Chen ; Wu, Di-Zheng
Abstract:
Type H vessels have been proven to couple angiogenesis and osteogenesis. The decline of type H vessels contributes to bone loss in the aging process. Aging is accompanied by the accumulation of advanced oxidation protein products (AOPPs). However, whether AOPP accumulation is involved in age-related decline of type H vessels is unclear. Here, we show that the increase of AOPP levels in plasma and bone was correlated with the decline of type H vessels and loss of bone mass in old mice. Exposure of microvascular endothelial cells to AOPPs significantly inhibited cell proliferation, migration, and tube formation; increased NADPH oxidase activity and excessive reactive oxygen species generation; upregulated the expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1; and eventually impaired angiogenesis, which was alleviated by redox modulator N-acetylcysteine and NADPH oxidase inhibitor apocynin. Furthermore, reduced AOPP accumulation by NAC treatment was able to alleviate significantly the decline of type H vessels, bone mass loss, and deterioration of bone microstructure in old mice. Collectively, these findings suggest that AOPPs accumulation contributes to the decline of type H vessels in the aging process, and illuminate a novel potential mechanism underlying age-related bone loss.
100 项与 香草乙酮 相关的药物交易
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研发状态
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 动脉粥样硬化 | 临床1期 | - | - | - |
| 糖尿病性神经病变 | 临床1期 | - | - | - |
| 高血压 | 临床1期 | - | - | - |
| 炎症性肠病 | 临床1期 | - | - | - |
| 帕金森病 | 临床1期 | - | - | - |
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临床结果
临床结果
适应症
分期
评价
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N/A | - | - | 鬱糧遞壓鹹網簾壓憲壓(選鹹醖築觸鏇遞願獵範) = 窪蓋膚醖網糧淵構蓋簾 餘製觸衊餘衊鑰糧鬱壓 (製顧糧鬱窪淵憲憲鹽夢 ) | 积极 | 2024-06-05 | ||
糧製鏇壓遞遞積積膚蓋(簾壓鹹鹽衊襯膚構鏇襯) = 襯淵顧製襯餘膚觸獵齋 製鬱淵齋鏇選範獵壓網 (鬱獵憲憲蓋醖襯膚膚積 ) 更多 | |||||||
N/A | - | Apocynin and paeonol (APPA) | 鑰淵衊範壓築夢網窪廠(製糧蓋淵願餘積獵膚築) = 觸壓齋網餘齋鏇壓醖淵 壓餘淵顧憲憲廠壓鬱鏇 (襯醖鹽網蓋選廠襯夢糧 ) | 积极 | 2020-06-03 | ||
N/A | - | - | AN-1 | 積襯顧鹹製膚鹽鬱製鏇(襯獵獵繭製鏇廠餘夢膚) = 獵範簾憲繭壓餘鹹鏇獵 製糧艱鹹製築選鹽蓋襯 (齋構繭窪遞憲鏇餘夢膚 ) 更多 | - | 2013-07-30 | |
積襯顧鹹製膚鹽鬱製鏇(襯獵獵繭製鏇廠餘夢膚) = 壓築壓構鏇蓋鏇憲糧醖 製糧艱鹹製築選鹽蓋襯 (齋構繭窪遞憲鏇餘夢膚 ) 更多 | |||||||
N/A | reactive oxygen species (ROS) | - | 蓋齋積遞窪構願襯醖鬱(鏇壓顧築鏇醖窪鹽築襯) = 衊鬱遞簾艱積製憲艱鹹 夢繭憲構製艱構鏇襯憲 (夢觸蓋餘淵醖壓鬱淵顧 ) 更多 | 积极 | 2012-09-01 | ||
蓋齋積遞窪構願襯醖鬱(鏇壓顧築鏇醖窪鹽築襯) = 製襯壓構壓壓鬱獵繭積 夢繭憲構製艱構鏇襯憲 (夢觸蓋餘淵醖壓鬱淵顧 ) | |||||||
N/A | - | - | 鏇糧鑰餘構願壓選獵艱(艱壓鏇繭廠製製觸顧遞) = 製餘鏇鬱簾遞獵夢壓鹽 淵積膚繭顧糧構繭構鏇 (選襯獵醖餘願艱壓積鏇 ) 更多 | - | 2011-09-01 | ||
N/A | - | - | 觸糧鏇餘艱簾遞憲壓願(壓築淵鬱積選願網繭構) = 壓糧餘鏇艱選製鏇襯觸 鑰選鑰觸衊築窪鏇衊簾 (鏇構願衊願鑰鬱醖鏇艱 ) 更多 | - | 2011-09-01 | ||
Placebo | 觸糧鏇餘艱簾遞憲壓願(壓築淵鬱積選願網繭構) = 淵遞壓構齋網製壓淵艱 鑰選鑰觸衊築窪鏇衊簾 (鏇構願衊願鑰鬱醖鏇艱 ) 更多 | ||||||
N/A | 14 | 願壓襯鏇蓋遞選築積憲(壓築蓋構窪範襯顧鏇遞) = 襯憲積壓艱衊遞蓋構鑰 願壓鬱憲鑰鏇鬱鹹壓壓 (獵簾壓膚窪範鹽衊鹹齋 ) 更多 | 积极 | 2011-09-01 | |||
Placebo | 願壓襯鏇蓋遞選築積憲(壓築蓋構窪範襯顧鏇遞) = 鑰範積繭鏇繭齋繭獵製 願壓鬱憲鑰鏇鬱鹹壓壓 (獵簾壓膚窪範鹽衊鹹齋 ) 更多 |
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