更新于：2024-12-07
Isoprenaline Hydrochloride
盐酸异丙肾上腺素
更新于：2024-12-07
概要
基本信息
最高研发阶段批准上市 |
首次获批日期 美国 (1956-03-09) |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构
分子式C11H18ClNO3 |
InChIKeyIROWCYIEJAOFOW-MERQFXBCSA-N |
CAS号5984-95-2 |
关联
22
项与 盐酸异丙肾上腺素 相关的临床试验Early Neurovascular Adaptations in Aging Women
Comparison of the Clinical Utility of Atropine and Isoprenaline in the Invasive Diagnosis of Arrhythmias
Sympathetic Neurovascular Transduction: Role of Adrenergic Receptors and Sex Differences
100 项与 盐酸异丙肾上腺素 相关的临床结果
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100 项与 盐酸异丙肾上腺素 相关的转化医学
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100 项与 盐酸异丙肾上腺素 相关的专利（医药）
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22,058
项与 盐酸异丙肾上腺素 相关的文献（医药）2024-12-01INTERNATIONAL IMMUNOPHARMACOLOGY
Interleukin(IL)-37 attenuates isoproterenol (ISO)-induced cardiac hypertrophy by suppressing JAK2/STAT3-signaling associated inflammation and oxidative stress
Article
作者: Wang, Pengfei ; Guo, Bingyan ; Zhang, Donglei ; Guo, Xiaohua ; Qian, Yuxing ; Wei, Huiqing ; Yan, Jie
BACKGROUND:
Inflammation and oxidative stress have drawn more and more interest in the realm of cardiovascular disease. In many different disorders, IL-37 acts as an anti-inflammatory and suppressor of inflammation. This study aimed to investigate whether IL-37 could alleviate cardiac hypertrophy by reducing inflammation and oxidative stress.
METHODS:
In vivo, a cardiac hypertrophy model was induced by 14 d of daily isoproterenol (ISO, 30 mg/kg/d) injection, followed by weeks of treatment with recombinant human IL-37 (1000 ng/animal), administered three times weekly. Assessments concentrated on markers of inflammation and oxidative stress, apoptosis, myocardial disease, and cardiac shape and function. In vitro, neonatal rat cardiomyocytes (NRCMs) were subjected to ISO (10 µM) to establish a cardiomyocytes hypertrophy model. Subsequent IL-37 treatment (100 ng/ml) was applied to determine its cardioprotective efficacy and to elucidate further the underlying mechanisms involved.
RESULTS:
Significant cardioprotective benefits of IL-37 were seen (in vitro as well as in vivo), primarily through the reduction of oxidative stress, inflammation, apoptosis, and heart hypertrophy markers. Furthermore, IL-37 treatment was associated with a decrease in JAK2 and STAT3 phosphorylation. It is interesting to note that WP1066, a JAK2/STAT3 inhibitor, exhibited antioxidant and anti-inflammatory properties comparable to IL-37, as well as synergistic effects when mixed with the latter.
CONCLUSION:
ISO-induced cardiac hypertrophy is lessened by IL-37 through the reduction of oxidative stress and inflammation. Additionally, the effects of IL-37 are closely related to inactivation of the JAK2/STAT3 signaling pathway. It is anticipated that IL-37 will one day be used to treat cardiovascular illnesses such as heart hypertrophy.
2024-12-01Molecular biology reports
Co-treatment with bone marrow-derived mesenchymal stem cells and curcumin improved angiogenesis in myocardium in a rat model of MI
Article
作者: Abedpour, Neda ; Mirfakhraie, Niki ; Javanmard, Masoumeh Zirak ; Shoorei, Hamed
BACKGROUND:
The cardioprotective properties of mesenchymal stem cells and the therapeutic potential of curcumin (CUR) have been explored. Combining these approaches may enhance stem cell effectiveness and expedite healing. This study aimed to investigate the synergistic effects of co-treating bone marrow mesenchymal stem cells (BMSCs) with curcumin on vascular endothelial growth factor (VEGF) levels, in a rat model of myocardial ischemia (MI).
METHODS AND RESULTS:
Sixty-five male rats were divided into four groups: G1 (healthy control), G2 (MI induced by isoproterenol hydrochloride), G3 (treated with BMSCs), and G4 (co-treated with curcumin and BMSCs). Blood and tissue samples were collected at specific time points (day 1, 7, 15 and 21) after MI induction. Serum levels of lactate dehydrogenase (LDH), creatine kinase (CK), cardiac troponin I (cTnI), aspartate aminotransferase (AST), CK-MB and VEGF were measured. VEGF mRNA and protein expression were evaluated using RT-qPCR and Western blot techniques. Histopathological assessments were performed using H&E staining and CD31 immunofluorescence staining. VEGF expression significantly increased on days 7 and 15 in the CUR-BMSCs group, peaking on day 7. Western blot analysis confirmed elevated VEGF protein expression on days 7 and 15 post-MI. ELISA results demonstrated increased serum VEGF levels on days 7 and 15, reaching the highest level on day 7 in CUR-BMSCs-treated animals. Treated groups showed lower levels of LDH, AST, CK, CK-MB and cTnI compared to the untreated MI group. H&E staining revealed improved myocardial structure, increased formation of new capillaries, in both treatment groups compared to the MI group.
CONCLUSION:
Combining curcumin with BMSCs promotes angiogenesis in the infarcted myocardium after 15 days of MI induction. These findings suggest the potential of this combined therapy approach for enhancing cardiac healing and recovery.
2024-12-01EXPERIMENTAL PHYSIOLOGY
CTRP6‐mediated cardiac protection in heart failure via the AMPK/SIRT1/PGC‐1α signalling pathway
Article
作者: Li, Mengli ; Zhu, Ningjun ; Lin, Xianhe ; Wang, Zhen ; Fan, Tingting
Abstract:
Heart failure (HF) remains a significant global health concern with limited effective treatments available. C1q/TNF‐related protein 6 (CTRP6) is a member of the CTRP family analogous to adiponectin and its role in HF pathogenesis remains unclear. Here, we investigated the impact of CTRP6 on HF progression. To mimic heart failure with reduced ejection fraction (HFrEF), we used isoproterenol injection in mice and administered adenovirus vectors expressing CTRP6 (Ad‐CTRP6) via tail vein injection. We assessed cardiac function through echocardiography and histology. CTRP6's effects on hypertrophy, fibrosis, apoptosis, oxidative stress and mitochondrial function were analysed. Downstream pathways (phosphorylated AMP‐activated protein kinase (p‐AMPK), sirtuin 1 (SIRT1) and peroxisome proliferator‐activated receptor γ coactivator 1‐α (PGC‐1α) were studied in heart tissues. In vitro, isoproterenol‐stimulated H9c2 cardiomyocytes were treated with CTRP6 to examine viability, apoptosis, F‐actin and signalling proteins. Compound C was used to assess AMPK involvement. CTRP6 expression was lower in the plasma of HF patients. In an isoproterenol‐induced HFrEF mouse model, adenovirus‐mediated overexpression of CTRP6 ameliorated cardiac dysfunction and reduced cardiomyocyte apoptosis, oxidative stress, inflammation and myocardial injury markers. Mechanistically, CTRP6 activation of the AMPK/SIRT1/PGC‐1α signalling pathway restored mitochondrial homeostasis, evidenced by reduced mitochondrial reactive oxygen species levels, increased ATP content, and enhanced mitochondrial complex I/III activities in cardiac tissues. In vitro studies using isoproterenol‐stimulated H9c2 cardiomyocytes corroborated these findings, demonstrating that CTRP6 upregulation attenuated hypertrophy, apoptosis, oxidative stress and mitochondrial dysfunction. Furthermore, these effects were partially reversed by the AMPK inhibitor Compound C, implicating the involvement of the AMPK pathway in CTRP6‐mediated cardioprotection. CTRP6 alleviates HF progression through the AMPK/SIRT1/PGC‐1α signalling pathway.
100 项与 盐酸异丙肾上腺素 相关的药物交易
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研发状态
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 心动过缓 | 日本 | 1987-04-16 | |
| 癫痫发作 | 日本 | 1987-04-16 | |
| 眩晕 | 日本 | 1975-12-09 | |
| 阿-斯综合征 | 美国 | 1956-05-25 | |
| 支气管痉挛 | 美国 | 1956-05-25 | |
| 心脏传导阻滞 | 美国 | 1956-05-25 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
N/A | 22,435 | Central neuraxial anesthesia+Glycopyrrolate+dopamine+Hydroxyethyl starch solutions+Epinephrine+desflurane+bupivacaine+Sodium Chloride 0.9%+propofol+atropine+Ephedrine+Isoflurane+Dobutamine+Vasopressin+Isoproterenol+norepinephrine+Prilocaine+Benzocaine+Procaine+Terlipressin+Tetracaine+ropivacaine+Articaine+levobupivacaine+Milrinone+phenylephrine+Sevoflurane+Mepivacaine+lidocaine+Chloroprocaine (Usual Care Group) | 憲顧壓觸襯淵壓積積選(醖襯觸顧範繭顧夢積鹽) = 鹽獵構鏇選夢遞遞繭獵 壓膚衊衊製醖製觸鏇壓 (願網窪壓網鏇顧餘壓網, 範廠醖襯製鑰鏇構淵繭 ~ 窪顧夢醖願淵鹽齋製構) 更多 | - | 2019-05-16 | ||
Central neuraxial anesthesia+Glycopyrrolate+dopamine+Hydroxyethyl starch solutions+Epinephrine+desflurane+bupivacaine+Sodium Chloride 0.9%+propofol+atropine+Ephedrine+Isoflurane+Dobutamine+Vasopressin+Isoproterenol+norepinephrine+Prilocaine+Benzocaine+Procaine+Terlipressin+Tetracaine+ropivacaine+Articaine+levobupivacaine+Milrinone+phenylephrine+Sevoflurane+Mepivacaine+lidocaine+Chloroprocaine (Hypotension Decision Support) | 憲顧壓觸襯淵壓積積選(醖襯觸顧範繭顧夢積鹽) = 鹹顧廠選範壓鏇窪蓋蓋 壓膚衊衊製醖製觸鏇壓 (願網窪壓網鏇顧餘壓網, 選廠廠選選獵簾築艱淵 ~ 醖積糧憲醖遞廠壓構獵) 更多 | ||||||
N/A | 40 | (Healthy Seniors) | 淵齋蓋構繭餘鏇選鹽鬱(願願積築襯鹽觸鏇獵築) = 窪襯壓窪構顧憲鹹鏇顧 構願鬱顧遞餘夢願鏇鹽 (廠鹹顧齋願糧觸獵簾夢, 醖夢鬱鹽餘窪鑰艱鏇簾 ~ 夢獵蓋構選襯壓鹽網網) 更多 | - | 2019-04-23 | ||
(HFpEF) | 淵齋蓋構繭餘鏇選鹽鬱(願願積築襯鹽觸鏇獵築) = 廠鹹壓廠築窪製窪衊鹹 構願鬱顧遞餘夢願鏇鹽 (廠鹹顧齋願糧觸獵簾夢, 衊築齋蓋衊膚淵築網網 ~ 遞糧鹹選願選艱壓膚製) 更多 | ||||||
N/A | 1,712 | 選醖獵範鹹選蓋廠淵淵(艱憲糧鑰鑰齋艱膚觸鹹) = 窪襯蓋廠餘築齋糧顧壓 醖窪鑰齋淵廠夢衊廠遞 (艱積範膚醖蓋廠鑰遞構 ) | - | 2018-03-18 | |||
選醖獵範鹹選蓋廠淵淵(艱憲糧鑰鑰齋艱膚觸鹹) = 鑰顧憲構積艱鑰艱鹹窪 醖窪鑰齋淵廠夢衊廠遞 (艱積範膚醖蓋廠鑰遞構 ) | |||||||
临床2期 | 131 | (Adenosine and Isoproterenol) | 淵淵廠獵糧齋範選鏇選(醖願蓋衊艱窪顧醖壓鹽) = 醖廠鬱憲選顧觸糧糧壓 襯鏇鏇範積築顧壓壓鹹 (膚鏇糧鹽窪獵醖繭顧襯, 構壓遞衊廠構糧觸鹹鹹 ~ 鏇繭衊憲築糧廠鏇鏇淵) 更多 | - | 2017-12-13 | ||
(Isoproterenol) | 淵淵廠獵糧齋範選鏇選(醖願蓋衊艱窪顧醖壓鹽) = 壓襯積選夢獵壓鬱膚廠 襯鏇鏇範積築顧壓壓鹹 (膚鏇糧鹽窪獵醖繭顧襯, 淵淵襯積觸範糧顧積選 ~ 鏇鹹觸膚壓簾夢夢壓蓋) 更多 | ||||||
N/A | - | (FDG/PET) | 觸壓獵築蓋衊糧鏇夢繭(壓願夢簾選餘網製糧製) = 艱齋糧壓遞觸淵製蓋鬱 獵構蓋網製網襯齋艱積 (選鑰鑰觸憲遞淵願憲繭 ) | - | 2017-05-24 | ||
(MIBI/SPECT) | 膚淵憲顧餘鑰窪遞衊願(衊積艱襯構餘繭顧構糧) = 餘淵鏇蓋醖鏇廠獵鹽製 餘鑰鏇壓鹹願簾積襯衊 (製夢蓋鏇鬱築顧糧鹽網 ) | ||||||
N/A | 224 | 膚廠窪糧醖鏇築積夢鹽(蓋簾繭餘簾窪醖顧構繭) = 齋鬱鑰範醖蓋艱鏇獵齋 憲鬱衊鏇範襯廠鹽糧獵 (構構簾遞鏇繭窪遞夢醖 ) | - | 2016-08-30 | |||
N/A | 20 | 淵廠窪顧積鏇網餘齋壓(製範鬱築繭窪蓋蓋繭繭) = 構鹹醖簾廠憲糧襯齋餘 壓壓廠膚糧選選蓋蓋鏇 (壓蓋遞繭構簾範積選醖, 壓獵衊膚醖構築衊襯壓 ~ 範鬱艱襯繭淵鹹遞夢膚) 更多 | - | 2015-02-23 | |||
临床1/2期 | 10 | 繭夢廠窪夢淵壓遞窪憲(觸鏇願鏇壓襯鹽製願襯) = 襯壓簾艱選衊膚艱膚膚 顧膚膚壓夢糧醖壓壓鬱 (築範繭夢廠構網鬱壓獵, 鏇鬱鹽糧襯窪網鬱觸鏇 ~ 淵遞願窪膚齋齋簾觸襯) 更多 | - | 2012-06-22 |
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