更新于：2024-12-06
Fosinopril Sodium
福辛普利钠
更新于：2024-12-06
概要
基本信息
在研机构 |
最高研发阶段批准上市 |
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C30H46NNaO7P |
InChIKeyNIDZYXQFQSHBTG-WATAJHSMSA-N |
CAS号88889-14-9 |
关联
11
项与 福辛普利钠 相关的临床试验一项在健康中国参加者中评估中国产与意大利产福辛普利钠片生物等效性的单剂量、开放性、随机、双向交叉研究
一项在健康中国参加者中评估中国产与意大利产 Monopril (10 mg) 片剂生物等效性的单剂量、开放性、随机、双向交叉研究
Comparison of Efficacy and Safety Between Benidipine and Hydrochlorothiazide in Fosinopril Treated Chronic Kidney Disease Patients With Hypertension: a Randomized Controlled Trial
100 项与 福辛普利钠 相关的临床结果
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100 项与 福辛普利钠 相关的转化医学
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100 项与 福辛普利钠 相关的专利（医药）
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593
项与 福辛普利钠 相关的文献（医药）2024-11-22Open Life Sciences
Fosinopril inhibits Ang II-induced VSMC proliferation, phenotype transformation, migration, and oxidative stress through the TGF-β1/Smad signaling pathway
Article
作者: Chen, Siqi ; Ye, Lingxiang
Abstract:
Fosinopril (FOS) is an angiotensin-converting enzyme inhibitor that can decrease angiotensin II (Ang II) formation, thereby reducing systemic vasoconstriction. This study investigated the impact of FOS on vascular smooth muscle cell (VSMC) phenotypic transformation in hypertension. Experiments using western blotting revealed that FOS inhibits the Ang II-induced downregulation of α-SMA and SM22α and the upregulation of OPN in VSMCs. In addition, CCK8 assays, EdU staining, and Transwell assays demonstrated that FOS reduces Ang II-induced increases in VSMC cell viability, proliferation, migration, and MMP2 and MMP9 expression. Moreover, immunofluorescence and ELISA experiments showed that FOS suppresses Ang II-induced increases in ROS levels, NAD(P)H activity, and NOX2 and NOX4 expression in VSMCs. Western blotting also indicated that FOS inhibits Ang II-induced increases in TGF-β1 and p-Smad2/3 expression in VSMCs. Finally, FOS mitigates Ang II-induced VSMC proliferation, phenotypic transformation, migration, and oxidative stress by inhibiting the TGF-β1/Smad signaling pathway. In conclusion, these results suggest that FOS could be effective in managing vascular diseases, including hypertension.
2024-06-01Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
[Modified Fangji Huangqi Decoction alleviates renal interstitial fibrosis by inhibiting TGF-β1/Smad/Snail signaling pathway during epithelial-mesenchymal transition].
Article
作者: Jin, Li ; Deng, Ya-Wen ; Chen, Dong-Ping
This study investigated the effects of modified Fangji Huangqi Decoction on the expression of proteins related to epithelial-mesenchymal transition(EMT) in a mouse model of unilateral ureteral obstruction( UUO) and in a rat renal tubular epithelial cell(NRK-52E) model of fibrosis induced by transforming growth factor β1(TGF-β1). It aims to decipher the molecular mechanism by which modified Fangji Huangqi Decoction alleviates renal interstitial fibrosis. C57/BL mice were subjected to UUO.After the surgery, the mice were treated with 0. 5-fold and 2-fold concentrations of modified Fangji Huangqi Decoction and fosinopril sodium(positive control) for 7 days. The interstitial collagen deposition in the kidney was assessed by Masson staining. Western blot and RT-qPCR were employed to determine the expression levels of TGF-β1, phosphorylated Smad2/3(p-Smad2/3), Smad2/3, Snail,epithelial cadherin(E-cadherin), alpha smooth muscle actin(α-SMA), and vimentin. The NRK-52E cell model induced by TGF-β1was treated with the serum samples collected from SD rats treated with different concentrations of modified Fangji Huangqi Decoction.The CCK-8 assay was employed to examine the effects of the serum samples on NRK-52E cell proliferation. The cell morphology in different groups was observed under a microscope. Furthermore, the modeled cells were treated with the serum containing 1-fold decoction. Western blot and RT-qPCR were then employed to measure the expression levels of p-Smad2/3, Smad2/3, Snail,E-cadherin, α-SMA, and vimentin in the cells. Under the same conditions, sh RNA was used to silence the Snail gene, and measurements were repeated before and after treatment with the serum containing 1-fold decoction. The results indicated that modified Fangji Huangqi Decoction alleviated the fibrotic injury in the mouse model of UUO and the fibrosis in the NRK-52E cell model. The treatment with the decoction down-regulated the protein and m RNA levels of EMT-related indicators including p-Smad2/3, α-SMA,Snail, and vimentin, while it up-regulated the expression of E-cadherin. After sh RNA silencing of the Snail gene, the protein and m RNA levels of E-cadherin, α-SMA, and vimentin showed no significant differences before and after treatment with the serum containing the decoction. The results suggest that modified Fangji Huangqi Decoction may alleviate renal interstitial fibrosis by inhibiting the TGF-β1/Smad/Snail signaling pathway and regulating the EMT process.
2024-01-01Journal of ethnopharmacology
Equivalent evaluation and biological ingredients of Syringa pinnatifolia against acute myocardial ischemia in mice
Article
作者: Chai, Xingyun ; Chen, Suyile ; Wuken, Shana ; Liu, Changxin ; Ma, Xiaojing ; Xu, Jixuan ; Gao, Xiaoli ; Liang, Yana ; Chen, Hongying ; Jiao, Shungang
ETHNOPHARMACOLOGICAL RELEVANCE:
The peeled roots, stems, and twigs of Syringa pinnatifolia Hemsl., known as Shan-Chen-Xiang (SCX) in Chinese, has the traditional effects such as anti-Khii, clearing heat and relieving pain. It has been clinically applied for the treatment of heart failure and mental abnormalities, and gradually replaced agarwood in Mongolian medicine.
AIM OF STUDY:
The present study aims to evaluate whether the key subfraction C (C), a half composition in mass of total ethanol extract (T) of SCX, exerts an equivalent effect against acute myocardial ischemia (AMI) compared to fraction I (I), and what was the potential pharmacologically active constituents of SCX.
MATERIALS AND METHODS:
Cardiac function, serum marker enzymes, and myocardial tissue pathology of infarcted mice with ligation of the anterior descending (LAD) branch of the left coronary artery were used to evaluate the anti-AMI effect of C and its equivalent potency to that of I. LCMS-IT-TOF was used to identify the main constituents in C and C-. The new and known compounds were isolated from C by a combination of mass spectrometry and bioactivity-guided fractionation methods, and structures were elucidated by extensive spectroscopic and chemical methods, including calculated 13C NMR data, calculated electronic circular dichroism, and single-crystal X-ray crystallography. The protective effect of isolates against oxidative injury induced by H2O2 in H9c2 cells was evaluated according to a previously reported protocol.
RESULTS:
The results of cardiac function, serum marker enzymes and myocardial tissue pathology observations (fosinopril as a positive drug) suggested that C (40 mg/kg, orally administered once a day for 7 days) possessed the anti-AMI effect and was equivalent to that of I, while C- did not show the positive effect. Then, 32 lignans were isolated from C, including the majors (8R,8'R,9S)-4,4'-dihydroxy-3,3',9-trimethoxy-9,9'-epoxylignan (24) and (8R,8'R,9R)-4,4'-dihydroxy-3,3',9-trimethoxy-9,9'-epoxylignan (25), which were confirmed by HPLC and LC-MS characterization. Among them, 15 ones were previously undescribed, including a pair of enantiomers (6a/6b), and 11 ones (1, 2, 6a/6b, 8, 10, 12, 16, 17, 24, and 25) exhibited protective effect against oxidative injury to H9c2 cells at different concentrations (ranged from 0.156 to 80 μM).
CONCLUSION:
C (40 mg/kg) exerts cardioprotective effect in mice, which was equivalent to that of I and T. Lignans, including both representative compounds (24, 25) and other undescribed molecules with low content, significantly contribute to the anti-AMI effect of SCX. However, the anti-AMI property assessment of SCX should not exclude the contribution from the representative sesquiterpenoid ZER. Hence, the exploration of the final potential substances in SCX requires further investigation.
100 项与 福辛普利钠 相关的药物交易
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 心脏衰竭 | 美国 | 1991-05-16 | |
| 高血压 | 美国 | 1991-05-16 |
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临床4期 | 291 | 鏇築顧鹹觸築鬱製鬱積(鏇廠築構獵繭襯顧積鏇) = 餘製顧襯衊築鬱憲範蓋 範選簾選範壓願網簾製 (製顧鹽顧顧鏇壓廠範衊, 糧遞繭壓鹽艱憲鹹範觸 ~ 夢廠夢鏇鏇壓觸鏇壓夢) 更多 | - | 2017-12-11 | |||
(ACEI Continuation) | 鏇築顧鹹觸築鬱製鬱積(鏇廠築構獵繭襯顧積鏇) = 糧簾選淵膚壓鑰艱範壓 範選簾選範壓願網簾製 (製顧鹽顧顧鏇壓廠範衊, 膚餘築醖淵鬱襯蓋憲遞 ~ 鏇簾鹹繭夢鏇製觸網簾) 更多 |
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