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  • 1
    Online Resource
    Online Resource
    Efficacy and Safety of Ciprofol for Sedation/Anesthesia in Patients Undergoing Hysteroscopy: A Randomized, Parallel-Group, Controlled Trial
    Informa UK Limited ; 2023
    In:  Drug Design, Development and Therapy Vol. Volume 17 ( 2023-06), p. 1707-1717
    Details
    In: Drug Design, Development and Therapy, Informa UK Limited, Vol. Volume 17 ( 2023-06), p. 1707-1717
    Type of Medium: Online Resource
    ISSN: 1177-8881
    URL: Article
    DOI: 10.2147/DDDT.S414243
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2023
    detail.hit.zdb_id: 2451346-5
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  • 2
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    Clinical effect of different doses of ciprofol for induction of general anesthesia in elderly patients: A randomized, controlled trial
    Wiley ; 2023
    In:  Pharmacology Research & Perspectives Vol. 11, No. 2 ( 2023-04)
    Details
    In: Pharmacology Research & Perspectives, Wiley, Vol. 11, No. 2 ( 2023-04)
    Abstract: Ciprofol is a newly developed intravenous anesthetic agent with improved pharmacokinetic properties. Compared to propofol, ciprofol exhibits stronger binding to the GABAA receptor and elicits a greater enhancement of GABAA receptor‐mediated neuronal currents in vitro. The aims of the present clinical trials were to examine the safety and efficacy of different doses of ciprofol for induction of general anesthesia in elderly patients. A total of 105 elderly patients undergoing elective surgery were randomized, in a 1:1:1 ratio, to receive one of three sedation regimens: (1) the C1 group (0.2 mg/kg ciprofol), (2) the C2 group (0.3 mg/kg ciprofol), (3) the C3 group (0.4 mg/kg ciprofol). The primary outcome was the incidence of various adverse events, including hypotension, hypertension, bradycardia, tachycardia, hypoxemia, and injection pain. The secondary outcomes of efficacy were the success rate of general anesthesia induction, the time to anesthesia induction, and the frequency of remedial sedation was recorded in each group. Adverse events occurred in 13 patients (37%) in group C1, 8 patients (22%) in group C2, and 24 patients (68%) in group C3. Compared with group C2, the total incidence of adverse events was significantly higher in group C1 and group C3 ( p   〈  .001).The success rate of general anesthesia induction in the three groups was 100%. Compared with group C1, the frequency of remedial sedation was significantly lower in group C2 and group C3. The outcomes demonstrated that ciprofol at a dose of 0.3 mg/kg has good safety and efficacy in the induction of general anesthesia in elderly patients. Overall, ciprofol is a new and viable option for the induction of general anesthesia in elderly patients undergoing elective surgery.
    Type of Medium: Online Resource
    ISSN: 2052-1707 , 2052-1707
    URL: Issue
    URL: Article
    DOI: 10.1002/prp2.v11.2
    DOI: 10.1002/prp2.1066
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2740389-0
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  • 3
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    Exacerbated cardiac fibrosis induced by β‐adrenergic activation in old mice due to decreased AMPK activity
    Wiley ; 2016
    In:  Clinical and Experimental Pharmacology and Physiology Vol. 43, No. 11 ( 2016-11), p. 1029-1037
    Details
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 43, No. 11 ( 2016-11), p. 1029-1037
    Abstract: Senescent hearts exhibit defective responses to β‐adrenergic receptor (β‐ AR ) over‐activation upon stress, leading to more severe pathological cardiac remodelling. However, the underlying mechanisms remain unclear. Here, we investigated the role of adenosine monophosphate‐activated protein kinase ( AMPK ) in protecting against ageing‐associated cardiac remodelling in mice upon β‐ AR over‐activation. 10‐week‐old (young) and 18‐month‐old (old) mice were subcutaneously injected with the β‐ AR agonist isoproterenol ( ISO ; 5 mg/kg). More extensive cardiac fibrosis was found in old mice upon ISO exposure than in young mice. Meanwhile, ISO treatment decreased AMPK activity and increased β‐arrestin 1, but not β‐arrestin 2, expression, and the effects of ISO on AMPK and β‐arrestin 1 were greater in old mice than in young mice. Similarly, young AMPK α2‐knockout ( KO ) mice showed more extensive cardiac fibrosis upon ISO exposure than that was observed in age‐matched wild‐type ( WT ) littermates. The extent of cardiac fibrosis in WT old mice was similar to that in young KO mice. Additionally, AMPK activities were decreased and β‐arrestin 1 expression increased in KO mice. In contrast, the AMPK activator metformin decreased β‐arrestin 1 expression and attenuated cardiac fibrosis in both young and old mice upon ISO exposure. In conclusion, more severe cardiac fibrosis is induced by ISO in old mice than in young mice. A decrease in AMPK activity, which further increases β‐arrestin 1 expression, is the central mechanism underlying the ageing‐related cardiac fibrosis induced by ISO . The AMPK activator metformin is a promising therapeutic agent for treating ageing‐related cardiac remodelling upon β‐ AR over‐activation.
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    URL: Article
    DOI: 10.1111/cep.2016.43.issue-11
    DOI: 10.1111/1440-1681.12622
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2020033-X
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  • 4
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    DataSheet1.docx
    Frontiers Media SA ; 2022
    In:  Frontiers in Pharmacology Vol. 13 ( 2022-2-17)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 13 ( 2022-2-17)
    Abstract: Resveratrol shows promizing anti-inflammatory effects in recent clinical trials, however its function in cardiovascular patients remains conflicting, suggesting there may be new mechanisms underlying its cardioprotective activity. Acute sympathetic stress induces early activation of the NLR family, pyrin domain containing 3 (NLRP3) inflammasome in cardiomyocytes as a critical step for triggering cardiac inflammation. Thus, this study explored targets of resveratrol activity involved in the inhibition of early inflammasome activation in cardiomyocytes following acute sympathetic stress. Network pharmacology was used to analyze common candidate targets in the sympathetic stress pathway, resveratrol activity, and myocardial inflammation and showed the Phosphoinositol 3—kinase (PI3K)/serine threonine protein kinase (Akt) signaling pathway and the target AKT1 may play a critical role. Molecular docking provided support for potential binding of resveratrol on AKT1. Furthermore, the effect of resveratrol on AKT1 activation was determined in cardiomyocytes. resveratrol dose-dependently inhibited AKT1 activation after activation of β-adrenoceptor. The AKT1 inhibitor A-674563 suppressed the activation of the NLRP3 inflammasome in cardiomyocytes following β-adrenoceptor activation, suggesting that AKT1 is a critical regulator molecule upstream of the NLRP3 inflammasome. Consistently, treatment with resveratrol suppressed β-adrenoceptor-mediated NLRP3 inflammasome activation in both cardiomyocytes and mouse hearts, as well as the resultant cardiac inflammation. In conclusion, resveratrol targets AKT1 to inhibit NLRP3 inflammasome activation in cardiomyocytes and cardiac inflammation following acute sympathetic stress. AKT1 is an important target of resveratrol, which should be considered as a treatment option for cardiovascular patients, especially those at risk of acute sympathetic stress.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
    URL: Article
    DOI: 10.3389/fphar.2022.818127
    DOI: 10.3389/fphar.2022.818127.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2587355-6
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  • 5
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    Tetramisole is a new I K1 channel agonist and exerts I K1 ‐dependent cardioprotective effects in rats
    Wiley ; 2022
    In:  Pharmacology Research & Perspectives Vol. 10, No. 4 ( 2022-08)
    Details
    In: Pharmacology Research & Perspectives, Wiley, Vol. 10, No. 4 ( 2022-08)
    Abstract: Cardiac ischemia, hypoxia, arrhythmias, and heart failure share the common electrophysiological changes featured by the elevation of intracellular Ca 2+ (Ca 2+ overload) and inhibition of the inward rectifier potassium (I K1 ) channel. I K1 channel agonists have been considered a new type of anti‐arrhythmia and cardioprotective agents. We predicted using a drug repurposing strategy that tetramisole (Tet), a known anthelminthic agent, was a new I K1 channel agonist. The present study aimed to experimentally identify the above prediction and further demonstrate that Tet has cardioprotective effects. Results of the whole‐cell patch clamp technique showed that Tet at 1–100 μmol/L enhanced I K1 current, hyperpolarized resting potential (RP), and shortened action potential duration (APD) in isolated rat cardiomyocytes, while without effects on other ion channels or transporters. In adult Sprague–Dawley (SD) rats in vivo, Tet showed anti‐arrhythmia and anticardiac remodeling effects, respectively, in the coronary ligation‐induced myocardial infarction model and isoproterenol (Iso, i.p., 3 mg/kg/day, 10 days) infusion‐induced cardiac remodeling model. Tet also showed anticardiomyocyte remodeling effect in Iso (1 μmol/L) infused adult rat ventricular myocytes or cultured H9c2 (2‐1) cardiomyocytes. Tet at 0.54 mg/kg in vivo or 30 μmol/L in vitro showed promising protections on acute ischemic arrhythmias, myocardial hypertrophy, and fibrosis. Molecular docking was performed and identified the selective binding of Tet with Kir2.1. The cardioprotection of Tet was associated with the facilitation of I K1 channel forward trafficking, deactivation of PKA signaling, and inhibition of intracellular calcium overload. Enhancing I K1 may play dual roles in anti‐arrhythmia and antiventricular remodeling mediated by restoration of Ca 2+ homeostasis.
    Type of Medium: Online Resource
    ISSN: 2052-1707 , 2052-1707
    URL: Issue
    URL: Article
    DOI: 10.1002/prp2.v10.4
    DOI: 10.1002/prp2.992
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2740389-0
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  • 6
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    Hemin mitigates contrast‐induced nephropathy by inhibiting ferroptosis via HO ‐1/Nrf2/ GPX4 pathway
    Wiley ; 2022
    In:  Clinical and Experimental Pharmacology and Physiology Vol. 49, No. 8 ( 2022-08), p. 858-870
    Details
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 49, No. 8 ( 2022-08), p. 858-870
    Abstract: Contrast‐induced nephropathy (CIN) is a common complication with adverse outcome after iodinated‐contrast injection, yet still lacking effective medication. Heme oxygenase‐1 (HO‐1) has been reported to play an important role against renal injuries. Hemin, a HO‐1 inducer and anti‐porphyria medicine, may have a promising effect against CIN. In this study, we aim to investigate the effect of hemin on CIN model and the underlying molecular mechanisms in human proximal tubule epithelial cells (HK‐2). To mimic a common condition in percutaneous coronary intervention (PCI) patients, CIN was induced by intravenous iopromide in high‐fat fed diabetic rats. We found hemin, given right before iopromide, mitigated CIN with enhanced antioxidative capacity and reduced oxidative stress. HK‐2 cells insulted by iopromide demonstrated decreased cell vitality and rising reactive oxygen species (ROS), which could also be inhibited by hemin. The effects of hemin involved a key molecule in ferroptosis, glutathione peroxidase (GPX4), whose down‐expression by small interfering RNA (siRNA) reversed the effect of hemin on HK‐2 cells. Furthermore, hemin's induction of GPX4 involved HO‐1 and nuclear factor erythroid 2‐related factor 2 (Nrf2). Either HO‐1 or Nrf2 inhibitor prevented hemin's effect on GPX4 to a comparable extent, and over‐expression of Nrf2 increased GPX4 expression. Moreover, intervention of ferroptosis inhibitor liproxstatin‐1 also alleviated CIN in vivo. Therefore, we showed hemin mitigated CIN, inhibiting oxidative stress and ferroptosis, by upregulation of GPX4 via activation of HO‐1/Nrf2. Hemin, as a clinical medicine, has a translational significance in treating CIN, and anti‐ferroptosis is a potential therapeutic strategy for CIN.
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    URL: Article
    DOI: 10.1111/cep.v49.8
    DOI: 10.1111/1440-1681.13673
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2020033-X
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  • 7
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    Disulfidptosis classification of hepatocellular carcinoma reveals correlation with clinical prognosis and immune profile
    Elsevier BV ; 2023
    In:  International Immunopharmacology Vol. 120 ( 2023-07), p. 110368-
    Details
    In: International Immunopharmacology, Elsevier BV, Vol. 120 ( 2023-07), p. 110368-
    Type of Medium: Online Resource
    ISSN: 1567-5769
    URL: Article
    DOI: 10.1016/j.intimp.2023.110368
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 2049924-3
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  • 8
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    Protective effects of a novel trimerized sTNFRII on acute liver injury
    Elsevier BV ; 2012
    In:  International Immunopharmacology Vol. 13, No. 1 ( 2012-05), p. 88-92
    Details
    In: International Immunopharmacology, Elsevier BV, Vol. 13, No. 1 ( 2012-05), p. 88-92
    Type of Medium: Online Resource
    ISSN: 1567-5769
    URL: Article
    DOI: 10.1016/j.intimp.2012.03.013
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2012
    detail.hit.zdb_id: 2049924-3
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  • 9
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    Regulation of cell survival by the HIP-55 signaling network
    Royal Society of Chemistry (RSC) ; 2014
    In:  Molecular BioSystems Vol. 10, No. 6 ( 2014), p. 1393-
    Details
    In: Molecular BioSystems, Royal Society of Chemistry (RSC), Vol. 10, No. 6 ( 2014), p. 1393-
    Type of Medium: Online Resource
    ISSN: 1742-206X , 1742-2051
    URL: Article
    DOI: 10.1039/c3mb70552h
    Language: English
    Publisher: Royal Society of Chemistry (RSC)
    Publication Date: 2014
    detail.hit.zdb_id: 2188635-0
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  • 10
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    A metabolite of Danshen formulae attenuates cardiac fibrosis induced by isoprenaline, via a NOX 2/ ROS /p38 pathway
    Wiley ; 2015
    In:  British Journal of Pharmacology Vol. 172, No. 23 ( 2015-12), p. 5573-5585
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 172, No. 23 ( 2015-12), p. 5573-5585
    Abstract: Cardiac fibrosis is a common feature of advanced coronary heart disease and is characteristic of heart disease. However, currently available drugs against cardiac fibrosis are still very limited. Here, we have assessed the role of isopropyl 3‐(3,4‐dihydroxyphenyl)‐2‐hydroxylpropanoate ( IDHP ), a new metabolite of D anshen D ripping P ills, in cardiac fibrosis mediated by the β ‐adrenoceptor agonist, isoprenaline, and its underlying mechanisms. Experimental Approach Identification of IDHP was identified by mass spectrometry, and proton and carbon nuclear magnetic resonance spectra. Myocardial collagen was quantitatively assessed with Picrosirius Red staining. Expression of mRNA for collagen was evaluated with real‐time PCR . Phosphorylated and total p 38 MAPK , NADPH oxidase ( NOX ) and superoxide dismutase ( SOD ) were analysed by W estern blot. Generation of reactive oxygen species ( ROS ) generation was evaluated by dihydroethidium ( DHE ) fluorescent staining. NOX2 was knocked down using specific siRNA . Key Results IDHP attenuated β ‐adrenoceptor mediated cardiac fibrosis in vivo and inhibited isoprenaline‐induced proliferation of neonatal rat cardiac fibroblasts ( NRCFs ) and collagen I synthesis in vitro . Phosphorylation of p 38 MAPK , which is an important mediator in the pathogenesis of isoprenaline‐induced cardiac fibrosis, was inhibited by IDHP . This inhibition of phospho‐ p 38 by IDHP was dependent on decreased generation of ROS . These effects of IDHP were abolished in NRCFs treated with siRNA for NOX2 . Conclusions and Implications IDHP attenuated the cardiac fibrosis induced by isoprenaline through a NOX2 / ROS /p38 pathway. These novel findings suggest that IDHP is a potential pharmacological candidate for the treatment of cardiac fibrosis, induced by β ‐adrenoceptor agonists. Linked Articles This article is part of a themed section on Chinese Innovation in Cardiovascular Drug Discovery. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-23
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    URL: Article
    DOI: 10.1111/bph.2015.172.issue-23
    DOI: 10.1111/bph.13133
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2029728-2
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