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  • Frontiers Media SA  (112)
  • Pharmacy  (112)
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  • Frontiers Media SA  (112)
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  • Pharmacy  (112)
  • 1
    Online Resource
    Online Resource
    Frontiers Media SA ; 2020
    In:  Frontiers in Pharmacology Vol. 11 ( 2020-11-6)
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 11 ( 2020-11-6)
    Abstract: Background: The pandemic of coronavirus disease 2019 (COVID-19) resulted in grave morbidity and mortality worldwide. There is currently no effective drug to cure COVID-19. Based on analyses of available data, we deduced that excessive prostaglandin E 2 (PGE 2 ) produced by cyclooxygenase-2 was a key pathological event of COVID-19. Methods: A prospective clinical study was conducted in one hospital for COVID-19 treatment with Celebrex to suppress the excessive PGE 2 production. A total of 44 COVID-19 cases were enrolled, 37 cases in the experimental group received Celebrex as adjuvant (full dose: 0.2 g, bid ; half dose: 0.2 g, qd ) for 7–14 days, and the dosage and duration was adjusted for individuals, while seven cases in the control group received the standard therapy. The clinical outcomes were evaluated by measuring the urine PGE 2 levels, lab tests, CT scans, vital signs, and other clinical data. The urine PGE 2 levels were measured by mass spectrometry. The study was registered and can be accessed at http://www.chictr.org.cn/showproj.aspx?proj=50474 . Results: The concentrations of PGE 2 in urine samples of COVID-19 patients were significantly higher than those of PGE 2 in urine samples of healthy individuals (mean value: 170 ng/ml vs 18.8 ng/ml, p & lt; 0.01) and positively correlated with the progression of COVID-19. Among those 37 experimental cases, there were 10 cases with age over 60 years (27%, 10/37) and 13 cases (35%, 13/37) with preexisting conditions including cancer, atherosclerosis, and diabetes. Twenty-five cases had full dose, 11 cases with half dose of Celebrex, and one case with ibuprofen. The remission rates in midterm were 100%, 82%, and 57% of the full dose, half dose, and control group, respectively, and the discharged rate was 100% at the endpoint with Celebrex treatment. Celebrex significantly reduced the PGE 2 levels and promoted recovery of ordinary and severe COVID-19. Furthermore, more complications, severity, and death rate were widely observed and reported in the COVID-19 group of elders and with comorbidities; however, this phenomenon did not appear in this particular Celebrex adjunctive treatment study. Conclusion: This clinical study indicates that Celebrex adjuvant treatment promotes the recovery of all types of COVID-19 and further reduces the mortality rate of elderly and those with comorbidities.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2020
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Frontiers Media SA ; 2022
    In:  Frontiers in Pharmacology Vol. 13 ( 2022-8-24)
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 13 ( 2022-8-24)
    Abstract: Background: The coronavirus disease of 2019 (COVID-19) is a severe public health issue that has infected millions of people. The effective prevention and control of COVID-19 has resulted in a considerable increase in the number of cured cases. However, little research has been done on a complete metabonomic examination of metabolic alterations in COVID-19 patients following treatment. The current project pursues rigorously to characterize the variation of serum metabolites between healthy controls and COVID-19 patients with nucleic acid turning negative via untargeted metabolomics. Methods: The metabolic difference between 20 COVID-19 patients (CT ≥ 35) and 20 healthy controls were investigated utilizing untargeted metabolomics analysis employing High-resolution UHPLC-MS/MS. COVID-19 patients’ fundamental clinical indicators, as well as health controls, were also collected. Results: Out of the 714 metabolites identified, 203 still significantly differed between COVID-19 patients and healthy controls, including multiple amino acids, fatty acids, and glycerophospholipids. The clinical indexes including monocytes, lymphocytes, albumin concentration, total bilirubin and direct bilirubin have also differed between our two groups of participators. Conclusion: Our results clearly showed that in COVID-19 patients with nucleic acid turning negative, their metabolism was still dysregulated in amino acid metabolism and lipid metabolism, which could be the mechanism of long-COVID and calls for specific post-treatment care to help COVID-19 patients recover.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 3
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 12 ( 2021-5-7)
    Abstract: Diabetes increases the risk of stroke, exacerbates neurological deficits, and increases mortality. Non-mitogenic fibroblast growth factor 1 (nmFGF1) is a powerful neuroprotective factor that is also regarded as a metabolic regulator. The present study aimed to investigate the effect of nmFGF1 on the improvement of functional recovery in a mouse model of type 2 diabetic (T2D) stroke. We established a mouse model of T2D stroke by photothrombosis in mice that were fed a high-fat diet and injected with streptozotocin (STZ). We found that nmFGF1 reduced the size of the infarct and attenuated neurobehavioral deficits in our mouse model of T2D stroke. Angiogenesis plays an important role in neuronal survival and functional recovery post-stroke. NmFGF1 promoted angiogenesis in the mouse model of T2D stroke. Furthermore, nmFGF1 reversed the reduction of tube formation and migration in human brain microvascular endothelial cells (HBMECs) cultured in high glucose conditions and treated with oxygen glucose deprivation/re-oxygenation (OGD). Amp-activated protein kinase (AMPK) plays a critical role in the regulation of angiogenesis. Interestingly, we found that nmFGF1 increased the protein expression of phosphorylated AMPK ( p -AMPK) both in vivo and in vitro . We found that nmFGF1 promoted tube formation and migration and that this effect was further enhanced by an AMPK agonist (A-769662). In contrast, these processes were inhibited by the application of an AMPK inhibitor (compound C) or siRNA targeting AMPK. Furthermore, nmFGF1 ameliorated neuronal loss in diabetic stroke mice via AMPK-mediated angiogenesis. In addition, nmFGF1 ameliorated glucose and lipid metabolic disorders in our mouse model of T2D stroke without causing significant changes in body weight. These results revealed that nmFGF1-regulated glucolipid metabolism and angiogenesis play a key role in the improvement of functional recovery in a mouse model of T2D stroke and that these effects are mediated by the AMPK signaling pathway.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 4
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 14 ( 2023-8-28)
    Abstract: Background: Pulmonary arterial hypertension (PAH) is a malignant pulmonary vascular disease that negatively impacts quality of life, exercise capacity, and mortality. This study sought to investigate the relationship between serum uric acid (UA) level and the disease severity and treatment response of patients with PAH and congenital heart disease (PAH-CHD). Methods: This study included 225 CHD patients and 40 healthy subjects. Serum UA was measured in all patients, and UA levels and haemodynamic parameters were re-evaluated in 20 patients who had received PAH-specific drug treatment for at least 7 ± 1 month. Results: Serum UA levels were significantly higher in PAH-CHD patients than in CHD patients with a normal pulmonary artery pressure and normal subjects (347.7 ± 105.7 μmol/L vs. 278.3 ± 84.6 μmol/L; 347.7 ± 105.7 μmol/L vs. 255.7 ± 44.5 μmol/L, p & lt; 0.05). UA levels in the intermediate and high risk groups were significantly higher than those in the low-risk group (365.6 ± 107.8 μmol/L vs. 311.2 ± 82.8 μmol/L; 451.6 ± 117.6 μmol/L vs. 311.2 ± 82.8 μmol/L, p & lt; 0.05). Serum UA levels positively correlated with mean pulmonary arterial pressure, WHO functional class, pulmonary vascular resistance, and NT-proBNP ( r = 0.343, 0.357, 0.406, 0.398; p & lt; 0.001), and negatively with mixed venous oxygen saturation (SvO 2 ) and arterial oxygen saturation (SaO 2 ) ( r = −0.293, −0.329; p & lt; 0.001). UA significantly decreased from 352.7 ± 97.5 to 294.4 ± 56.8 μmol/L ( p = 0.001) after PAH-specific drug treatment for at least 6 months, along with significant decreases in mean pulmonary arterial pressure and pulmonary vascular resistance and increases in cardiac index and mixed SvO 2 . Conclusion: Serum UA can be used as a practical and economic biomarker for risk stratification and the evaluation of PAH-specific drug treatment effects for patients with PAH-CHD.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
    Location Call Number Limitation Availability
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  • 5
    Online Resource
    Online Resource
    Frontiers Media SA ; 2022
    In:  Frontiers in Pharmacology Vol. 13 ( 2022-9-8)
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 13 ( 2022-9-8)
    Abstract: Background: Previous studies have suggested that proton pump inhibitors could impair the antiplatelet effect of clopidogrel. It is uncertain whether ilaprazole affects the antiplatelet effect of clopidogrel. This study aimed to determine the drug-drug interaction between ilaprazole and clopidogrel. Methods: A randomized crossover trial of 40 healthy subjects was performed. Clopidogrel was administered alone or in combination with ilaprazole for 7 days. The maximal platelet aggregation (MPA) to 5 μmol/L adenosine diphosphate was measured by light transmission aggregometry and the platelet reactivity index (PRI) was determined by vasodilator-stimulated phosphoprotein P2Y 12 assay. High on-treatment platelet reactivity (HOPR) was defined as a MPA of & gt;40%. The inhibition of platelet aggregation (IPA) and PRI in the two phases were compared between two regimens after the last dosing. Results: IPA was comparable between the two regimens at 0, 10 and 24 h ( p & gt; 0.05), but higher at 4 h in the clopidogrel alone regimen compared with that in the combined treatment regimen (75.66 ± 18.44% vs. 70.18 ± 17.67%, p = 0.031). The inhibition of PRI was comparable between the two regimens at 0 and 24 h. There were no significant differences in the area under the time-IPA% curve (AUC) or the incidence of HOPR at all time-points between the two regimens. Conclusion: In healthy subjects, ilaprazole has limited effect on the pharmacodynamics of clopidogrel and it may not be clinically relevant. Clinical Trial Registration : [ www.chictr.org.cn ], identifier [ChiCTR2000031482] .
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
    Location Call Number Limitation Availability
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  • 6
    Online Resource
    Online Resource
    Frontiers Media SA ; 2018
    In:  Frontiers in Pharmacology Vol. 9 ( 2018-9-13)
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 9 ( 2018-9-13)
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2018
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
    Location Call Number Limitation Availability
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  • 7
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 8 ( 2017-03-31)
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2017
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
    Location Call Number Limitation Availability
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  • 8
    Online Resource
    Online Resource
    Frontiers Media SA ; 2018
    In:  Frontiers in Pharmacology Vol. 9 ( 2018-9-21)
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 9 ( 2018-9-21)
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2018
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 9
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 12 ( 2021-11-17)
    Abstract: Gonggan (Citrus reticulata Blanco var. gonggan) is one of the most popular citruses. In this study, the effect of Gonggan peel extract (GPE) on gastric injury was investigated. The components in GPE were analysed by HPLC and the gastric injury model in mice was established by ethanol/hydrochloric acid. After treatment by GPE, the pathological changes of gastric tissue were observed by optical microscope. The levels of oxidative stress and inflammation were measure by kit. And the mRNA expression of related gene was determined by qPCR assay. HPLC result showed GPE mainly contained the flavonoids narirutin, hesperidin, nobiletin, tangeretin and 5-demethylnobiletin. Morphological and pathological analysis of gastric tissue revealed that GPE could relieve gastric injury. Also, GPE increased the levels of SOD, GSH-Px, and CAT and decreased the level of MDA. Moreover, GPE decreased the levels of the inflammatory cytokines TNF-α, IFN-γ, IL-1β, and IL-6 to suppress inflammation. In addition, the q-PCR results showed that GPE upregulated the mRNA expression of SOD1, SOD2, γ-GCS, GSH-Px, CAT, and IκBα and downregulated the mRNA expression of NF-κB. In conclusion, GPE alleviated gastric injury caused by ethanol/hydrochloric acid by inhibiting oxidative stress and the inflammatory response. The mechanism by which GPE protects gastric tissues may involve the antioxidative pathway. Therefore, GPE has great potential to be developed as a product to prevent gastric injury.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
    Location Call Number Limitation Availability
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  • 10
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 15 ( 2024-5-17)
    Abstract: Primary Sjögren’s Syndrome (pSS) is a complex autoimmune disorder characterized by exocrine gland dysfunction, leading to dry eyes and mouth. Despite growing interest in biologic therapies for pSS, FDA approval has proven challenging due to trial complications. This review addresses the absence of a molecular-target-based approach to biologic therapy development and highlights novel research on drug targets and clinical trials. A literature search identified potential pSS treatment targets and recent advances in molecular understanding. Overlooking extraglandular symptoms like fatigue and depression is a notable gap in trials. Emerging biologic agents targeting cytokines, signal pathways, and immune responses have proven efficacy. These novel therapies could complement existing methods for symptom alleviation. Improved grading systems accounting for extraglandular symptoms are needed. The future of pSS treatment may involve gene, stem-cell, and tissue-engineering therapies. This narrative review offers insights into advancing pSS management through innovative biologic interventions.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2024
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
    Location Call Number Limitation Availability
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