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  • Ovid Technologies (Wolters Kluwer Health)  (9)
  • Pharmacy  (9)
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  • Ovid Technologies (Wolters Kluwer Health)  (9)
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  • Pharmacy  (9)
  • 1
    In: Pharmacogenetics and Genomics, Ovid Technologies (Wolters Kluwer Health), Vol. 24, No. 6 ( 2014-06), p. 306-313
    Type of Medium: Online Resource
    ISSN: 1744-6872
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2048376-4
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Journal of Cardiovascular Pharmacology Vol. 76, No. 2 ( 2020-08), p. 246-254
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 76, No. 2 ( 2020-08), p. 246-254
    Abstract: Cardiac hypertrophy causes heart failure and is associated with hyperglycemia in patients with diabetes mellitus. Mibefradil, which acts as a T-type calcium channel blocker, exerts beneficial effects in patients with heart failure. In this study, we explored the effects and mechanism of mibefradil on high-glucose–induced cardiac hypertrophy in H9c2 cells. H9c2 cells were incubated in a high-glucose medium and then treated with different concentrations of mibefradil in the presence or absence of the Akt inhibitor MK2206 or mTOR inhibitor rapamycin. Cell size was evaluated through immunofluorescence, and mRNA expression of cardiac hypertrophy markers (atrial natriuretic peptide, brain natriuretic peptide, and β-myosin heavy chain) was assessed by using quantitative real-time polymerase chain reaction. Changes in the expression of p-PI3K, p-Akt, and p-mTOR were evaluated using Western blotting, and autophagosome formation was detected using transmission electron microscopy. Our results indicate that mibefradil reduced the size of H9c2 cells, decreased mRNA expression of atrial natriuretic peptide, brain natriuretic peptide, and β-myosin heavy chain, and decreased the level of autophagic flux. However, MK2206 and rapamycin induced autophagy and reversed the effects of mibefradil on high-glucose–induced H9c2 cells. In conclusion, mibefradil ameliorated high-glucose–induced cardiac hypertrophy by activating the PI3K/Akt/mTOR pathway and inhibiting excessive autophagy. Our study shows that mibefradil can be used therapeutically to ameliorate cardiac hypertrophy in patients with diabetes mellitus.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 3
    In: Pharmacogenetics and Genomics, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 5 ( 2023-07), p. 101-110
    Abstract: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by deficits in social communication and restrictive behaviors. Mouse nerve growth factor (mNGF), a neurotrophic factor, is critical for neuronal growth and survival, and the mNGF treatment is considered a promising therapy for neurodegeneration. In light of this, we aimed to evaluate the effect of mNGF on neurological function in ASD. Methods An ASD rat model was established by intraperitoneal injection of valproic acid (VPA). Social behavior, learning, and memory of the rats were measured. TdT-mediated dUTP Nick-end labeling and Nissl assays were performed to detect neuronal apoptosis and survival in the hippocampus and prefrontal cortex. Apoptosis-related proteins and oxidative stress markers were detected. Results mNGF improved locomotor activity, exploratory behavior, social interaction, and spatial learning and memory in VPA-induced ASD rats. In the hippocampus and prefrontal cortex, mNGF suppressed neuronal apoptosis, increased the number of neurons, superoxide dismutase, and glutathione levels, and decreased reactive oxygen species, nitric oxide, TNF-α, and IL-1β levels compared with the VPA group. In addition, mNGF increased the levels of Bcl-2, p-phosphoinositide-3-kinase (PI3K), and p-serine/threonine kinase (Akt), and decreased the levels of Bax and cleaved caspase-3, while the PI3K inhibitor LY294002 reversed these effects. Conclusion These data suggest that mNGF suppressed neuronal apoptosis and ameliorated the abnormal behaviors in VPA-induced ASD rats, in part, by activating the PI3K/Akt signaling pathway.
    Type of Medium: Online Resource
    ISSN: 1744-6872
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2048376-4
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Journal of Cardiovascular Pharmacology Vol. 79, No. 6 ( 2022-03-02), p. 925-934
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 79, No. 6 ( 2022-03-02), p. 925-934
    Abstract: Activation of adventitial fibroblasts (AFs) on vascular injury contributes to vascular remodeling. Hydrogen sulfide (H 2 S), a gaseous signal molecule, modulates various cardiovascular functions. The aim of this study was to explore whether exogenous H 2 S ameliorates transforming growth factor-β1 (TGF-β1)–induced activation of AFs and, if so, to determine the underlying molecular mechanisms. Immunofluorescent staining and western blot were used to determine the expression of collagen I and α-smooth muscle actin. The proliferation and migration of AFs were performed by using cell counting Kit-8 and transwell assay, respectively. The mitochondrial morphology was assessed by using MitoTracker Red staining. The activation of signaling pathway was evaluated by western blot. The mitochondrial reactive oxygen species and mitochondrial membrane potential were determined by MitoSOX and JC-1 (5,5′,6,6′-tetrachloro-1,1,3,3′-tetraethylbenzimidazolyl carbocyanine iodide) staining. Our study demonstrated exogenous H 2 S treatment dramatically suppressed TGF-β1–induced AF proliferation, migration, and phenotypic transition by blockage of dynamin-related protein 1 (Drp1)–mediated mitochondrial fission and regulated mitochondrial reactive oxygen species generation. Moreover, exogenous H 2 S reversed TGF-β1–induced mitochondrial fission and AF activation by modulating Rho-associated protein kinase 1–dependent phosphorylation of Drp1. In conclusion, our results suggested that exogenous H 2 S attenuates TGF-β1–induced AF activation through suppression of Drp1-mediated mitochondrial fission in a Rho-associated protein kinase 1–dependent fashion.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 5
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Therapeutic Drug Monitoring Vol. 38, No. 3 ( 2016-06), p. 343-349
    In: Therapeutic Drug Monitoring, Ovid Technologies (Wolters Kluwer Health), Vol. 38, No. 3 ( 2016-06), p. 343-349
    Type of Medium: Online Resource
    ISSN: 0163-4356
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2048919-5
    SSG: 15,3
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  • 6
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Journal of Cardiovascular Pharmacology Vol. 74, No. 1 ( 2019-07), p. 71-79
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 74, No. 1 ( 2019-07), p. 71-79
    Abstract: Ganglioside has been implicated to play important roles in modulating various cell signaling and biological functions. However, the functional analysis of a single ganglioside in a zebrafish model is so far lacking. In this study, we investigated the angiogenic effects of 2 monosialoganglioside compounds isolated from GM1 in zebrafish embryos. First, we showed the tested compounds are adequate safe. Then, we found that these compounds exhibited significant proangiogenic effect through enhancement of endothelial cell proliferation, migration, and differentiation. Furthermore, the 2 compounds were proved to promote angiogenesis through, at least partially, modulating the level of Notch signaling. This study provides the novel insights into the clinical application of the 2 ganglioside compounds and GM1.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 7
    In: Clinical Neuropharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 44, No. 2 ( 2021-3), p. 53-56
    Abstract: Major depressive disorder (MDD) is a heterogeneous psychiatric disorder and considered to be one of the most common mental diseases worldwide. The antidepressant venlafaxine, as a serotonin noradrenaline reuptake inhibitor, is applied to MDD relief. Solute carrier family 6 member 4 ( SLC6A4 ) has been reported to promote the reuptake of serotonin and to be closely correlated to depression. The present study examined whether rs6354 and rs1487971 in SLC6A4 are associated with remission after venlafaxine treatment in MDD patients. Methods This study consisted of 195 Han Chinese patients with MDD, who accepted a 6-week treatment with venlafaxine. Two SLC6A4 single-nucleotide polymorphisms (SNPs) were selected from database of SNP and genotyped by matrix-assisted laser desorption/ionization time of flight mass spectrometer in MassARRAY Analyzer 4 platforms. The 17-item Hamilton Depression Scale was used to access the severity of major depression. Allele and genotype frequencies between patients in remission and nonremission were calculated with online software SHEsis. Results No significant differences in allele or genotype frequencies were observed in rs6354 and rs1487971. There were no significant associations between 2 SNPs and venlafaxine treatment outcome. Conclusions It suggested that rs6354 or rs1487971 within SLC6A4 appears not to be involved in the venlafaxine treatment outcome in Han Chinese patients with MDD.
    Type of Medium: Online Resource
    ISSN: 1537-162X , 0362-5664
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2048796-4
    SSG: 15,3
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  • 8
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Journal of Cardiovascular Pharmacology Vol. 81, No. 1 ( 2022-08-23), p. 85-92
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 81, No. 1 ( 2022-08-23), p. 85-92
    Abstract: Salidroside has anti-inflammatory and antiatherosclerotic effects, and mitochondrial homeostasis imbalance is closely related to cardiovascular disease. The aim of this study was to investigate the effect of salidroside on mitochondrial homeostasis after macrophage polarization and elucidate its possible mechanism against atherosclerosis. RAW264.7 cells were stimulated with 1 μg·mL −1 Lipopolysaccharide and 50 ng·mL −1 IFN-γ establish M1 polarization and were also pretreated with 400 μM salidroside. The relative expression of proinflammatory genes was detected by RT-PCR whereas that of mitochondrial homeostasis–related proteins and nuclear factor kappa-B (NF-κB) was detected by WB. Levels of intracellular reactive oxygen species (ROS), mitochondrial membrane potential, and mass were measured by chemifluorescence whereas that of NF-κB nuclear translocation was detected by immunofluorescence. Compared with the Mφ group, the M1 group demonstrated increased mRNA expression of interleukin-1β , inductible nitric oxide synthase (iNOS), and tumor necrosis factor-α ; increased protein expression of iNOS, NOD-like receptor protein 3, putative kinase 1 , and NF-κB p65 but decreased protein expression of MFN2, Tom20, and PGC-1α; decreased mitochondrial membrane potential and mass; and increased ROS levels and NF-κB p65 nuclear translocation. Salidroside intervention decreased mRNA expression of interleukin-1β and tumor necrosis factor-α compared with the M1 group but did not affect that of iNOS. Furthermore, salidroside intervention prevented the changes in protein expression, mitochondrial membrane potential and mass, ROS levels, and NF-κB p65 nuclear translocation observed in the M1 group. In summary, salidroside ultimately inhibits M1 macrophage polarization and maintains mitochondrial homeostasis after macrophage polarization by increasing mitochondrial membrane potential, decreasing ROS levels, inhibiting NF-κB activation, and in turn regulating the expression of proinflammatory factors and mitochondrial homeostasis–associated proteins.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
    Location Call Number Limitation Availability
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  • 9
    In: Therapeutic Drug Monitoring, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. 2 ( 2021-04), p. 292-297
    Abstract: With the outbreak of COVID-19, it has become very important to improve biosafety measures taken by medical staff. Fewer pretreatment steps correspond to lower chances of infection. The authors established a direct injection technique to analyze levetiracetam (LEV) concentrations in human serum and studied its application in therapeutic drug monitoring. Methods: Serum samples were prepared by hollow fiber centrifugal ultrafiltration and the filtrate was directly injected into a ultra-high performance liquid chromatography apparatus (Waters UPLC BEH C18 column: 50 × 2.1 mm, 1.7 μm) for analysis. The mobile phase consisted of acetonitrile and water (8:92) at a flow rate of 1.0 mL/min. The column temperature was maintained at 30°C. The detected wavelength was 210 nm. Results: A linear relationship was obtained for LEV from 0.625 to 80 mcg/mL ( r 2 = 0.999). The limit of detection for the analysis of LEV was 0.125 mcg/mL. The analysis time was shortened to 4 minutes. The recovery rate of LEV based on the current method was 96.6%–100.1%, whereas the absolute recovery rate was 93.2%–96.8%. The relative SD of intraday and interday precision was 〈 7.3%. Stability was achieved at room temperature for 24 hours after 3 freeze–thaw cycles and at −80°C for 21 days. The method was successfully applied to determine LEV concentrations in the serum of 19 patients. Conclusions: The present method is simple, accurate, and sensitive, and can improve biosafety with the direct injection technique. It is suitable for the analysis of LEV concentrations in therapeutic drug monitoring.
    Type of Medium: Online Resource
    ISSN: 0163-4356
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2048919-5
    SSG: 15,3
    Location Call Number Limitation Availability
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