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1.
J Affect Disord ; 339: 384-391, 2023 10 15.
Artículo en Inglés | MEDLINE | ID: mdl-37442452

RESUMEN

BACKGROUND: Negative life events are major triggers for depression. How individual physical qualities and psychological resources affect the relationship between negative life events and depression in college students remains to be studied. Therefore, we constructed a structural equation model to explore the mediating effect of trait anxiety and the moderating effect of self-esteem in the relationship between negative life events and depression among college students. METHODS: A total of 6224 Chinese college students (aged 16-25) in Jiangxi Province in the central area of China completed the online survey. A moderated mediation model was tested to verify the hypothesis. RESULTS: The mediation analysis showed a significant indirect effect of negative life events on depression through trait-anxiety. Mediation was moderated by self-esteem, which significantly interacted with negative life events to reduce their effect on both anxiety and depression. LIMITATIONS: All measures were self-reported. The cross-sectional design only provides evidence of correlation. CONCLUSIONS: The results in this study revealed that self-esteem as a component of psychological defense mechanism to reduce the harm of environmental threats to individuals. Low self-esteem college students are more likely to have adverse effects when experiencing low-level life events. University mental health education reduces the effects of negative life events on trait anxiety and depression of college students by raising their self-esteem levels.


Asunto(s)
Ansiedad , Autoimagen , Humanos , Universidades , Estudios Transversales , Ansiedad/epidemiología , Ansiedad/psicología , Estudiantes/psicología
2.
Drug Metab Dispos ; 51(6): 782-791, 2023 06.
Artículo en Inglés | MEDLINE | ID: mdl-36921993

RESUMEN

The anti-hypertensive agent hydralazine is a time-dependent inhibitor of the cytosolic drug-metabolizing enzyme aldehyde oxidase (AO). Glutathione (GSH) was found to suppress the inhibition of AO by hydralazine in multiple enzyme sources (human liver and kidney cytosol, human liver S9, rat liver S9, and recombinant human AO) and with different AO substrates (zoniporide, O6 -benzylguanine, and dantrolene). Hydralazine-induced AO inactivation was unaffected when GSH was added to the incubation mixture after pre-incubation of hydralazine with AO (rather than during the pre-incubation), suggesting that GSH traps a hydralazine reactive intermediate prior to enzyme inactivation. Consistent with previous reports of 1-phthalazylmercapturic acid formation when hydralazine was incubated with N-acetylcysteine, we detected a metabolite producing an MS/MS spectrum consistent with a 1-phthalazyl-GSH conjugate. O6 -Benzylguanine, an AO substrate, did not protect against hydralazine-induced AO inactivation, implying that hydralazine does not compete with O6 -benzylguanine for binding to the AO active site. Catalase also failed to protect AO from hydralazine-induced inactivation, suggesting that hydrogen peroxide is not involved. However, an allosteric AO inhibitor (thioridazine) offered some protection, indicating a catalytic role for AO in the bioactivation of hydralazine. AO inhibition by phthalazine (a substrate and inhibitor of AO and a metabolite of hydralazine) was unaffected by the presence of GSH. GSH also prevented hydralazine from inhibiting the nitro-reduction of dantrolene by AO. Furthermore, the GSH-hydralazine combination stimulated dantrolene reduction. Phthalazine inhibited only oxidation reactions, not reduction of dantrolene. Together, these results support the hypothesis that hydralazine is converted to a reactive intermediate that inactivates AO. SIGNIFICANCE STATEMENT: These studies suggest that a reactive intermediate of hydralazine plays a primary role in the mechanism of aldehyde oxidase (AO) inactivation. Inactivation was attenuated by glutathione and unaffected by catalase. Phthalazine (hydralazine metabolite) inhibited AO regardless of the presence of glutathione; however, phthalazine inhibited only oxidation reactions, while hydralazine inhibited both oxidation and reduction reactions. This report advances our mechanistic understanding of hydralazine as an AO inhibitor and provides information to facilitate appropriate use of hydralazine when probing AO metabolism.


Asunto(s)
Aldehído Oxidasa , Espectrometría de Masas en Tándem , Ratas , Animales , Humanos , Aldehído Oxidasa/metabolismo , Catalasa , Dantroleno , Hidralazina/farmacología , Ftalazinas/metabolismo , Glutatión
3.
Front Aging ; 2: 636390, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-35822039

RESUMEN

Early prevention from accelerated neurocognitive declines with advanced aging and the delay of the onset of dementia have became paramount for the achievement of active aging. The present study examined whether the proposed non-pharmaceutical, multi-component exercise training which combined Tai-Chi exercise, Aerobic fitness, and thera-band therapy protects against age-related neurocognitive and physical deterioration in the older participants with amnestic mild cognitive impairment (aMCI). Participants with aMCI in the quasi-experimental design were assigned to the multi-component exercise group or care control group. Evaluations of neuropsychological function and functional fitness were performed before and after 12-weeks intervention, and after 24-weeks follow-up. Our results showed that the multi-component intervention significantly improved various domains of neurocognitive function, particularly in memory- and frontal-related cognition, and better performance on functional fitness, including muscle strength, cardiopulmonary endurance, and agility. Furthermore, such beneficial effects were preserved after 24 weeks. The findings provide supportive evidence that non-pharmaceutically multi-component intervention with Tai-Chi style practice as a core exercise may protect against age-related neurocognitive and physical deficits and lay the path on developing age-friendly intervention programs to delay, or even reverse, the progression of MCI to dementia.

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