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1.
J Glob Antimicrob Resist ; 24: 215-219, 2021 Jan 15.
Artículo en Inglés | MEDLINE | ID: mdl-33460843

RESUMEN

Fusarium species cause many diseases in plants and humans, which results in a great number of economic losses every year. The management of plant diseases and related human diseases caused by Fusarium is challenging as many kinds of Fusarium may be intrinsically resistant to antifungal drugs, not to mention the fact that they can acquire drug resistance, which is common in clinical practice. To date, the drug resistance of Fusarium is mainly related to target alterations, drug efflux and biofilm formation. This article reviews recent studies related to the mechanism of Fusarium resistance, and summarizes the key molecules affecting resistance.

2.
Eur J Pharmacol ; 845: 56-64, 2019 Feb 15.
Artículo en Inglés | MEDLINE | ID: mdl-30582911

RESUMEN

Cerebral ischemia-reperfusion injury is a thorny issue in the treatment of stroke. Energy depletion and oxidative stress are the core mechanisms underlying cerebral ischemia-reperfusion injury. Mitochondrial function is involved in energy production and oxidative stress. It has been reported that mitochondrial uncoupling protein 2 (UCP2) may be involved in the regulation of cerebral ischemia-reperfusion injury. We hypothesized that UCP2 can regulate cerebral ischemia-reperfusion injury by regulating energy supply and oxidative stress. To test this hypothesis, we used a middle cerebral artery occlusion model in male C57BL/6 mice with/without genipin--an UCP2-specific inhibitor. We measured the expression and/or activity of UCP2, SIRT3, the level of ATP, and antioxidant-related molecules in the cerebral cortex and the LDH in serum after ischemia-reperfusion, the level of apoptosis was reflected by the level of cleaved-caspase3 and tunel staining. The results showed an increase in the expression of UCP2, coinciding with an increase in the level of apoptosis, NAD+/NADH ratio, SIRT3 activity, LDH release and a decrease in the level of ATP and antioxidant-related molecules after 1 h of ischemia and 24 h of reperfusion. These findings suggest that UCP2 may regulate energy supply and oxidative stress in ischemia-reperfusion injury. Interestinly, above changes can be reserved by administration of genipin with the brain damage level going down. In conclusion, the UCP2-SIRT3 signaling pathway is involved in the regulation of cerebral ischemia-reperfusion injury as a bridge between energy metabolism and oxidative stress. Genipin protects against cerebral ischemia-reperfusion injury by inhibiting UCP2.


Asunto(s)
Iridoides/uso terapéutico , Mitocondrias/metabolismo , Fármacos Neuroprotectores/uso terapéutico , Daño por Reperfusión/prevención & control , Sirtuina 3/metabolismo , Accidente Cerebrovascular/tratamiento farmacológico , Proteína Desacopladora 2/metabolismo , Animales , Apoptosis , Metabolismo Energético , Iridoides/farmacología , Masculino , Ratones , Ratones Endogámicos C57BL , Fármacos Neuroprotectores/farmacología , Estrés Oxidativo , Especies Reactivas de Oxígeno , Transducción de Señal
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