RESUMEN
Spinal cord injury (SCI) is terrible damage leading to the deficiencies and results in infinite inconvenience to sufferers. The effective treatment for SCI still meets a larger number of problems. Herein, the underlying molecular mechanism and novel therapy of SCI are urgently to investigate. Arachidonate 12-lipoxygenase (ALOX12) is widely expressed in various cell types and plays important role in modulating different cellular processes, such as platelet aggregation, cell migration and cancer cell proliferation. Nevertheless, the effects of ALOX12 on SCI are unclear. In the study, SCI model was established in wild type (WT) mice and ALOX12 knockout mice. First, ALOX12 expression was up-regulated in spinal cord tissues of WT mice after SCI. ALOX12-knockout mice exhibited improved behavior after SCI operation. Glial activation triggered by SCI was also alleviated in mice with the loss of ALOX12, as evidenced by the down-regulated expression of glial fibrillary acidic protein (GFAP) and Iba-1 in spinal cord samples. Further, SCI-induced inflammation was markedly prevented in ALOX12-knockout mice through blocking inhibitor of NF-κB α (IκBα)/nuclear factor-κB (NF-κB) pathway signaling. Additionally, reducing ALOX12 expression attenuated apoptosis in spinal cord tissues of SCI mice by decreasing Cyto-c, cleaved Caspase-3 and poly (ADP-ribose) polymerases (PARP) expression. The protective role of ALOX12-decrease against SCI was verified in LPS-incubated glial cells through repressing inflammatory response and apoptotic formation. Moreover, transgenic mice with ALOX12 over-expression showed accelerated SCI, associated with intensified inflammation and apoptosis. Based on these results, strategies for inhibiting ALOX12 could be used to prevent SCI development by repressing inflammation and apoptosis.
Asunto(s)
Araquidonato 12-Lipooxigenasa/genética , Regulación de la Expresión Génica , Traumatismos de la Médula Espinal/genética , Traumatismos de la Médula Espinal/prevención & control , Médula Espinal/enzimología , Animales , Apoptosis/efectos de los fármacos , Apoptosis/genética , Araquidonato 12-Lipooxigenasa/deficiencia , Proteínas de Unión al Calcio/genética , Proteínas de Unión al Calcio/metabolismo , Caspasa 3/genética , Caspasa 3/metabolismo , Citocromos c/genética , Citocromos c/metabolismo , Proteína Ácida Fibrilar de la Glía/genética , Proteína Ácida Fibrilar de la Glía/metabolismo , Lipopolisacáridos/farmacología , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Proteínas de Microfilamentos/genética , Proteínas de Microfilamentos/metabolismo , Inhibidor NF-kappaB alfa/genética , Inhibidor NF-kappaB alfa/metabolismo , FN-kappa B/genética , FN-kappa B/metabolismo , Neuroglía/efectos de los fármacos , Neuroglía/metabolismo , Neuroglía/patología , Poli(ADP-Ribosa) Polimerasas/genética , Poli(ADP-Ribosa) Polimerasas/metabolismo , Transducción de Señal , Médula Espinal/patología , Traumatismos de la Médula Espinal/enzimología , Traumatismos de la Médula Espinal/patologíaRESUMEN
A facile approach to fabricate nanoholes on the surface of a phosphor via a carbothermal reaction between C and BaMgAl10O17 was adopted. Drilling nanoholes greatly enhanced excitation light absorption and consequently increased the quantum efficiency, which provided new insight to help improve the luminescence efficiency of oxygen-containing phosphors.