ABSTRACT
La epilepsia es un trastorno neurológico que afecta aproximadamente al 1% de la población mundial. Estudios realizados en humanos y animales de experimentación sugieren que mediadores de inflamación, como las citocinas, participan en la fisiopatología de la epilepsia; entre ellos, la interleucina-1beta (IL-1ß) podría participar en la susceptibilidad para generar crisis convulsivas así como en la muerte neuronal causada por las convulsiones, aunque algunos hallazgos son contradictorios. En este documento se revisa el conocimiento actual que establece una relación entre la IL-1ß, las crisis convulsivas y la muerte neuronal.
Epilepsy is a neurological disorder affecting almost 1% of the world population. Experimental human and animal studies suggest that inflammation mediators, like cytokines, participate in the physiopathology of epilepsy. Interleukin-1beta (IL-1ß) could influence susceptibility for seizures, as well as neuronal death caused by seizures, although some findings are contradictory. This document reviews the current knowledge establishing a connection between IL-1ß, seizures and neuronal death.
Subject(s)
Animals , Humans , Interleukin-1beta/physiology , Neurons/physiology , Seizures/etiology , Cell Death/physiologyABSTRACT
En general, los factores genéticos influencian la respuesta inflamatoria e inmune, haciendo que losindividuos puedan responder de manera diferente a un mismo cambio en el ambiente. Así, el perfil genéticode cada individuo modula o influencia esa respuesta. La interleukina 1ß (IL-1 ß) es un potente activadorde la actividad osteoclástica y una variación genética de la proteína, conocida como polimorfismo, puedeaumentar su efecto, lo que afectaría negativamente el pronóstico en los tratamientos odontológicos. Elestudio de los polimorfismos genéticos de las interleuquinas se ha convertido en tema de gran interésy debate académico en diferentes ramas de la salud, debido a la importancia que parecen tener comomoduladores de los procesos de reabsorción ósea. Porque los polimorfismos genéticos pueden ayudar a explicar las diferentes respuestas al tratamiento endodóntico en diferentes pacientes. El propósito de estarevisión es actualizar la información previamente publicada relacionada con los polimorfismos genéticos.
Genetic factors influence inflammatory and immune responses in general, and individuals may responddifferently to common environmental challenges. Therefore the genetic profile for every individual moduleor influence that response. Interleukin 1ß (IL-1 ß) is a potent activator of osteoclastic activity and geneticvariation of the protein, known as polymorphism, may increase its effect, which would negatively affectthe prognosis of dental treatment. The study of genetic polymorphisms of interleukins has become atopic of great interest and academic debate in different areas of health, given the importance they seemto have as modulators of bone resorption processes. Because of the genetic polymorphisms might helpexplain the different responses to endodontic treatment in different patients, the purpose of this literaturereview is to update previously published information regarding genetic polymorphism.
Subject(s)
Humans , Cytokine-Induced Killer Cells , Interleukin-1beta , Periodontal Diseases , Polymorphism, GeneticABSTRACT
Objective To observe the effect of intrathecal injection of siRNA targeting Toll-like receptor 4 (TLR4) on neuropathic pain and spinal cord levels of TLR4, IL-1β, and TNF-α in rat model of chronic constriction injury (CCI). Methods Male Sprague-Dawley rats were randomly divided into four groups (n = 10): the sham group (intrathecal normal saline, IT NS), CCI group (CCI+IT NS), mismatch siRNA group (CCI+IT mismatch siRNA), and siRNA-TLR4 group (CCI+IT siRNA-TLR4). The lumbar intrathecal catheters were implanted in rats and CCI models were established as previously described. The TLR4 siRNA were administered intrathecally for 7 days starting from 1 day before surgery. The spinal cord expression of TLR4 mRNA was assessed by real-time PCR. Levels of TNF-α and IL-1β in spinal cord were detected by ELISA. The thermal and mechanical nociceptive thresholds were assessed by paw withdrawal latency (PWL) to radiant heat and von Frey filaments. Results Compared with the sham group, animals in CCI group had significantly lower mechanical and thermal pain thresholds, higher expression of TLR4 mRNA and levels of IL-1β, TNF-α in the spinal cord (P<0.05). Rats in the siRNA-TLR4 group had significantly higher mechanical and thermal pain thresholds (at 1, 3, and 7 days after ligation, P<0.05) and significantly lower expression of TLR4 mRNA and levels of IL-1β, TNF-α in the spinal cord compared with those in the CCI group and mismatch siRNA group(P<0.05). Conclusion Intrathecal injection of siRNA-TLR4 can decrease the levels of inflammatory factors by silencing the TLR4 in the spinal cord of rats, and subsequently relieve the neuropathic pain induced by CCI.