RESUMEN
We evaluated the potentially protective effect of nimodipine on rat spinal cord injury. Sprague-Dawley rats received spinal cord injury, and were separated into nimodipine (N = 12) and saline groups (N = 12). Within 1 h of the injury, rats were treated intraperitoneally with nimodipine (1.0 mg/kg) or an equal amount of saline. Treatment was performed 3 times a day for 1 week. Operation BBB score and track experiment were used to measure the physical function of the hind legs 1 and 2 weeks after injury. Two weeks after the injury, malondialdehyde (MDA) content and spinal cord myeloperoxidase (MPO) activity of the injured part were determined, and the glial scar and dead room were studied using the immune tissue chemical test. ED1 was used to observe active gitter cell and macrophages. The physical function of the nimodipine group improved significantly (P < 0.01). Two weeks after injury, spinal cord MDA content in the spinal cord in the nimodipine group (nmol/g, 25.6 ± 9.7 vs 68.5 ± 16.7) and MPO activity (U/g, 252.2 ± 63.9 vs 382.8 ± 108.2) decreased significantly (P < 0.01); nimodipine whole dead space (mm2, 4.45 ± 1.28 vs 6.16 ± 2.65) and ED1 antibody immunity colored positive room (mm2, 1.87 ± 0.42 vs 2.86 ± 1.01) reduced significantly (P < 0.01). Nimodipine treatment could reduce oxidative injury after spinal cord injury, reduce the whole dead space and inflammation, and repair spinal cord injury.
Asunto(s)
Nimodipina/uso terapéutico , Traumatismos de la Médula Espinal/tratamiento farmacológico , Traumatismos de la Médula Espinal/fisiopatología , Animales , Bloqueadores de los Canales de Calcio/uso terapéutico , Radicales Libres , Inmunohistoquímica , Macrófagos/efectos de los fármacos , Masculino , Malondialdehído/química , Microscopía Fluorescente , Destreza Motora , Estrés Oxidativo , Peroxidasa/química , Propilenglicol/química , Ratas , Ratas Sprague-Dawley , Médula Espinal/efectos de los fármacos , Médula Espinal/patologíaRESUMEN
Numerous studies have evaluated the association between the X-ray repair cross-complementing group 1 (XRCC1) DNA repair gene polymorphism -77T>C and lung cancer risk. However, this association is controversial. We used PubMed and Embase to identify 5 case-control studies, which included 2488 lung cancer cases and 2576 controls, for inclusion in a comprehensive meta-analysis in order to assess this association. Two independent reviewers extracted data from the studies, and ORs with 95%CIs were calculated. When all studies were pooled, we found a significant association between the -77T>C polymorphism and lung cancer risk (TT vs CC: OR = 0.52, 95%CI = 0.34-0.80, P = 0.49; TT vs CT: OR = 0.71, 95%CI = 0.62-0.81, P = 0.69; dominant model: OR = 1.45, 95%CI = 1.27-1.66, P = 0.64; recessive model: OR = 0.54, 95%CI = 0.36-0.82, P = 0.24). In a subgroup analysis of nationalities, the -77T>C polymorphism was significantly associated with lung cancer risk in Asian patients. In conclusion, the XRCC1 -77T>C polymorphism might be related to increased risk of lung cancer in Asians. Future studies are needed for conclusive evidence about this association.