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Objective: To study the nuclear factor-κB (NF-κB) the hippocampal neurons cyclooxygenase -2 (COX-2) after traumatic brain injury (TBI), caspases -3 (Caspase- 3) the regulation of expression, explore progesterone (progesterone, PROG) TBI rat hippocampal neurons protective effect after its possible mechanisms. Methods: Male SD rats were randomly divided into sham group, trauma group and PROG group 90 in accordance with the modified Feeney freefall injury device production in rat brain trauma model (1) trauma group (TBI-1): 1 h after injury, intraperitoneal injection saline (16 mg / kg body weight), 6h after injury to brain tissue; ② trauma group (TBI-2): 1 h after injury, 6h intraperitoneal injection of saline (16 mg / kg body weight) at 24 h after injury ③ trauma group (TBI-3): 1h, 6h intraperitoneal injection of normal saline (16 mg / kg body weight) after injury, after injury, 1d, 2d subcutaneous injection of normal saline (16 mg / kg body weight), in brain tissue; 72h after injury to brain tissue. ④ PROG-1: after injury 1h intraperitoneal injection of PROG (16 mg / kg body quality), 6 h after injury to take brain tissue; ⑤ PROG-2: 1 h after injury, 6h intraperitoneal injection of PROG (16 mg / kg body quality), in injury 24h after brain tissue; ⑥ PROG-3: 1 h after injury, 6h intraperitoneal injection of PROG (16 mg / kg body weight), 1d, 2d subcutaneous injection of PROG (16 mg / kg body weight) after injury, after injury 72h take brain organization. ⑦ sham group (sham-operated): intraperitoneal injection of normal saline was the same phase, and 6h after injury, 24h, 72h animals were sacrificed. HE method, Nissl staining groups of pathological changes in the hippocampal CA1 region. The immunohistochemical method immune Western blotting, observe the injured side of rats hippocampus of NF-κB, COX-2 and prostaglandin E2 (PGE2) and Caspase-3 expression changes observed PROG of these indicators change. Specific protein-positive cell counts and western blot with a semi-quantitative analysis using computer image analysis of immunohistochemistry. All data for statistical analysis using SPSS 13.0 statistical analysis software, to P lt; 0.05 as statistically significant. Results: 6 hours after injury, trauma group hippocampal CA1 region of NF-κB positive neurons (13.5 ± 2.2) compared with sham group increased, COX-2 (16.3 ± 1.9), PGE2 (15.0 ± 2.6), Caspase-3 (11.7 ± 3.3) positive neurons in the number of significant increase compared with sham group. 24 hours after injury, trauma group hippocampal CA1 region of NF-κB positive neurons (24.0 ± 2.5) compared with sham group, a significant increase in the number of COX-2 (35.9 ± 2.7), PGE2 (34.4 ± 2.9) positive neurons significantly increased compared with the sham group (P lt; 0.05), not significantly increase the number of caspase-3-positive neurons (25.1 ± 2.7) compared with sham group; 72 hours after injury, compared with sham-operated rats, the trauma group hippocampal CA1 region of NF-κB (12.8 ± 2.3), COX-2 (22.8 ± 2.7), PGE2 (22.4 ± 2.3), the number of positive neurons was significantly increased, and Caspase-3 positive neurons (33.8 ± 3.8) significantly increased compared with the sham group (P lt; 0.05). To the in PROG therapy, six hours after the injury, number of positive neurons in hippocampal CA1 region of NF-κB (7.9 ± 1.7) compared with the trauma group decreased significantly (P lt; 0.05). 24 hours after injury, NF-kappa B (14.2 ± 1.8), COX-2 (16.6 ± 2.7) PGE2 (16.5 ± 2.0) positive neurons decreased significantly compared with the trauma group (P lt; 0.05). 72 hours after the injury, Caspase-3 positive neurons significantly reduced compared with the trauma group (16.9 ± 1.4) (P lt; 0.05). Conclusion: NF-κB hippocampal neurons, COX-2 and Caspase-3 from the role after TBI; PROG by down-regulating NF-κB to regulate the expression of COX-2, thereby inhibiting Caspase-3-mediated apoptosis program can also by down-regulating NF-κB regulating Caspase-3-mediated apoptosis process in order to achieve the protective effect of rat hippocampal neurons after TBI.
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