Eslami Mansoureh, Alizadeh Leila, Morteza-Zadeh Parastoo, Sayyah Mohammad
Department of Basic Sciences, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran.
Neurol Res. 2020 Feb;42(2):91-98. doi: 10.1080/01616412.2019.1709139. Epub 2020 Jan 8.
: Traumatic brain injury (TBI) is a serious medical problem that affects the quality of life. Apoptosis is a form of programmed cell death that happens after trauma. Effector caspases are responsible for initiating apoptosis.: In the present study, we examined the effect of LPS preconditioning (0.1 and 0.5 mg/kg, ip; 5 days prior controlled cortical injury) on apoptosis, 4 and 12 hours after trauma. We investigated possible mechanisms on the expression of caspase3 and caspase7 in hippocampal CA1 and CA3 areas by using immunohistochemistry and Western blotting techniques and also TUNEL-positive cells.: Higher expression of caspase3 and caspase7 were accompanied by a higher number of dead neurons in traumatic rats 4 and 12 hours after trauma(P < 0.05). LPS preconditioning decreased caspase3 and caspase7over-expression and the number of dead neurons in the hippocampus(P < 0.05).: Our data indicate that LPS preconditioning inhibits neural damage and apoptosis induced by trauma in the hippocampus.
创伤性脑损伤（TBI）是一个影响生活质量的严重医学问题。细胞凋亡是创伤后发生的一种程序性细胞死亡形式。效应半胱天冬酶负责启动细胞凋亡。
在本研究中，我们检测了脂多糖预处理（0.1和0.5mg/kg，腹腔注射；在控制性皮质损伤前5天）对创伤后4小时和12小时细胞凋亡的影响。我们通过免疫组织化学和蛋白质印迹技术以及TUNEL阳性细胞研究了海马CA1和CA3区域中半胱天冬酶3和半胱天冬酶7表达的可能机制。
创伤后4小时和12小时，创伤大鼠中半胱天冬酶3和半胱天冬酶7的高表达伴随着更多的死亡神经元（P<0.05）。脂多糖预处理降低了海马中半胱天冬酶3和半胱天冬酶7的过度表达以及死亡神经元的数量（P<0.05）。
我们的数据表明，脂多糖预处理可抑制创伤诱导的海马神经损伤和细胞凋亡。
