Mansoureh Eslami1, Leila Alizadeh2, Parastoo Morteza-Zadeh3, Mohammad Sayyah4. 1. Department of Basic Sciences, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. 2. Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran. 3. Department of Biology, Faculty of Basic Sciences, Kharazmi University, Tehran, Iran. 4. Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.
Abstract
Objectives: 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. Methods: 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. Results: 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).Discussion: Our data indicate that LPS preconditioning inhibits neural damage and apoptosis induced by trauma in the hippocampus.
Objectives: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. Methods: 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. Results: Higher expression of caspase3 and caspase7 were accompanied by a higher number of dead neurons in traumaticrats 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).Discussion: Our data indicate that LPS preconditioning inhibits neural damage and apoptosis induced by trauma in the hippocampus.
Authors: Cole Vonder Haar; Sarah K Wampler; Henna S Bhatia; Jenny E Ozga; Cory Toegel; Anastasios D Lake; Christopher W Iames; Caitlyn E Cabral; Kris M Martens Journal: Front Behav Neurosci Date: 2022-03-11 Impact factor: 3.558