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ENGLISH ABSTRACT
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
[Protective effects of heat shock preconditioning on the experimental autoimmune encephalomyelitis rats].
OBJECTIVE: To study the effects of heat shock preconditioning on the expression of heat shock protein-70 (HSP70) and apoptosis of the neuron in experimental autoimmune encephalomyelitis (EAE) rats.
METHODS: Thirty-six Wistar rats were randomly divided into control, EAE and heat shock preconditioning groups (n=12 each). The EAE animal model was induced with guinea pig myelin basic protein. Heat shock preconditioning was performed 24 hrs prior to the EAE model inducement. No treatment was done in the control group. The neurological signs were observed after immunization. The spinal cords were removed and stained with hematoxylin and eosin. HSP70 was detected by immunohistochemistry. Apoptosis of the neuron was measured by TUNEL.
RESULTS: Heat shock preconditioning significantly alleviated clinical signs and neuronal injury. HSP70 expression in the heat shock preconditioning group was significantly higher than in the untreated EAE group (21.08 +/- 0.87 vs 10.17 +/- 0.51; P < 0.01). Heat shock preconditioning suppressed apoptosis of the neuron compared with the EAE group (apoptosis rate: 21.92 +/- 1.00% vs 58.92 +/- 1.67%; P < 0.01).
CONCLUSIONS: Heat shock preconditioning might improve the neurological outcome in EAE rats, possibly through the induction of HSP70 synthesis and the reduction of apoptosis of the neuron in spinal cords.
METHODS: Thirty-six Wistar rats were randomly divided into control, EAE and heat shock preconditioning groups (n=12 each). The EAE animal model was induced with guinea pig myelin basic protein. Heat shock preconditioning was performed 24 hrs prior to the EAE model inducement. No treatment was done in the control group. The neurological signs were observed after immunization. The spinal cords were removed and stained with hematoxylin and eosin. HSP70 was detected by immunohistochemistry. Apoptosis of the neuron was measured by TUNEL.
RESULTS: Heat shock preconditioning significantly alleviated clinical signs and neuronal injury. HSP70 expression in the heat shock preconditioning group was significantly higher than in the untreated EAE group (21.08 +/- 0.87 vs 10.17 +/- 0.51; P < 0.01). Heat shock preconditioning suppressed apoptosis of the neuron compared with the EAE group (apoptosis rate: 21.92 +/- 1.00% vs 58.92 +/- 1.67%; P < 0.01).
CONCLUSIONS: Heat shock preconditioning might improve the neurological outcome in EAE rats, possibly through the induction of HSP70 synthesis and the reduction of apoptosis of the neuron in spinal cords.
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