2012China Medical HeraldRequires access

Influences on ERK signal transduction pathways to nerve cell apoptosis in rats after trauma

Junling Gao

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Abstract

Objective To study the mechanism of ERK signal transduction pathways to nerve cell apoptosis in rats after trauma.Methods Heavy diffuse brain injury(TMI) model was established.Male SD rats(n = 70) were randomly divided into two groups: trauma group and control group.Tuma group was divided into 7 subgroups according to time phase following brain injury: 10,30 min,3,6,24,48,72 h.The expression of p-ERK1/2 and caspase-3 were detected by immunity histochemistry staining;the apoptosis of nerve cell was detected by TUNEL.Results The expression of p-ERK1/2,caspase-3 in the hippocampasl CA1 area in TBI group were increased significantly after injury 3 h compared to those in the control group(P 0.05),and reached the peak at 6 h(P 0.01),the overexpression of p-ERK1/2 and caspase-3 continued to 24 h and 72 h respectively;TUNEL positive cells were increased in TBI group from 3 h to 72 h,and reach the peak at 48 h(P 0.01).Conclusion The activation of ERK signal transduction pathway and expression of caspase-3 may is one of mechanisms of nerve cell apoptosis following traumatic brain injury in rats.

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Objective To study the mechanism of ERK signal transduction pathways to nerve cell apoptosis in rats after trauma.Methods Heavy diffuse brain injury(TMI) model was established.Male SD rats(n = 70) were randomly divided into two groups: trauma group and control group.Tuma group was divided into 7 subgroups according to time phase following brain injury: 10,30 min,3,6,24,48,72 h.The expression of p-ERK1/2 and caspase-3 were detected by immunity histochemistry staining;the apoptosis of nerve cell was detected by TUNEL.Results The expression of p-ERK1/2,caspase-3 in the hippocampasl CA1 area in TBI group were increased significantly after injury 3 h compared to those in the control group(P 0.05),and reached the peak at 6 h(P 0.01),the overexpression of p-ERK1/2 and caspase-3 continued to 24 h and 72 h respectively;TUNEL positive cells were increased in TBI group from 3 h to 72 h,and reach the peak at 48 h(P 0.01).Conclusion The activation of ERK signal transduction pathway and expression of caspase-3 may is one of mechanisms of nerve cell apoptosis following traumatic brain injury in rats.

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Available abstract

Objective To study the mechanism of ERK signal transduction pathways to nerve cell apoptosis in rats after trauma.Methods Heavy diffuse brain injury(TMI) model was established.Male SD rats(n = 70) were randomly divided into two groups: trauma group and control group.Tuma group was divided into 7 subgroups according to time phase following brain injury: 10,30 min,3,6,24,48,72 h.The expression of p-ERK1/2 and caspase-3 were detected by immunity histochemistry staining;the apoptosis of nerve cell was detected by TUNEL.Results The expression of p-ERK1/2,caspase-3 in the hippocampasl CA1 area in TBI group were increased significantly after injury 3 h compared to those in the control group(P 0.05),and reached the peak at 6 h(P 0.01),the overexpression of p-ERK1/2 and caspase-3 continued to 24 h and 72 h respectively;TUNEL positive cells were increased in TBI group from 3 h to 72 h,and reach the peak at 48 h(P 0.01).Conclusion The activation of ERK signal transduction pathway and expression of caspase-3 may is one of mechanisms of nerve cell apoptosis following traumatic brain injury in rats.

Key concepts: Apoptosis, Medicine, TUNEL assay, Signal transduction, MAPK/ERK pathway, Immunohistochemistry, Cell, Caspase 3

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