2005Acta Academiae Medicinae XuzhouRequires access

The correlation of TNF - #alpha# and ICAM - 1 in rats with ischemia/reperfusion injury

Jie Xiang, Xia Shen, Yang Rongli, Cheng Qiantao

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Abstract

Objective To study the expression of tumor necrosis factor alfa (TNF-α) and inflammatory cell adhesion molecules-1 (ICAM-1) in rats with cerebral ischemia/reperfusion injury(I/R).Methods The model of cerebral I/R was established in S D rats by inducing MCAO ( middle cerebral artery occlusion) for 2 h followed by reperfusion for 0, 2, 6, 12, 24,48 and 96 h separately. Experiments were carried out in a host of groups: i.e. normal control, sham operation, ischemia, ischemia/reperfusion for varied lengths. The expressions of TNF-α and ICAM-1 were determined by immunohistochemistry.Results The expressions of TNF-α and ICAM-1 were higher in the I and I/R groups than in the sham operation and control groups (P0.01). The peak expression of TNF-α appeared earlier than that of ICAM-1; they two were found to have positive correlationship after 24, 48 and 96 h of reperfusion (P0.05), and were present in the same localities in the brain.Conclusion TNF-α and ICAM-1 participate in the inflammatory process in the brain after cerebral I/R in a correlated manner. It is possible that TNF-α induce an upregulation of ICAM-1 expression, playing a role in the process of delayed neuronal necrosis.

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Objective To study the expression of tumor necrosis factor alfa (TNF-α) and inflammatory cell adhesion molecules-1 (ICAM-1) in rats with cerebral ischemia/reperfusion injury(I/R).Methods The model of cerebral I/R was established in S D rats by inducing MCAO ( middle cerebral artery occlusion) for 2 h followed by reperfusion for 0, 2, 6, 12, 24,48 and 96 h separately. Experiments were carried out in a host of groups: i.e. normal control, sham operation, ischemia, ischemia/reperfusion for varied lengths. The expressions of TNF-α and ICAM-1 were determined by immunohistochemistry.Results The expressions of TNF-α and ICAM-1 were higher in the I and I/R groups than in the sham operation and control groups (P0.01). The peak expression of TNF-α appeared earlier than that of ICAM-1; they two were found to have positive correlationship after 24, 48 and 96 h of reperfusion (P0.05), and were present in the same localities in the brain.Conclusion TNF-α and ICAM-1 participate in the inflammatory process in the brain after cerebral I/R in a correlated manner. It is possible that TNF-α induce an upregulation of ICAM-1 expression, playing a role in the process of delayed neuronal necrosis.

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Available abstract

Objective To study the expression of tumor necrosis factor alfa (TNF-α) and inflammatory cell adhesion molecules-1 (ICAM-1) in rats with cerebral ischemia/reperfusion injury(I/R).Methods The model of cerebral I/R was established in S D rats by inducing MCAO ( middle cerebral artery occlusion) for 2 h followed by reperfusion for 0, 2, 6, 12, 24,48 and 96 h separately. Experiments were carried out in a host of groups: i.e. normal control, sham operation, ischemia, ischemia/reperfusion for varied lengths. The expressions of TNF-α and ICAM-1 were determined by immunohistochemistry.Results The expressions of TNF-α and ICAM-1 were higher in the I and I/R groups than in the sham operation and control groups (P0.01). The peak expression of TNF-α appeared earlier than that of ICAM-1; they two were found to have positive correlationship after 24, 48 and 96 h of reperfusion (P0.05), and were present in the same localities in the brain.Conclusion TNF-α and ICAM-1 participate in the inflammatory process in the brain after cerebral I/R in a correlated manner. It is possible that TNF-α induce an upregulation of ICAM-1 expression, playing a role in the process of delayed neuronal necrosis.

Key concepts: Ischemia, ICAM-1, Tumor necrosis factor alpha, Immunohistochemistry, Medicine, Reperfusion injury, Necrosis, Downregulation and upregulation

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