2006World Journal of GastroenterologyOpen access

Expression of macrophage inflammatory protein-1α in Kupffer cells following liver ischemia or reperfusion injury in rats

Wei Ma

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Abstract

AIM: To explore the expression of macrophage inflammatory protein-1alpha (MIP-1alpha) in Kupffer cells (KCs) following liver ischemia/reperfusion injury IRI in rats. METHODS: Forty male SD rats were divided randomly into five groups. A model of partial warm ischemia/reperfusion injury in the rat liver was established. KCs were isolated and incubated one hour, six hours, 12 h, and 24 h after the reperfusion. Tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in the supernatants were measured by ELISA. MIP-1alpha in KCs was detected by immunocytochemical and RT-PCR. RESULTS: No or few MIP-1alpha protein and mRNA were expressed in the KCs of the control group. Its expression in the IRI group had a significant increase after the reperfusion (P < 0.05), which was contrary to the control group. CONCLUSION: The active behavior of the MIP-1alpha gene in KCs following liver ischemia/reperfusion injury is assumed to be one of the major causes for the hepatic ischemia/reperfusion injury.

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AIM: To explore the expression of macrophage inflammatory protein-1alpha (MIP-1alpha) in Kupffer cells (KCs) following liver ischemia/reperfusion injury IRI in rats. METHODS: Forty male SD rats were divided randomly into five groups. A model of partial warm ischemia/reperfusion injury in the rat liver was established. KCs were isolated and incubated one hour, six hours, 12 h, and 24 h after the reperfusion. Tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in the supernatants were measured by ELISA. MIP-1alpha in KCs was detected by immunocytochemical and RT-PCR. RESULTS: No or few MIP-1alpha protein and mRNA were expressed in the KCs of the control group. Its expression in the IRI group had a significant increase after the reperfusion (P < 0.05), which was contrary to the control group. CONCLUSION: The active behavior of the MIP-1alpha gene in KCs following liver ischemia/reperfusion injury is assumed to be one of the major causes for the hepatic ischemia/reperfusion injury.

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Available abstract

AIM: To explore the expression of macrophage inflammatory protein-1alpha (MIP-1alpha) in Kupffer cells (KCs) following liver ischemia/reperfusion injury IRI in rats. METHODS: Forty male SD rats were divided randomly into five groups. A model of partial warm ischemia/reperfusion injury in the rat liver was established. KCs were isolated and incubated one hour, six hours, 12 h, and 24 h after the reperfusion. Tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in the supernatants were measured by ELISA. MIP-1alpha in KCs was detected by immunocytochemical and RT-PCR. RESULTS: No or few MIP-1alpha protein and mRNA were expressed in the KCs of the control group. Its expression in the IRI group had a significant increase after the reperfusion (P < 0.05), which was contrary to the control group. CONCLUSION: The active behavior of the MIP-1alpha gene in KCs following liver ischemia/reperfusion injury is assumed to be one of the major causes for the hepatic ischemia/reperfusion injury.

Key concepts: Ischemia, Reperfusion injury, Medicine, Tumor necrosis factor alpha, Macrophage, Macrophage inflammatory protein, Liver injury, Kupffer cell

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