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AIM: To explore the expression of macrophage inflammatory protein-la (MlP-1α) 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-α) and interleukin-1beta (IL-1β) in the supernatants were measured by ELISA. MIP-1αin KCs was detected by immunocytochemical and RT-PCR. RESULTS: No or few MIP-1αprotein 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-1αgene in KCs following liver ischemia/reperfusion injury is assumed to be one of the major causes for the hepatic ischemia/reperfusion injury.
AIM: To explore the expression of macrophage inflammatory protein-la (MlP-1α) 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 KI was isolated and incubated for one hour, six hours, 12 h, and 24 h after the reperfusion. Tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL- ) in the supernatants were measured by ELISA. MIP-1αin KCs were detected by immunocytochemical and RT-PCR. RESULTS: No or few MIP-1αprotein and mRNA were expressed in the KCs of the control group. Its expression in the IRI group had a CONCLUSION: The active behavior of the MIP-1αgene in KCs following liver ischemia / reperfusion injury was assumed to be one of the major causes for the hepatic ischemia / reperfusion injury.