Abstract

Objective To investigate the effect of hemorrhagic shock on dendritic cell accumulation in rat lung and lung injury, and to observe the protective effect of vitamin C. Methods Forty-two Sprague-Dawley rats (6 to 7 weeks old) were randomly divided into 7 groups (n=61 group): control group, hemorrhagic shock groups (HS 2 hours, HS 6 hours and HS 24 hours), and hemorrhagic shock+ vitamin C groups (HS+ VitC 2 hours, HS+ VitC 6 hours and HS+ VitC 24 hours). The rat hemorrhagic shock model was established by withdrawing blood through femoral arteriy. We used immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) technology to detect the expression level of dendritic cell specific intercellular adhesion molecule -3 (DC-SIGN) in rat lung tissues. The mRNA expression levels of TNF-α and IL-6, the myeloperioxidase activity in the lung tissues were tested, the lung injury scours were assessed simultaneously. Results There were few DC-SIGN proteins in rat lungs in control group. The expression levels of DC-SIGN protein increased markedly in hemorrhagic shock groups. The DC-SIGN mRNA concentration in rat lungs increased significantly 2 hours after hemorrhagic shock (P<0.05), and kept in high levels in 24 hours. The TNF-α and IL-6 mRNA concentration, the myeloperoxidase activity in lung tissues, and the histological damage scores of lungs were all increased in hemorrhagic shock groups compared with control group (P<0.05). All these phenomena induced by hemorrhagic shock were relieved when vitamin C was treated before resuscitation (P<0.05). Conclusions Perhaps hemorrhagic shock induced acute lung injury by promoting dendritic cell accumulation in rat lungs.Vitamin C curbed this phenomenon. Key words: Shock, Hemorrhagic; Dendritic cells; Acute lung injury

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