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The first part hydrochloric penehyclidine pretreatment of NF-κB expression in rats with hemorrhagic shock induced acute lung injury in lung tissue Objective: To investigate the hydrochloric acid penehyclidine rats with hemorrhagic shock induced acute lung injury in lung tissue NF- κB activation. Methods: 24 healthy adult Wistar rats, body weight 200 ~ 250 g, male or female, were randomly divided into 3 groups (n = 8): sham operation group (S group), hemorrhagic shock induced acute lung injury model group (A group), hydrochloric acid penehyclidine, group (P group). S group action, venipuncture, and not prepared ALI model; A and P groups after cannulation of the right common carotid artery to monitor blood pressure, the left femoral artery and venous catheters were used for bloodletting reinfusion of blood and administration MAP 35 ~ 45 mmHg 1 h, phlebotomy and blood transfusion to maintain all the loss of blood and saline equivalent to the amount of blood loss and transfusion, preparation ALI model; P group at the bloodletting immediately before intravenous injection of hydrochloric acid penehyclidine 2 mg / kg . In bloodletting completed after 6 h, plasma TNF-α concentrations were measured by ELISA. Calculate the lung wet to dry weight ratio, using immunohistochemical method detection of lung tissue the NF-κBp65 the expression, light microscopy of lung tissue. Results: compared with S group, group A and P plasma TNF-α concentration increased lung tissue expression of NF-κB p65 upregulation (P lt; 0.01) pathological damage; compared with group A, P plasma TNF- α concentration decreased lung tissue downregulation of NF-κB p65 (P lt; 0.05), lung tissue injury is significantly reduced. Conclusion: hydrochloride penehyclidine, can inhibit the inflammatory response by inhibiting the activation of NF-κB in lung tissue, thereby reducing hemorrhagic shock induced acute lung injury. Affect the purpose of the second part of hydrochloric acid penehyclidine rats with hemorrhagic shock induced acute lung injury in lung tissue CD40, CD40L expression: the observation hydrochloric penehyclidine hemorrhagic shock induced acute lung injury in lung tissue of CD40 and CD40L expression impact, explore the lung protection mechanisms, hydrochloride of penehyclidine, as well as different time administration its treatment effect. Methods: A healthy adult rats 40, were randomly divided into five groups (n = 8), the sham group (S, 8), hemorrhagic shock induced acute lung injury model group (A, 8), hydrochloric acid before penehyclidine ether bloodletting immediate administration group (P1 group), hydrochloric acid penehyclidine ether bloodletting completed immediately after administration group (P2 group), the hydrochloric acid penehyclidine reperfusion immediately before administration group (P3 group) at more time points were given the hydrochloric acid penehyclidine 2mg/kg. The remaining four groups of animals except group S Preparation of hemorrhagic shock and acute lung injury model. The calculated lung tissue wet-dry weight ratio, Immunohistochemical detection of lung tissue CD40 and CD40L expression changes detected by ELISA in plasma TNF-α, IL-10 expression changes, pathological changes of lung tissue stained with HE. Results: Compared with S group, group A pathological damage lung tissue of CD40, CD40L expression was significantly increased (P lt; 0.05), plasma TNF-α, IL-10 levels increased (P lt; 0.05). P1, P2, P3 group than in the group A of CD40 and CD40L content was significantly decreased (P lt; 0.05), TNF-α, IL-10 content decreased (P lt; 0.05), lung histopathology relief. Where P1, P2 group compared to the P3 group changes obvious, P1, P2 group difference was not statistically significant. Conclusion: of penehyclidine hydrochloride rat hemorrhagic shock-reperfusion lung tissue of CD40, CD40L expression further reduce TNF-α, IL-10 synthesis and expression, so as to reduce lung injury, lung protective effect. And, given early the hydrochloric penehyclidine of these indicators improve more obvious.
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