| Background and objective: Systemic inflammatory response syndrome (SIRS) is a new concept proposed by American college of chest physician (ACCP) and society for critical care medicine (SCCM) in august 1991. At the same time, the standard has been formulated. The concept reflects a systemic response syndrome induced from intrinsic immune response of body, and the syndrome independence to some cause. The systemic response syndrome induces the body to be out of control to inflammatory response. The imbalance and excess inflammatory is the path foundation of the organ damage. It can induce the microcirculation disturbance and proceeded shock and multiple organ dysfunction syndrome (MODS). Once MODS happen, it is very difficult to cure. The medical cost and the mortality will boost largely. Accordingly, blocking the progression from SIRS to MODS is the key point to decrease mortality. Polymorph nuclear europhiles is the most active and the shortest one of the leukocyte. Brown has found that the quantity of PMN and variation of the function correlated closely with the generation and the development. If the PMN can not be cleared, it can release the mediators of inflammation, such as IL-6, IL-8, protease, and oxradical, and to invoke the"breath burst". Then the infernal circle happened and SIRS will be aggravated. So the apoptosis of PMN was regarded as an important mechanism that the inflammatory reaction decreases without injury. Consequently controlling the inflammatory response by promoting PMN apoptosis, is the new concept that deal with inflammatory and infectious diseases. ICAM-3 is a member in the immunoglobulin. It is the third receptor of LFA-1 besides ICAM-1 and ICAM-2. It can participate the cell adhesion, stimulate in coordination, and signal conduction. It play the initialization role in the initial stage of immune reaction. At president it has been found that the leukocyte mainly expresses ICAM-3, especially the rest lymphocyte, monocytes, PMN. The ICAM-3 of apoptosis cell with CD14 of macrophage induces the Ca2+ flow by some bridging molecule. It leads to phosphatidyl serine (PS) ectropion, accordingly the apoptosis cell is promoted to clean up. This experiment intends to research the extra organ effect of emodin and dexamethasone on ICAM-3 of peritoneal macrophage of acute pancreatitis in SIRS.Method:The SAP/SIRS model of SD rat was established by retrograde injection of 1.5% concentration of sodium deoxycholate into common biliopancreatic duct. SIRS model of severe acute pancreatitis The preparation stage of SIRS model of SAP: 20 SD rats were randomly divided into 2 groups, that is, sham operation group , model group of SIRS in SAP, 10 SD rats each group. Macrophage, MΦdosing stage: Macrophages which were taken out from sham-operated group were divided into a separate group (SO group).Macrophage which took out from SIRS in SAP model group was divided into 3 groups. That is, Emodin (EMO) intervention group, Dexamethasone(DEX) intervention group , control group (CON). EMO intervention group (Final intervention consistency: 5ug/ml, final ethanol consistency <0.1%); Dex intervention group (Final intervention consistency: 0.1umol/ml), each intervention group was dosed emodin after macrophages adherent (MΦculture 24h). Selected samples made pathological examination and object detection after making model 24h.The pathological alteration of pancreas was examined with microscope. Detect the expression of ICAM-3 by flow cytometry. Application of MPO method to detect macrophage phagocytosis ability, application technology immunofluorescence to test ICAM-3.Result:1. Sham-operated group and the SIRS model group the patho- logical changes of pancreas specimens: comparison with the sham-operated group, SIRS model group was significant patho- logical changes.2. PMФof rats in each group phagocytic capacity of PMN apoptosis compared:(1). Compared with the sham-operated group, SIRS model group phagocytic capacity decreased with significant difference (2.0±0.5 vs. 3.4±0.6, P <0.05).(2). With the control group, emodin intervention group significantly increased phagocytic capacity (2.8±0.2 vs. 2.0±0.5, P <0.05), phagocytic ability of dexamethasone intervention group than drug blank control group (2.4±0.3 vs. 2.0±0.5, P <0.05).(3). To compare each groups: emodin intervention group and dexamethasone intervention group, emodin intervention group significantly increased phagocytic capacity (2.8±0.2 vs. 2.4±0.3, P <0.05).3. In each group the expression of ICAM-3 compared by flow cytometre.(1). Compared with sham-operated group, SIRS model group ICAM-3 expression was significantly decreased (12.57±5.37 vs. 26.12±3.32, P <0.05).(2). Compared with the control group, the expression of ICAM-3 of emodin intervention group was significantly increased (22.40±2.25vs.12.57±5.37, P < 0.05), the expression of ICAM-3 of dexamethasone intervention group significantly increased (16.64±5.36 vs. 12. 57±5.37, P <0.05).(3). To compare each group: emodin intervention group and dexamethasone intervention group, emodin intervention group of ICAM-3 expression was significantly increased (22.40±2.25 vs. 16.64±5.36, P <0.05).4. In each group the expression of ICAM-3 compared by immunofluorescence technique.(1) .Compared with sham-operated group, control group ICAM-3 expression was significantly decreased (37.5% vs. 80%, P <0.05).(2).Compared with the control group, the expression of ICAM-3 of emodin intervention group was significantly increased (87.5%vs37.5%, P < 0.05), the expression of ICAM-3 of dexamethasone intervention group significantly increased (75% vs37.5%, P<0.05).Conclusion: Compared with sham-operated group, the pathological alteration of pancreas in SIRS group was changed at extent severely. The expression of PMФICAM-3 in emodin intervention group was higher than control group and dexamethasone intervention group. It hint that emodin maybe change the expression level of ICAM-3 of cell membrane, and promote the phagocytic capacity of PMФand the capacity of clearing of PMN.
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