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目的探讨重症急性胰腺炎(SAP)大鼠血清高迁移率族蛋白-1(HMGB1)水平对胰腺腺泡细胞胀亡的影响。方法将32只SD大鼠随机分为假手术组(SO组,n=8)和SAP组(n=24)。SO组大鼠开腹后仅翻动肠管,SAP组大鼠采用胆胰管内逆行注射3%牛磺胆酸钠的方法建立SAP模型。建模成功后,将SAP组大鼠随机均分为6、12及24 h组,每组8只,分别于上述时点处死大鼠,取静脉血及胰腺组织,行HE染色以观察胰腺组织的病理学改变,行ELISA法检测血清中的HMGB1浓度,以流式细胞仪检测胰腺腺泡细胞的胀亡百分比。结果 SO组大鼠的胰腺腺泡结构完整,偶见单个炎症细胞浸润。SAP-6 h组可见胰腺腺泡肿胀、间质水肿,炎症细胞浸润;SAP-12 h组及SAP-24 h组见胰腺病理学损伤加重,部分腺泡细胞坏死,间质血管瘀血,局灶坏死,且随时间延长病理学损伤加重。3个SAP亚组大鼠的血清HMGB1浓度和胰腺腺泡细胞胀亡百分比均高于SO组(P<0.01),且随时间延长,SAP大鼠的血清HMGB1浓度和胰腺腺泡细胞胀亡百分比均增高(P<0.05)。24 h内SAP大鼠的血清HMGB1浓度与胰腺腺泡细胞胀亡百分比呈正相关(r=0.846,P<0.01)。结论 SAP时,HMGB1在介导炎症反应的同时,可能诱导胰腺腺泡细胞胀亡,从而参与SAP的病理生理过程。
Objective To investigate the effects of serum high mobility group box-1 (HMGB1) on pancreatic acinar cell infiltration in severe acute pancreatitis (SAP) rats. Methods Thirty-two SD rats were randomly divided into sham operation group (SO group, n = 8) and SAP group (n = 24). In the SO group, only the intestine was turned open after laparotomy. The SAP model was established by retrograde injection of 3% sodium taurocholate into the pancreatic duct in the SAP group. After successful modeling, rats in SAP group were randomly divided into 6, 12 and 24 h groups, with 8 rats in each group. Rats were sacrificed at the above time points, and venous blood and pancreatic tissues were obtained. HE staining was performed to observe pancreatic tissues The pathological changes were detected by ELISA, serum HMGB1 concentration was detected by flow cytometry pancreatic acinar cell swelling percentage. RESULTS: The pancreatic acinar structure of SO group was intact, occasionally infiltrating with single inflammatory cells. SAP-6 h group showed pancreatic acinar swelling, interstitial edema and inflammatory cell infiltration. In SAP-12 h group and SAP-24 h group, pancreatic pathological injury was aggravated, part of acinar necrosis and interstitial blood vessel stasis were observed Foci necrosis, and pathological injury over time increased. Serum HMGB1 concentration and pancreatic acinar cell swelling percentages in three SAP subgroups were higher than those in SO group (P <0.01). With the prolongation of time, the levels of serum HMGB1 and pancreatic acinar cell expansion (P <0.05). The serum HMGB1 concentration in SAP rats was positively correlated with the percentage of pancreatic acinar cell expansion within 24 h (r = 0.846, P <0.01). Conclusions HMGB1 may be involved in the pathophysiological process of SAP when it is involved in the inflammatory response of SAP.