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目的:探讨瘦素及瘦素受体在大鼠高脂血症性胰腺炎(HLAP)中的动态变化。方法:将60只SD雄性大鼠随机分为3组:正常对照组(NC组),高脂血症组(HL组),高脂血症性胰腺炎组(HLAP组)。采用高脂饲料喂养3周后经腹腔注射L-精氨酸500 mg/100 g体重制作大鼠高脂血症性胰腺炎模型。各组分别于造模后24 h、36 h处死半数大鼠,观察血清淀粉酶、瘦素水平、细胞因子IL-1β、TNF-α和IL-10的变化。并对胰腺的病理学评分、胰腺组织瘦素、瘦素受体的表达和定位评分。结果:HL组血清IL-1β、TNF-α、瘦素水平较NC组高(P<0.01);而IL-10水平、病理学评分以及胰腺组织瘦素和瘦素受体表达与NC组无差异。造模后24 h,HLAP组血淀粉酶和IL-1β、TNF-α、瘦素水平均较HL组及NC组升高(P<0.01),而IL-10与HL组相当;HLAP组的胰腺瘦素、瘦素受体表达较HL组及NC组增加(P<0.01),胰腺组织损害也明显增强(P<0.01)。造模后36 h,HLAP组血淀粉酶和瘦素水平下降。HLAP组IL-1β、TNF-α及IL-10水平继续上升,胰腺病理损害进一步加重(P<0.01)。此外,HLAP组瘦素及瘦素受体表达也均下降(P<0.01)。结论:正常胰腺中有瘦素及其受体的存在。在HLAP时作为保护性机制,内源性的瘦素表达能够明显增加;但这种内源性瘦素的增加出现早,维持时间短,不足以抑制强烈的炎症反应。
Objective: To investigate the dynamic changes of leptin and leptin receptor in rat hyperlipidemic pancreatitis (HLAP). Methods: Sixty SD male rats were randomly divided into three groups: normal control group (NC group), hyperlipidemia group (HL group) and hyperlipidemic pancreatitis group (HLAP group). The model of hyperlipidemic pancreatitis was established by intraperitoneal injection of L-arginine 500 mg / 100 g body weight after high-fat diet for 3 weeks. Half of the rats in each group were killed at 24 h and 36 h after modeling, and the changes of serum amylase, leptin, cytokines IL-1β, TNF-α and IL-10 were observed. The pathological score of pancreas, the expression of leptin and the localization of leptin in pancreatic tissue were also evaluated. Results: The levels of IL-1β, TNF-α and leptin in HL group were significantly higher than those in NC group (P <0.01). The levels of IL-10, pathological score and the expression of leptin and leptin in pancreatic tissues were significantly lower than those in NC group difference. The level of serum amylase, IL-1β, TNF-α and leptin in HLAP group were significantly higher than those in HL group and NC group (P <0.01) at 24 h after modeling, while IL-10 was the same in HL group Pancreatic leptin, leptin receptor expression than the HL group and NC group increased (P <0.01), pancreatic tissue damage was also significantly increased (P <0.01). At 36 h after modeling, the levels of serum amylase and leptin in HLAP group decreased. The level of IL-1β, TNF-α and IL-10 in HLAP group continued to increase, and the pathological damage of pancreas further aggravated (P <0.01). In addition, leptin and leptin receptor expression also decreased in HLAP group (P <0.01). Conclusion: There are leptin and its receptor in normal pancreas. As a protective mechanism in HLAP, endogenous leptin expression can be significantly increased; but this increase in endogenous leptin early, maintaining a short time, not enough to suppress a strong inflammatory response.