目的  探讨木犀草素对重症急性胰腺炎（SAP）小鼠胰腺的保护作用及其可能的分子机制。  方法  将60只SPF级健康雄性C57BL/6小鼠随机分为3组，对照组、SAP模型组和治疗组，每组各20只。采用雨蛙素法构建模型，成功构建SAP模型后，应用ELASA法检测脂肪酶、淀粉酶、血红素加氧酶（HO)-1、肿瘤坏死因子（TNF）-α、丙二醛（MDA）及超氧化物歧化酶（SOD）水平。使用Western blotting和Real-time PCR测定各组小鼠核因子（NF）-κB、P38及p-P38 蛋白和mRNA水平。  结果  与对照组比较，模型组和治疗组小鼠胰腺干湿重比、脂肪酶及淀粉酶、TNF-α水平、氧化应激指标HO-1及MDA水平均明显升高，SOD水平明显降低（P<0.05）；与模型组小鼠比较，治疗组小鼠胰腺干湿重比、脂肪酶及淀粉酶，TNF-α、MDA水平均明显降低，HO-1、SOD水平均明显升高（P<0.05）。与对照组比较，模型组和治疗组小鼠NF-κB、p-P38蛋白和mRNA水平明显升高（P<0.05），P38蛋白和mRNA表达水平无显著变化（P>0.05）；与模型组小鼠比较，治疗组小鼠NF-κB、p-P38蛋白和mRNA水平均明显降低（P<0.05）。  结论  木犀草素对SAP小鼠胰腺具有一定的保护作用，其可能的分子机制为缓解炎症应激和氧化应激，下调NF-κB及p-P38 蛋白的表达。

Objective  To analyze the protective effect of luteolin on the pancreas of mice with severe acute pancreatitis and to explore its possible molecular mechanism.   Methods  Sixty healthy male C57/BL mice of SPF grade were divided into three groups according to the random number table method, the control group, the severe acute pancreatitis (SAP) model group and the treatment group, 20 cases in each group. The model was established by the caerulein method. The levels of lipase, amylase, heme oxygenase（HO）-1, tumor necrosis factor（TNF）-α, malondialdehyde（MDA）and superoxide dismutase（SOD）were measured by ELASA method . The protein and mRNA levels of nuclear factor（NF)-κB, P38 and p-P38 in each group were determined by Western blotting and Real-time PCR.   Results  Compared with the control group, the pancreas dry-wet weight ratio, lipase and amylase, inflammatory factors Ho-1, TNF-α levels, oxidative stress index MDA levels increased significantly, while SOD levels were significantly lower in the model group and the treatment group (P<0.05). Compared with the model group, the pancreas dry-wet weight ratio, lipase and amylase, TNF-α and MDA levels in the treated group decreased significantly, while HO-1 and SOD levels increased significantly (P<0.05). Compared with the control group, the levels of NF-κB and p-P38 protein and mRNA in the model group and the treatment group increased significantly (P<0.05), and there was no significant change in P38 mRNA protein and expression level (P>0.05). Compared with the model mice, the levels of NF-κB, p-P38 protein and mRNA in the treated group decreased significantly (P<0.05).   Conclusion  Luteolin has a protective effect on SAP mice. Its possible molecular mechanism is to relieve inflammatory stress and oxidative stress, and down-regulate the expression of NF-κB and p-P38 protein.