吸烟及饮酒致胰腺损伤的实验研究

Experiment study on pancreatic injury induced by smoking inhalation and alcohol consumption

目的研究单纯吸烟以及吸烟和饮酒同时存在时的胰腺损伤情况，探讨其可能作用机制。方法将Wistar大鼠分为对照组10只、吸烟组30只、饮酒组42只和吸烟＋饮酒组48只，测定4、8、12周时血清白细胞介素（IL）-6水平，胰腺组织中超氧化物歧化酶（SOD）活性、单核细胞趋化蛋白-1（MCP-1）及羟脯氨酸水平。HE染色观察胰腺组织病理学改变，免疫组化染色观察a-平滑肌肌动蛋白（a-sMA）表达情况。结果自第8周起，单纯吸烟和饮酒都能够导致胰腺腺泡胞质空泡样变，与对照组相比，胰腺内a—SMA、羟脯氨酸含量升高（P〈0．01），吸烟和饮酒同时存在时能够加重上述改变（与饮酒组比较，P〈0．05）；吸烟组血清IL-6及胰腺组织MCP-1表达明显高于对照组（P〈0．01），饮酒组MCP-1低于对照组（P〈0．01）；单纯吸烟和饮酒均可降低胰腺内SOD活性，吸烟＋饮酒组降低更加明显升高（P〈0．01）。结论吸烟能够导致大鼠胰腺组织损伤。吸烟和饮酒同时存在能够加重胰腺损伤。其机制之一可能是两者同时存在时能够进一步加重胰腺组织内的氧化应激反应。

Objective To eveluate the pancreatic injury induced by smoking alone or combined with alcohol consumption, and its possible mechanism. Methods The Wistar rats were divided into control group （n= 10）, smoking group （n=30）, drinking group （n=42） and smoking combined with drinking group （combination group, n= 48）. Serum levels of interleukin （IL）-6, superoxide dismutase （SOD） activities, monocyte chemoattractant protein-1 （MCP 1） and hydroxyproline were determined at 4th-,8th- and 12th week. The pathohistological changes of the pancreas were examined using HE staining and the expression of a-smooth muscle actin （ a SMA ） were measured by immunohistochemistry. Results In contrast to control group, pancreatic changes including cytoplasmic vaeuolation and increased levels of a-SMA and hydroxyproline were found in both smoking and drinking groups at the 8thweek （P 〈 0. 01 ）. Whereas these changes were aggravated in combination group （P〈0.05）. Serum level of IL-6 and MCP-1 expression in pancreatic tissue were significantly increased in smoking group when compared with control group. But MCP-1 expression was lower in drinking group than control group. Moreover, the SOD activity in pancreatic tissue decreased in smoking and drinking groups, especially in combination group. Conclusions Long-term smoking can induce cytoplasmic vacuolation in pancreatic acinar cells, enhance inflammatory factors and chemokine expression and aggravate oxidative stress response in pancreas. These changes are aggravated when smoking and drinking coexisted. The mechanism behind it may be associated with increased oxidative stress response in pancreas.