CAJ | 학술논문

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α-平滑肌肌动蛋白(α-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α-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.
목적 연구단순흡연이급흡연화음주동시존재시적이선손상정황,탐토기가능작용궤제.방법 장Wistar대서분위대조조10지、흡연조30지、음주조42지화흡연+음주조48지,측정4、8、12주시혈청백세포개소(IL)-6수평,이선조직중초양화물기화매(SOD)활성、단핵세포추화단백-1(MCP-1)급간포안산수평.HE염색관찰이선조직병이학개변,면역조화염색관찰α-평활기기동단백(α-SMA)표체정황.결과 자제8주기,단순흡연화음주도능구도치이선선포포질공포양변,여대조조상비,이선내α-SMA、간포안산함량승고(P<0.01),흡연화음주동시존재시능구가중상술개변(여음주조비교,P<0.05);흡연조혈청IL-6급이선조직MCP-1표체명현고우대조조(P<0.01),음주조MCP-1저우대조조(P<0.01);단순흡연화음주균가강저이선내SOD활성,흡연+음주조강저경가명현승고(P<0.01).결론 흡연능구도치대서이선조직손상.흡연화음주동시존재능구가중이선손상.기궤제지일가능시량자동시존재시능구진일보가중이선조직내적양화응격반응.
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 α-smooth muscle actin (α-SMA) were measured by immunohistochemistry.ResultsIn contrast to control group,pancreatic changes including cytoplasmic vacuolation and increased levels of α-SMA and hydroxyproline were found in both smoking and drinking groups at the 8th-week (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.