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目的探讨高脂饮食诱导肥胖小鼠下丘脑及肺内SH2-Bβ表达与肥胖和炎症之间关系。方法c57BL/6小鼠45只,随机分为对照组和肥胖组,对照组20只,肥胖组25只;高脂饮食制备肥胖模型。利用免疫组织化学法,测定各组小鼠肺内SH2-Bβ表达变化;western blot检测下丘脑SH2-Bβ蛋白变化;应用小鼠肺功能仪检测气道阻力变化。结果肥胖小鼠肺内可见大量炎性细胞浸入,气道上皮及炎性细胞均高表达SH2-Bβ,肥胖组小鼠肺内SH2-Bβ平均光密度值为(0.685±0.025),明显高于对照组的(0.127±0.019)(t=56.19,P<0.01),下丘脑SH2-Bβ免疫阳性产物平均光密度值为(0.686±0.016),明显低于对照组的(2.487±0.014)(t=267.88,P<0.01);肥胖组小鼠气道阻力较对照组明显增高(P<0.01)。结论高脂饮食可使小鼠下丘脑内SH2-Bβ表达下调近而导致肥胖;肺内气道上皮和炎性细胞SH2-Bβ过表达使气道阻力增加。
Objective To investigate the relationship between the expression of SH2-Bβ in the hypothalamus and lung and obesity and inflammation induced by high-fat diet in obese mice. Methods Forty five c57BL / 6 mice were randomly divided into control group and obesity group, 20 in control group and 25 in obesity group. Obesity model was made by high fat diet. The expression of SH2-Bβ in the lungs of each group was detected by immunohistochemistry. The changes of SH2-Bβ protein in the hypothalamus were detected by western blot. The changes of airway resistance were measured by the lung function analyzer. Results Large numbers of inflammatory cells were infiltrated into the lungs of obese mice, and SH2-Bβ was highly expressed in airway epithelium and inflammatory cells. The mean optical density of SH2-Bβ in obese mice was (0.685 ± 0.025) The mean optical density of SH2-Bβ immunoreactive products in the hypothalamus was (0.68 ± 0.016) in control group (0.127 ± 0.019) (t = 56.19, P <0.01), which was significantly lower than that in control group (2.487 ± 0.014) = 267.88, P <0.01). The airway resistance of obese mice was significantly higher than that of the control group (P <0.01). Conclusion High-fat diet can down-regulate the expression of SH2-Bβ in the hypothalamus and lead to obesity. Over-expression of SH2-Bβ in the airway epithelium and inflammatory cells in the lungs increases airway resistance.