目的观察脓毒症模型大鼠肺组织中凋亡相关因子的表达情况。方法 30只雌性SD大鼠随机分为脓毒症模型组(n=20)及正常对照组(n=10)。以经典盲肠结扎穿孔法(CLP)成功制作脓毒症大鼠模型。分别在造模后3h及12h处死大鼠,石蜡切片HE染色光镜观察各时间点肺组织的病理变化;取血清ELISA法检测肿瘤坏死因子(TNF-α)的表达水平;免疫组织化学染色法检测造模12hBcl-2及Bax蛋白在大鼠肺组织的表达情况,并计算两种蛋白的累积吸光度值。结果模型组大鼠在造模后3h开始出现脓毒症的相关表现;3h及12h肺组织石蜡切片HE染色可见肺组织炎症反应明显,肺血管充血,肺泡萎陷,炎细胞渗出,并随着观察时间延长有加重趋势。对照组与模型组血清(3h及12h)TNF-α平均吸光度值分别为0.2510±0.0038、0.7392±0.0526及0.4203±0.0256;对照组与模型组2个观察时间点的TNF-α的平均吸光度值差异均有统计学意义(P=0.000;P=0.000),模型组在2个观察时间点的TNF-α的平均吸光度值差异有统计学意义(P=0.000)。免疫组化结果可见Bcl-2蛋白及Bax蛋白在对照组及模型组12h均有表达,但Bcl-2表达在对照组高于模型组(P=0.002),而Bax表达在对照组低于模型组(P=0.012)。结论细胞凋亡可能在脓毒症肺组织损伤中发挥重要作用。 Objective To observe the expression of apoptosis related factors in lung tissue of septic rats. Methods Thirty female SD rats were randomly divided into sepsis model group (n = 20) and normal control group (n = 10). The sepsis rat model was successfully established by classical cecal ligation and puncture (CLP). The rats were sacrificed at 3h and 12h respectively. The pathological changes of lung tissue were observed under light microscope with paraffin sections at different time points. The expression of tumor necrosis factor (TNF-α) was detected by ELISA. The expression of TNF- The expression of 12h Bcl-2 and Bax protein in rat lung tissue was detected and the cumulative absorbance values ​​of two proteins were calculated. Results Compared with the model group, the sepsis began to appear at 3h after model establishment. The inflammatory reaction of lung tissue was obvious at 3h and 12h after paraffin sections of HE staining. Pulmonary vascular congestion, alveolar collapse and infiltration of inflammatory cells were observed With the observation of time to increase the trend of aggravating. The mean absorbance values ​​of TNF-α in serum of control group and model group at 3h and 12h were 0.2510 ± 0.0038, 0.7392 ± 0.0526 and 0.4203 ± 0.0256, respectively. The difference of mean absorbance of TNF-α between control group and model group at two observation time points (P = 0.000; P = 0.000). The mean absorbance of TNF-α in the model group at two observation time points was significantly different (P = 0.000). Immunohistochemical results showed that Bcl-2 protein and Bax protein were expressed in both control group and model group at 12h, but Bcl-2 expression was higher in the control group than in the model group (P = 0.002), while Bax expression was lower in the control group Group (P = 0.012). Conclusion Apoptosis may play an important role in lung injury in sepsis.