论文部分内容阅读
目的:研究挤压伤致股骨干骨折引起的挤压综合征(CS)对大鼠心肌细胞损伤的作用机制。方法:将32只SD雄性大鼠随机分为对照组、CS后再灌注0 h组(CS-0组)，CS后再灌注12 h组(CS-12组)、CS后再灌注24 h组(CS-24组)，每组8只。CS组采用自制挤压器制作大鼠CS模型，利用4%多聚甲醛灌注0、12、24 h。采用苏木伊红染色法观察各组大鼠心肌组织形态，TUNEL法检测凋亡心肌细胞情况，并采用试剂盒检测心肌匀浆液中丙二醛(MDA)、超氧化物歧化酶(SOD)、乳糖脱氢酶(LDH)、白介素-6(IL-6)、白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)水平及活性，并通过Western blot检测心肌细胞中半胱氨酸蛋白酶-3(Caspase-3)、Bax、Bcl-2、核转录因子-κB(NF-κB)蛋白表达情况。结果:与对照组相比，CS模型组大鼠心肌组织均有不同程度形态损伤，表现为心肌纤维断裂、排序紊乱、间质水肿和炎症细胞浸润；与对照组相比，CS-0组、CS-12组、CS-24组心肌细胞凋亡率、Caspase-3、Bax蛋白表达水平均显著升高(n P<0.05)，Bcl-2蛋白表达水平显著降低(n P<0.05)；与对照组相比，CS-0组、CS-12组、CS-24组心肌匀浆中MDA、LDH、IL-6、IL-1β、TNF-α水平及P65蛋白磷酸化均显著升高(n P<0.05)，SOD活性显著降低(n P<0.05)。n 结论:CS后再灌注可能通过激活NF-κB途径抑制氧化应激并诱导炎症反应从而损伤大鼠心肌细胞。“,”Objective:To investigate the mechanism of crush syndrome (CS) induced by crush injury on myocardial cells in rats.Methods:Thirty two male Sprague Dawley (SD) rats were randomly divided into control group, CS-0 group, CS-12 group and CS-24 group with 8 rats in each group. CS model was made by self-made extruder and perfused with 4% paraformaldehyde for 0, 12 and 24 h. The morphological changes of myocardial tissue were observed by hematoxylin staining. The apoptosis of cardiomyocytes was detected by terminal dexynucleotide transferase-mediated nick end labeling (TUNEL). The levels and activities of malondialdehyde (MDA), superoxide dismutase (SOD), lactose dehydrogenase (LDH), interleukin-6 (IL-6), interleukin-1 β (IL-1 β), tumor necrosis factor-α (TNF- α) in myocardial homogenate were detected by enzyme-linked immunosorbent assay (ELISA). The expressions of Caspase-3, Bax, Bcl-2 and necrosis factor-κB (NF-κ B) were detected by Western blot.Results:Compared with the control group, the myocardial tissue of CS model group had different degrees of morphological damage; compared with the control group, the apoptosis rate, Caspase-3 and Bax protein expression levels of CS-0 group, CS-12 group and CS-24 group were significantly increased (n P<0.05), and the expression level of Bcl-2 protein was significantly decreased (n P<0.05); compared with the control group, the levels of MDA, LDH, IL-6, IL-1β, TNF-α and p65 protein phosphorylation in the myocardial homogenate of CS-0 group, CS-12 group and CS-24 group were significantly increased (n P<0.05), and SOD activity was significantly decreased (n P<0.05).n Conclusions:CS may inhibit oxidative stress and induce inflammatory reaction by activating NF-κ B pathway, thus damaging myocardial cells in rats.