| 管小萌,徐桂萍,王晓丽.大鼠肝缺血再灌注后肺细胞凋亡及七氟醚对细胞凋亡及NF-κBp65的影响[J].安徽医药,2015,19(12):2272-2275. |
| 大鼠肝缺血再灌注后肺细胞凋亡及七氟醚对细胞凋亡及NF-κBp65的影响 |
| Pneumocyte apoptosis after hepatic ischemia-reperfusion in rats and the effect of sevoflurane on apoptosis and NF-κBp65 |
| 投稿时间：2015-07-28 |
| DOI： |
| 中文关键词: 七氟醚 细胞凋亡 缺血再灌注 |
| 英文关键词: sevoflurane cell apoptosis ischemia-reperfusion |
| 基金项目:国家自然科学基金 (No 81160016) |
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| 摘要点击次数: 2742 |
| 全文下载次数: 212 |
| 中文摘要: |
| 目的 探讨七氟醚预处理对大鼠肝缺血再灌注后肺细胞凋亡的影响。方法 24只 Wister大鼠随机分为3组(n=8):假手术组,缺血再灌注组,七氟醚组,阻断肝门30 min后建立大鼠70%肝缺血再灌注模型。假手术组(S组)仅游离肝门,但不阻断；肝缺血再灌注组(IR组)采用阻断肝门30 min,再灌注1 h的方法制备大鼠肝缺血再灌注损伤模型；七氟醚预处理组(SP组)吸入2.1%七氟醚30 min,停止吸入10 min后制备肝缺血再灌注模型。于再灌注1 h时处死动物,留取肺组织, 测定湿/干重比(W/D比),采用比色法检测超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量,采用原位末端转移酶法(TUNEL)检测细胞凋亡,计算细胞凋亡指数(AI),采用Western blot法测定核蛋白NF-κBp65 表达,光镜下观察肺组织病理学结果。结果 与S组比较,IR组和SP组再灌注各时点肺组织W/D比值、细胞凋亡指数(AI)和NF-κB 活性水平及MDA含量均显著增高(均P<0.05)；SOD活性显著降低(P<0.05)；与IR组比较,SP组W/D比值、细胞凋亡指数(AI)、NF-κB表达水平与MDA含量显著降低(均P<0.05)；而SOD活性显著增加(P<0.05)；SP组肺组织损伤较IR组减轻。结论 细胞凋亡可能在肝缺血再灌注肺损伤发生过程中具有重要意义；七氟醚对大鼠肝缺血再灌注后肺细胞凋亡具有抑制作用,其作用机制可能通过降低肺组织NF-κB的活性,从而清除自由基、抑制脂质过氧化有关。 |
| 英文摘要: |
| Objective To explore the influences of sevoflurane pretreatment on apoptosis of rat lung cells after hepatic ischemia reperfusion. Methods Twenty-four Wister rats were randomized into 3 groups (n=8):sham-operation group, hepatic ischemia reperfusion group and sevoflurane group. After 30 min of hepatic portal occlusion, rat models with 70% hepatic ischemia and reperfusion were established. Porta hepatis was only separated but not blocked in the sham-operation group (group S); hepatic ischemia reperfusion rat model was established by 30 min of hepatic portal occlusion and 1 h of reperfusion in hepatic ischemia reperfusion group (group IR); In sevoflurane pretreatment group (group SP), the rats were inhaled with 2.1% of sevoflurane for 30 min, and then stopped. 10 min later, hepatic ischemia reperfusion model was established. The animals were executed at 1h after reperfusion. The lung tissue was taken. Wet/dry weight ratio (W/D ratio) was determined. Colorimetry was adopted to determine activity of superoxide dismutase (SOD) and content of malondialdehyde (MDA). Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) was used to determine cell apoptosis. Cell apoptosis index (AI) was calculated. Western blot was used to determine expressions of NF-κBp65. Pathological results of lung tissue were observed under microscope. Results W/D ratios, AIs, NF-κB activity and MDA content of group IR and group SP at each time after reperfusion were significantly increased compared with group S (All P<0.05); SOD activity was decreased significantly (P<0.05); W/D ratios, AIs, NF-κB activity and MDA content of group SP were significantly lower than those of group IR (All P<0.05); and SOD activity was obviously increased (P<0.05); lung tissue injury of group SP was decreased compared with group IR. Conclusions Cell apoptosis may play an important role in lung tissue injury due to hepatic ischemia reperfusion. Sevoflurane has a certain inhibition on rat lung cell apoptosis after hepatic ischemia reperfusion, which may eliminate free radicals and inhibit lipid peroxidation by reducing activity of NF-κB in lung tissue. |
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