衰老大鼠急性肺损伤诱导肝功能受损的研究

目的　观察脂多糖 (LPS)致衰老大鼠的急性肺损伤 (ALI)是否可进一步诱发肝功能受损及银杏叶提取物 (GBE)对其是否有保护作用。方法　雄性Wistar大鼠 3 0只复制成衰老模型。再随机分成对照组 (静脉注射生理盐水 ) ;LPS组 (静脉注射LPS)及GBE +LPS组 (注LPS前 7天开始每天GBE灌胃 1次 )。注LPS后 2、6h收集血液并取肺、肝。制备肺、肝组织匀浆待测。结果　衰老大鼠在注射LPS后 2、6h时形成ALI。对照组注射LPS表明 ,2h血中总胆红素含量及谷丙转氨酶 (GPT)活性为(10 9± 0 6)mg/L、(2 6± 3 )U ,LPS 6h组为 (3 0 1± 2 1)mg/L、(88± 12 )U ,两组比较差异有显著性 (P均<0 0 0 1) ;对照组注射LPS表明 ,2h血和肺组织中每毫克蛋白中丙二醛 (MDA)含量分别为 (15 9±1 8) μmol/L、(18 8± 2 1)nmol,LPS 2h组为 (2 2 1± 1 9) μmol/L、(2 8 8± 3 1)nmol,两组比较差异有显著性 (P均 <0 0 0 1) ;而每毫克蛋白血和肺组织中超氧化物歧化酶 (SOD)活性对照组分别为 (2 5 5±2 6)mU/L、(3 6 1± 2 4)U ,LPS 2h组分别为 (2 0 6± 1 9)mU/L、(3 2 0± 2 7)U ,两组比较差异有显著性(P <0 0 1和 0 0 5 )。对照组注射LPS表明 ,2h时肺组织中每毫克蛋白中谷胱甘肽过氧化物酶 (GSH PX)及Na+ K+ ATP酶活性

Hepatic injury induced by acute lung injury in aging rats

OBJECTIVE: To investigate the induction of hepatic function damage by acute lung injury (ALI) in aging rats and the effect of Ginkgo Biloba extract (GBE) on this process. METHODS: Thirty male Wistar rats were used to produce the aging animal model. Aging rats were randomly divided into three groups: the control group, the lipopolysaccharide (LPS, intravenous injection) group, and the GBE + LPS group (GBE given 7 days before experiment, once a day, via the esophagus). Samples from the blood, the lung and the liver were collected 2 and 6 h after LPS or saline administration. RESULTS: ALI was induced by intravenous injection of LPS in aging rats. Compared with the aging control, the total bilirubin content and the glutamic pyruvic transaminase (GPT) activity in serum did not change at 2 h after LPS administration. But at 6 h, they were increased, respectively from (10.9 +/- 0.6) mg/L and (26 +/- 3) U in the control group to (30.1 +/- 2.1) mg/L and (88 +/- 12) U in the LPS group (P < 0.001). MDA content increased in the blood and the lung tissue at 2 has compared to the control group, from (15.9 +/- 1.8) micro mol/L and (18.8 +/- 2.1) nmol/mg protein to (22.1 +/- 1.9) micro mol/L and (28.8 +/- 3.1) nmol/mg protein (all P < 0.001), respectively. SOD activity in the lung tissue was decreased significantly, from (25.5 +/- 2.6) mU/L and (36.1 +/- 2.4) U/mg protein to (20.6 +/- 1.9) mU/L and (32.0 +/- 2.7) U/mg protein, respectively (P < 0.05, P < 0.001). The GSH-P(X) activity and the Na(+)-K(+)-ATPase activity in the lung tissue at 2 hours after LPS administration were decreased markedly, from (28.2 +/- 2.8) U/mg protein and (4.9 +/- 0.5) micromol Pi x mg(-1) protein x h(-1). to (21.1 +/- 2.7) U/mg protein and (3.1 +/- 0.3) micromol Pi x mg(-1) protein x h(-1). These changes lasted 6 h after LPS administration. These parameters did not change significantly in the hepatic tissue at 2 h after LPS administration. But after 6 h, MDA content was increased from (7.9 +/- 0.9) nmol/mg protein to (10.9 +/- 0.7) nmol/mg protein; while the GSH-P(X) and the Na(+)-K(+)-ATPase activities were decreased markedly, from (59.0 +/- 3.9) U/mg protein and (0.87 +/- 0.04) micromol Pi x mg(-1) protein x h(-1) to (49.2 +/- 3.0) U/mg protein and (0.77 +/- 0.04) micromol Pi x mg(-1) protein x h(-1) (P < 0.001, P < 0.01). There was no obvious change in the SOD activity. All the changes were significantly attenuated in the GBE + LPS group (P < 0.05, P < 0.01). CONCLUSION: Hepatic function damage could be induced by ALI in aging rats. GBE showed a protective effect on ALI and hepatic function damage in this animal model.