目的:研究大豆异黄酮对D半乳糖致衰老大鼠抗氧化能力的影响。方法:用D半乳糖注射Wistar雄性大鼠5个月,建立衰老模型。对致衰老模型组、大豆异黄酮组肝脏、心脏和前列腺丙二醛(MDA)含量、超氧化物歧化酶(SOD)、谷胱甘肽过氧化酶(GSHPx)活性进行测定及比较。结果:低、中、高不同剂量大豆异黄酮灌喂组与模型组大鼠相比,各脏器MDA含量(μmol/L)(心脏:695±093,562±112,435±112比802±111;肝脏:815±085,647±120,515±112比935±135;前列腺:715±092,558±115,423±125比833±124)均有降低,差异有统计学意义(Plt;005),而SOD酶活性(nmol/L)(心脏:4732±308,5518±428,6120±368比3225±370;肝脏:18121±506,19015±706,19720±570比17213±512;前列腺:4156±301,4607±421,5015±335比3374±305)和GSHPx酶活性(nmol/L)(心脏:905±096,1111±245,1313±146比713±151;肝脏:902±105,1150±223,1362±192比698±160;前列腺:435±085,613±102,747±155比312±106)有升高,差异同样具有统计学意义(Plt;005);大豆异黄酮摄入量越高,MDA含量越低,而SOD、GSHPx酶活性越高。结论:摄入适量大豆异黄酮可有效增强大鼠机体抗氧化能力,从而延缓D半乳糖诱发的大鼠衰老。
Objective To investigate the protective effects of endotoxin pretreatment on lung injury of rats with endotoxemia. Methods The rat model of acute endotoxemia was established by injecting lipopolysaccharide (LPS) intraperitoneally. Seventy-two male Wistar rats were randomly divided into three groups, ie. a saline control group (N, n=24) , a LPS-treated group (L, n=24) , and a LPS pretreated group ( P, n=24) . Each group was divided into 2 h, 4 h, 6 h, and 12 h subgroups. The rats in group P were firstly administered with introperitoneal injection of 0.25 mg/kg LPS. After 24 hours, they were subjected to the injection of 0.5 mg/kg LPS. The rats in group N and L received injection of equivalent amount of saline. After 72 hours, the rats in group L and P were challenged with intravenous injection of 10 mg/kg LPS, otherwise saline in group N. Six rats were killed at 2, 4, 6 and 12 hours respectively after injection of LPS in group L and P. The lungs were removed for detecting intercellular adhesion molecule-1 ( ICAM-1) , superoxide dismutase ( SOD) , and malondialdehyde (MDA) . Meanwhile the level of tumor necrosis factoralpha ( TNF-α) in serum was measured, and the pathological changes of lung were also examined. Results The contents of ICAM-1, MDA and TNF-α in the LPS-treated 4 h group were 75.07 ±0. 53, ( 3.93 ± 0.42) μmol/g, and (478.62 ±45.58) pg/mL respectively, significantly higher than those in the saline control group. The endotoxin pretreatment reduced the above indexes to 42.40 ±0.44, ( 2.89 ±0.49) μmol / g and ( 376.76 ±43.67) pg/mL respectively (Plt;0.05) . The content of SOD in the LPS-treated 4 h group was ( 6.26 ±0.31) U/mg, significantly lower than that in the saline control group. The endotoxin pretreatment increased SOD to ( 8.79 ±0.35) U/mg. Conclusion Endotoxin pretreatment can suppress the progress of lung injury in rats with endotoxemia and protect the lung tissue by down-regulating the inflammatory response and oxygen free radical production.
Objective To study the effect of various doses of estrogen on tissue injury, blood supply and survival area of skin flap and to investigate its mechanism. Methods Thirty New Zealand white rabbits aged 3-4 months old and weighing 1.5-2.2 kg (male or female) were used. Random pattern skin flap (12 cm × 3 cm in size) taking the central l ine of the rabbit dorsum as axis and with the pedicle attached at the proximal end was prepared, and the flap pedicle division was performed 7 days after operation. The rabbits were divided randomly into three groups (n=10 rabbits per group). At 2, 4, and 6 days after operation, the proximal edge of flap in group A and B received 100 ?g/kg and 50 ?g/kg subcutaneous injection ofestradiol benzoate, respectively, while group C received no further treatment serving as control group. General condition ofthe rabbits was observed after injection, gross observation was performed 3 and 7 days after injection, survival area of the skin flap was measured 7 days after injection, contents of malondialdehyde (MDA) and nitric oxide (NO) were tested 5 days after injection, and the flaps were harvested 4 and 7 days after injection to receive histology and no significant difference was noted between group A and group B (P gt; 0.05). The NEU counts 4 days after injection were (18.20 ±6.24) cells/HP in group A, (21.27 ± 5.34) cells/HP in group B, and (28.78 ± 7.92) cells/HP in group C, and at 7 days after injection, there were (15.16 ± 7.02) cells/HP in group A, (18.12 ± 6.44) cells/HP in group B, and (29.67 ± 9.12) cells/HP in group C. The VEGF score 4 days after injection was (4.02 ± 0.48) points in group A, (4.19 ± 0.66) points in group B and (3.67 ± 0.49) points in group C, and at 7 day after injection, it was (4.96 ± 0.69) points in group A, (5.12 ± 0.77) points in group B, and (3.81 ± 0.54) points in group C. Significant difference was evident between 4 days and 7 days after injection in group A or B in terms of NEU counts and VEGF score (P lt; 0.05), and difference between 4 days and 7 days after injection in group C was not significant (P gt; 0.05), and the differences among 3 groups were significant (P lt; 0.05). Conclusion Estrogen injection can increase VEGF expression and NO content of flap, decrease MDA content and NEU infiltration of flat, and improve survival area of flap.
Objective To explore the effect of oxygen inhalation on the retinae of newborn rats and its mechanism.Methods We mimicked the retinopathy of prematurity(ROP) by putting the newborn rats in high concentrated oxygen. One-day old rats were put into the oxygen box with the oxygen concentration of 80% for continuous 7 days; then in air condition for 7 days. The arterial blood oxygen pressure, retinal superoxide dismutase (SOD), and malondialdehyde (MDA) of the rats (1,2,4,7,8,9,11,14 days old) were examined. The diameter of retinal vessels′main branch and the coverage rate of peripheral vessels were measured in 7- and 14-day-old rats by ink perfusion. The retinal neovascularization of rats (8,9,11, 14 days old) were observed by HE staining. The rats of the same age fed in air condition were in the control group.Results The differential pressures of blood oxygen of rats (1,2,4,7 days old) in study group were significantly higher than those in the control group (P＜0.01), while the differential pressures of blood oxygen of rats (8,9,11,14 days old) in study group were lower than those in the control group (P＞0.05). The contents of SOD of the retinae in the rats ( 1,2,4,7,8 days old) were significantly lower than those in the control group(P＜0.01, P＜0.05 ), while the contents of MDA were significantly higher than those in the control group (P＜0.01,P＜0.05). The diameter of retinal vessels′main branch in 7-day rats was 75% of the control group, and the coverage rate of peripheral vessels was 22% of the control group; and was 61% and 73% respectively in 14-day-old rats. The neovascularization could be seen in 16.7% of the rats in the study group and nought in the control group.Conclusion The damage of free radical of the retina in high concentrated oxygen and hypoxia situation after oxygen supply may be one of the most important mechanism of ROP. (Chin J Ocul Fundus Dis，2003，19：269-332)
Objective：To observe the histochemical changes of retinal photochemical damage in rats. Methods：The changes of retinal ultrastructure were observed.The concentration of malondaldehyde(MDA) was tested and the activity the histochemical change of cytochrome oxidase (CCO) and (Mg ++ -ATPasw) were evaluated on the retnal photochemical damage in SD rats. Results：At the 6th hour after light exposure,the swelling appwared at the nuclei of photoreceptor,the mitochondria of inner segment.The apical microvilli of RPE disappeared and lysosomes increased in RPE.On the 6th day after light exposure,the changes became more obvious.While on the 14th day after light expose the nuclei of photoreceptors and the inner segments renewed but the arrangement of the disk was lose;and the microvilli appeared of the disk was lose;and the microvilli appeared at the tip of RPE.The Activity of CCO and Mg ++ -ATPase decreased and MDA increased in retina at the 6th hour and on the 6th day and they recovered on the 14th day after light exposure. Conclusion：Lipd peroxidation that broke the cell membrane system of photoreceptor which induced changes of the cell ultrastru cture abd the activity of enzyme might relate to pathogenesis in retinal photochemical damage. (Chin J Ocul Fundus Dis,1998,14:38-40)
Objective To investigate the effects of glutathione (GSH) on survival of the random skin flap in rats and the probable mechanism that contribute to this effect. Methods Twenty SD rats with 200-250 g in weight, were randomly divided into the experimental group and control group(n=10). Random flap of 8 cm×2 cm in size was made on the back of each rat with the pedicel on the angular of the scapular. GSH(250 mg/kg) and NS of the same dose were injected into the abdominal cavity of rats in the experimental groupand the control group immediately after the operative, 1st and 2nd days respectively. The rats were killed on the 7th day after the operation. The tissue pathology, the survival rate of the flap, the superoxide dismutase(SOD) activity and malonyldialdehyde (MDA) level were compared between two groups. Results The mean survival rate of the flap on the 7th day in the experimental group（56.77%±10.67%） was higher than that in the control group(40.16%±7.12%)(Plt;0.05).SOD activity in experimental group （306.06±84.87 U/mgprot）was higher than that in the control group （224.79±27.12 U/mgprot）, while MDA level （3.835±0.457 nmol/mgprot）was lower than that in the control group (6.127±0.837 nmol/mgprot)(Plt;0.05). Histological observation showed that the neutrophil infiltration was less in experimental group than that in the control group; that the experimental group was surperior to the control group in angiogenesis, fibroblasts, fair cells and cuaneous gland. Conclusion The intraperitoneal use of GSH may promote the survival rate of the random flaps and the possible mechanism for improvement may lies in that the GSH can reduce the level of oxygen free radical and lipidperoxidation,and lessen neutrophil infiltration.
Objective To observe the levels of malonaldehyde (MDA) , interleukin-8 (IL-8) and tumor necrosis factor-α(TNF-α) in lung tissues of subjects with or without chronic obstructive pulmonary disease (COPD) , and investigate their roles in the the pathogenesis of COPD. Methods The content of MDA, IL-8 and TNF-αin lung tissues of smokers with COPD (n=9) , ex-smokers with COPD (n=8) , non-smokers with COPD (n=7) , healthy smokers (n=9) , healthy ex-smokers (n=8) and healthy nonsmokers (n=6) was measured with enzyme-linked immunosorbent assay ( ELISA) and corrected by creatinine. Results The levels of MDA, IL-8 and TNF-α in lung tissues of the COPD patients were significantly higher than those in the healthy subjects (Plt;0.05) , which were also significantly higher in the smokers when compared with the non-smokers (Plt;0.05) , whether suffering from COPD or not. In the COPD patients, not the levels of IL-8 but MDA and TNF-αin lung tissues of the smokers were significantly higher than those in the ex-smokers (Plt;0.05) ; whereas in the healthy cases, no statistical significance was revealed between the smokers and the ex-smokers on the levels of MDA and IL-8 in lung tissues except TNF-α( Pgt;0.05) . Conclusion The abnormal increase of MDA, IL-8 and TNF-αin lung tissues caused by chronic smoking may play an important role in the the pathogenesis of COPD.
ObjectiveTo detect the level of oxidative stress markers in serum, including malondialdehyde (MDA), protein carbonyls (PC), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and total antioxidant capacity (TAC), in patients with stable chronic obstructive pulmonary disease (COPD), and explore the impacts of oxidant/antioxidant imbalance in pathogenesis of COPD. MethodsTwo hundred stable COPD patients (the COPD group) and 100 healthy individuals (the control group) were recruited in the study. The concentrations of MDA, PC, 8-OHdG and TAC in serum were detected. Pulmonary function test was performed and the general informations for each subjects were collected. The COPD patients were divided into a smoking subgroup and a non-smoking subgroup, or divided into a mild-moderate airflow limitation subgroup and a severe-extremely severe airflow limitation subgroup. ResultsThe levels of serum MDA, PC and 8-OHdG in the COPD group were significantly higher than those in the control group (all P < 0.01), but the level of serum TAC was significantly lower than that in the control group (P < 0.01). In the COPD patients, the levels of PC and 8-OHdG in the smoking subgroup were significantly higher than those in the non-smoking subgroup (both P < 0.05). The level of PC in the severe-extremely severe airflow limitation subgroup was significantly higher when compared with the mild-moderate airflow limitation subgroup (P < 0.01). Multiple linear regression analysis showed that the levels of PC and 8-OHdG were negatively related with FEV1% pred in the COPD patients, and the PC had greater impacts than 8-OHdG (β=-0.230, -0.219, P < 0.01). ConclusionSmoking can induce the abnormal increase of PC and 8-OHdG in serum which are negatively related with FEV1% pred in COPD patients, which suggests that oxidative stress might play an important role in pathogenesis of COPD.
Hyperuricemia is a risk factor for various diseases, but knowledge on acute hyperuricemia is still not sufficient. The present study was aimed to investigate the effect of acute hyperuricemia on red blood cells from hemorheological point of view, and to provide the reference for clinical treatment. The rats were gavaged with 500 mg/kg hypoxanthine and intraperitoneally injected with 100 mg/kg oxonate to induce the model of acute hyperuricemia. The same volume of blood samples were drawn within time period of 0, 1, 2, 3 and 6 h, respectively, from the inner canthus of rats to measure the serum uric acid, hemorheological parameters and the malondialdehyde level. It was found that in each period of 1, 2 and 3 h, the rats had significantly higher levels of uric acid. The integrated deformation index and relax index were increased. The hemolysis rate was significantly reduced. The plasma malondialdehyde level was obviously decreased at the end of 2 h. The results suggested that short-term elevated uric acid could improve the hemorheological parameters and the lipid oxidative level in red blood cells.