目的 探讨地震应激对胃泌素、生长抑素、血清超氧化物歧化酶（SOD）活性和丙二醛（MDA）水平的影响，为震后灾区人群应激性溃疡的防治提供理论依据。 方法 随机抽取四川省人民医院2008年5月15日－31日间收治的60名5.12汶川地震灾民为研究组，58名健康体检者作为对照组。分别对两组人群进行心理调查，采用酶联免疫吸附法测定血清胃泌素和生长抑素水平，利用生化法检测血清SOD活性和MDA含量，并对上述各指标在两组间的分布进行比较。 结果 研究组症状自评量表得分高于对照组（P＜0.05）；两组血清胃泌素分别为（1.04 ± 0.67）、（0.74 ± 0.58） ng/mL，研究组高于对照组（P＜0.01）；两组MDA水平分别为（7.16 ± 5.58）、（4.83 ± 4.48） nmol/mL，研究组高于对照组（P＜0.05）；而两组生长抑素分别为（0.74 ± 0.94）、（1.92 ± 3.05） ng/mL，研究组低于对照组（P＜0.01）；两组SOD分别为（6.06 ± 2.20）、（7.79 ± 1.58）U/mL，研究组低于对照组（P＜0.01）。 结论 地震可引起生理应激状态，导致机体在免疫、抗氧化能力、胃肠激素等方面出现一系列变化，胃泌素、生长抑素等均参与应激性疾病的形成，这些变化可能导致地震灾区消化性溃疡高发。
【摘要】 目的 探讨抗氧化应激是否参与参附注射液预处理诱导的肾脏保护作用。 方法 健康成年雄性SD大鼠21只随机分为假手术对照组（Sham组）、肾脏缺血再灌注组（I/R组）和参附注射液组（SF组）；SF组给予参附注射液10 mL/kg腹腔注射，每日1次，连续给药7d。麻醉下行右肾切除后，用无损伤动脉夹钳夹左侧肾蒂60min，再灌注24 h，制备肾缺血再灌注损伤动物模型。比较各组SD大鼠再灌注24 h肾脏组织中超氧化物歧化酶（superonidedismutase，SOD）水平、过氧化氢酶（catalese，CAT）和丙二醛（malonicalaldehyed，MDA）含量。 结果 与Sham组相比，I/R和SF组肾脏组织SOD和CAT显著降低，而MDA明显升高（Plt;0.05）；与I/R组比，参附注射液能明显增加SOD和CAT水平（Plt;0.05），降低MDA含量（Plt;0.05）。 结论 参附注射液预处理可增强缺血再灌注损伤肾脏组织抗氧化应激，其表现为增强SOD和CAT的活力，减少MDA的生成。【Abstract】 Objective To explore the protective effect of Shenfu injection combined with antioxidant system on rats’ kidney after ischemia-reperfusion injury. Methods Twenty-one male Sprague Dawley (SD) rats were randomly divided into 3 groups: sham operation group (Sham group), ischemia-reperfusion group (IR group), and shenfu injection treated group (SF group). The rats were anesthetized with valebarbitone. Bilateral kidneys were exposed through midline incision. The right kidney underwent the nephrectomy and left renal pedicels were occluded for 60 minutes with a traumatic mini-clamp and then unclamped for 24 hours. Animals in SF group received Shenfu injection (10 mL/kg) through intraperitoneal injection every day for 7 days. About 24 hours after reperfusion, superoxide dismutase (SOD), CAT and malonical aldehyde (MDA) were measured. Results The levels of MDA were lower in SF group than those in IR group (Plt;0.05). The level of SOD and CAT in SF group increased more significantly than which did in IR group (Plt;0.05). Conclusion Our finding suggests that antioxidant system in SF group works more efficiently than IR group to overcome oxidative stress in renal ischemia-reperfusion injury.
Through dog models of common bile duct obstruction (BDO), the contents of liver superoxide dismutase (SOD) and malondialdehyde(MDA) were measured 2,3,4 and 5 weeks after BDO. Results indicated that the hepatic MDA content was increased 2 weeks after BDO as compared with control group (Ｐ＜0.01), the hepatic SOD content was decreased 3 weeks after BDO (Ｐ＜0.05). When bile duct obstructing, these changed were more serious. The results suggest that liver has little ability to eliminate the superoxide free radicals after BDO, whereas the lipid peroxidation products increase. It may be one of the mechanisms of liver damage after BDO.
Objective To investigate the influence of chronic alcohol ingestion on the severity of acute lung injury (ALI) induced by oleic acid and lipopolysaccharide (LPS).Methods Thirty-two SD rats were randomly administrated with alcohol or water for 6 weeks，then instilled with oleic acid and LPS to induce ALI or with normal saline as control.Thus the rats were randomly divided into two injury groups [ethanol group and water group] and two control groups [ethanol group and water group] (n=8 in each group). PaO2,Wet to dry lung weight ratio (W/D)，levels of γ-glutamylcysteinylglycine (GSH) and malonaldehyde (MDA) in the lung tissue were measured.Results Compared to corresponding control groups，the PaO2 and GSH significantly decreased，and the lung W/D and MDA level were significantly increased in the injury groups (all Plt;0.05).In the injury groups，the changes of above parameters were more significant in the alcohol group than thoe in the water group (all Plt;0.05)，except the lung W/D with no significant difference.Conclusion Chronic ethanol ingestion was relevalent to oxidation/ antioxidation imbalance and more severe lung injury in rats with severe septic after trauma,which suggests that chronic alcohol abuse could increase the severity of acute lung injury.
Objective To explore the potential protective effect in vivo of Edaravone, a free radical scavenger on model of acute lung injury in rats with sepsis. Methods Twenty-four male Wistar rats were randomly divided into three groups, ie. a control group( NS group) , a model group( LPS group) , a Edaravone treatment group( ED group) . ALI was induced by injecting LPS intravenously( 10 mg/ kg) in the LPS group and the ED group. Meanwhile the ED group was intravenously injected with Edaravone( 3 mg/ kg) . The NS group was injected with normal saline as control. The lung tissue samples were collected at 6 h after intravenous injection. The wet / dry ( W/D) weight ratio of lung tissue was measured. The levels of myeloperoxidase ( MPO) , malondialdehyde ( MDA ) and superoxide dismutase ( SOD) in lung tissue homogenate were assayed. The pathological changes and expression of nuclear factor-kappa B( NF-κB) in lung tissue were also studied. Results Compared with the NS group, The W/D, pathological scores, NF-κB expression, MPO and MDA levels in the LPS group were significantly higher( all P lt; 0. 01) , and the level of SOD was apparently lower( P lt; 0. 01) . The W/D, pathological scores, NF-κB expression, MPO and MDA levels in the ED group were significantly lower than those in the LPS group( all P lt; 0. 01) and higher than those in the NS group( all P lt; 0. 01) . And the level of SOD in lung tissue of the ED group was higher than that in the LPS group and lower than that in the NS group ( P lt; 0. 01) . Conclusions Edaravone has protective effect on ALI rat model. The mechanismmay be related to its ability of clearing the reactive oxygen species, inhibiting the activation of the signal pathway of NF-κB and inflammatory cascade.
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.
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 investigate the effects of ecdysterone on the survival of the dorsal random-pattern skin flap with large length-to-width ratio in rats and its possible mechanisms. Methods Twenty-four healthy adult SD rats (male and/or female) weighing 200-250 g were randomly divided into the experimental group and the control group (n=12 per group).A caudally based dorsal random pattern skin flap, measuring 8 cm × 2 cm, was symmetrically raised. Ecdysterone (5 mg/kg) and normal sal ine (5 mg/kg) were injected into the abdominal cavity of rats in the experimental group and the control group at 10 minutes before operation and from the first to the fifth day after operation, respectively. The general condition of the rats was observed after operation. At 7 days after operation, the survival rate of the flap was detected, the superoxide dismutase (SOD) activity and the malonyldialdehyde (MDA) level were tested, HE and immunohistochemistry staining observation of the flap were performed. VIII factor dried microvessels in the middle part of the flap (4 cm far away from pedicle) were counted. Results All the rats survived until the end of the experiment. At 7 days after operation, the survival rate of the flap was 62.323% ± 7.046% in the experimental group and 47.753% ± 2.952% in the control group (P lt; 0.001); SOD activity was (54.560 ± 4.535) U/mgprot in the experimental group and (23.962 ± 3.985) U/mgprot in the control group (P lt; 0.001); MDA level was (8.445 ± 0.992) nmol/mgprot in the experimental group and (14.983 ± 0.929) nmol/mgprot in the control group (P lt; 0.001). Histology observation: compared with the control group, the inflammatory cells infiltration was less and the hyperplasia of fibers was more obvious in the experimental group. The microvessel counting in the middle part of the flap was 17.817 ± 2.420 in the experimental group and 8.967 ± 2.000 in the control group (P lt; 0.001). Conclusion Perioperative intraperitoneal injection of ecdysterone can promote the survival of the random-pattern skin flaps with large length-to-width ratio. Its mechanism may be related to its effects of improving SOD activity, decreasing l ipid peroxidation, and promoting angiogenesis of skin flaps.
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.
To study the variations of l ipid peroxidation products and copper, zinc-superoxide dismutase(CuZn-SOD) in pathological scars (hypertrophic scars and keloids). Methods The specimens were gained from patients of voluntary contributions from May 2005 to August 2005. The tissues of hypertrophic scar (10 cases, aged 16-35 years, the mean course of disease was 2.2 years), keloid (10 cases, aged 17-32 years, the mean course of disease was 8 months) and normal skin (8 cases, aged 16-34 years) were obtained. The content of malonaldehyde (MDA)and CuZn-SOD activity were detected by spectrophotometric method. The expression of CuZn-SOD was evaluated by immunohistochemistry technique. Results The contents of MDA and CuZn-SOD activity were significantly higher in hypertrophic scars[MDA (1.139 0 ± 0.106 7)nmoL/mg prot, CuZn-SOD (31.65 ± 2.21)U/mg prot, (P lt; 0.05)]and keloids[MDA (1.190 0 ± 0.074 8)nmoL/ mg prot, CuZn-SOD (34.36 ± 5.01)U/mg prot (P lt; 0.05)] than those of normal skin tissues [MDA (0.821 3 ± 0.086 4)nmoL/mg prot, CuZn-SOD (20.60 ± 5.56)U/mg prot]. Immunohistochemical studies indicated that the brown particles were CuZn-SOD positive signals, which mainly located cytoplasm in normal skin tissues, hypertrophic scars as well as keloids epidermal keratinocytes and dermal fibroblasts. CuZn-SOD expression evaluation in hypertrophic scars (4.14 ± 0.90, P lt; 0.05) and keloids epidermal keratinocytes (4.43 ± 0.79, P lt; 0.05) markedly increased when compared with normal skin tissues (2.20 ± 0.45). The expression of CuZn-SODin hypertrophic scars (4.00 ± 0.82, P lt; 0.05) and keloids dermal fibroblasts (4.43 ± 0.53, P lt; 0.05) were significantly higher than that of normal skin tissues (1.60 ± 0.89). There were no differences in the content of MDA, CuZn-SOD activity and expression evaluation between hypertrophic scars and keloids (P gt; 0.05). Conclusion In pathological scars, the contents of MDA and CuZn-SOD activity increase and the expressions of CuZn-SOD are enlarged.