【Abstract】Objective To investigate the expressions of TNF-α and superoxide dismutase (SOD) mRNA in myocardium of rats with obstructive jaundice (OJ). Methods The expressions of TNF-α and SOD mRNA were semi-quantitatively analyzed after amplification of cDNA in myocardium of the rats with OJ by RTPCR. Results The expression of TNF-α mRNA increased and that of SOD mRNA decreased in the myocardium of rats with OJ. The level of plasm TNF-α increased and SOD synthesis in myocardium decreased. Conclusion The injury of myocardium in OJ is correlated with increasing expression of TNF-α mRNA and decreasing expression of SOD mRNA.
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.
Electron spin resonance (ESR) spectroscopy and spin trapping agent PBN were applied to measure directly the changes of oxygen free redicals (OFR) in gastric mucosa of rats with portal hypertension (PHT) injured by shockreperfusion, and treated with superoxide dismutase (SOD), radix salviae miltiorrhizae (RSM), with concomitant monitoring activity of SOD and pathology of gastric mucosa. Results showed that the amount of OFR increased markedly in gastric mucosa of PHT rats during the shock-reperfusion. The pathological changes were in accordance with alteration of the amount of OFR and the activity of SOD. Gastric mucosa in PHT was more susceptible to shock-reperfusion insult than normal controls. The anti-oxidant SOD, RSM used at early stage exerted mild gastric mucosal insult through different mechanisms.
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 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 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.
Perfusion of free flaps from groin of rabbits, after 12 hours of complete ischemia, with superoxide dismutase (SOD), an oxygen free radical scavenger, would significantly increase the survival rate of these flaps from 18.75% to 75% in the control group. Tissue levels of SOD and malonydialdehyde (MDA, an end product of lipoperoxidation) were measured before ischemia, after ischemia but before reperfusion, and 60 minites after reperfusion. In untreated flap, after 12 hours- ischemia, the SOD content of skin decreased significantly as compared with the SOD content before ischemia, and reperfusion further decreased SOD activity, while the concentration of MDA increased after ischemia and further increased after reperfusion. In the treated flaps, the concentration of SOD was not decrease and MADnot increased after reperfusion. There was a negative correlation between the values of SOD and MDA. These findings suggested that free oxygen radicals playedan important role in the free flap ischemia reperfusion injury. SOD could increase the survival of ischemic free-flaps by reducing lipoperoxidation. The results had significant clinical implications with regard to organ preservation and transplantation.
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 study the effects of malondialdehyde (MDA), superoxide dismutase (SOD) and tumor necrosis factor-α (TNF-α) on brain tissue in rats with pancreatic encephalopathy (PE). Methods Thirty-six Wistar rats were randomly divided into control group (n=6) and PE model group (n=30). In control group, rats were injected with normal saline by internal carotid artery (0.1 ml/100 g) and were killed on the first day after the injection. In PE model group, rats were injected with phospholipases A2 (0.1 ml/100 g, 1 000 U/0.1 ml) by internal carotid artery, to establish animal model of PE in rat and 10 rats were killed on day 1, 3, 7 respectively after the injection. The changes of water content in the brain were measured. Leucocytes aggregation and margination in the microvessels, and the changes of cerebral cells and nerve fibers were observed. The levels of MDA, TNF-α and the activity of SOD were tested in the brain homogenate in rats. Results In PE model group, water contents of brain increased; The phenomena of leucocytes accumulation and margination, cellular edema of neurons and demyelination of nerve fibers became more obvious; The levels of MDA and TNF-α increased significantly than those in the control group, while the activity of SOD reduced (P＜0．05， P＜0.01)． Conclusion Inthe rat model of PE, MDA, SOD, and TNF-α play important roles on the occurrence and development of brain injury.
ObjectiveTo explore the feasibility of medical ozone in treatment of pulmonary fibrosis. MethodsForty Wistar rats were randomly divided into an experimental group and a control group, with 20 rats in each group.All rats were intratreacheally instilled with bleomycin to induce pulmonary fibrosis.Then the rats were intraperitoneally injected with physiological saline every other day in the control group, and with medical ozone every other day in the experimental group.After 28 days, 10 rats in each group were sacrificed after lung function test.Right lung tissues were sampled for pathological examination, and left lung tissues were sampled for measurement of superoxide dismutase (SOD) and hydroxyproline.The remaining 10 rats in each group continued to be normally fed and intraperitoneally injected for observation of the survival time. ResultsThe lung function of the control group significantly decreased compared with the experimental group.The degree of lung fibrosis in the control group was more severe than that in the experimental group (lung fibrosis score: 1.9±0.5 vs.1.2±0.4, P < 0.05). The level of SOD in lung tissue was significantly higher and the level of hydroxyproline was significantly lower in the experimental group compared with the control group [(208.48±29.37)U·mg-1·pro-1 vs.(163.34±21.42) U·mg-1·pro-1, (2.25±0.28) mg/g vs.(2.68±0.37) mg/g, P < 0.05].The rats in the experimental group had longer survival time compared with the control group (79 d vs.59 d, P < 0.05). ConclusionMedical ozone can delay the progress of pulmonary fibrosis in rats.