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Objective:To investigate the relevance between spatial learning and memory impairment and the changes of inducible nitric oxide synthase (iNOS) activity,superoxide dismutase (SOD) activity and malondiadehyde (MDA) content in hippocampus from Type 1 diabetic mice.Methods:Sixty male mice were randomly assigned into a control group (NC group,20 mice) and a Type 1 diabetic group (DM group,40 mice).Type 1 diabetic mouse models were established by a large dose intraperitoneal injection of streptozotocin (100 mg/kg).The spatial learning and memory abilities of mice were assessed by Morris water maze (MWM) test.After MWM test,we chose 20 mice (diabetic encephalopathy mice) with the worst spatial learning and memory abilities from diabetic model group,and detected the iNOS activity,SOD activity and MDA content in hippocampus in both groups.Results:Compared with the NC group,the escape latency was significantly extended and platform crossings were significantly declined in diabetic mice (P＜0.01).Furthermore,the activity of iNOS and the content of MDA were markedly increased,and the activity of SOD was significantly decreased in hippocampus of diabetic encephalopathy mice (P＜0.01).Conclusion:The established Type 1 diabetic mice show symptoms of cognitive dysfunction,which might be related to the increase of oxidative stress in hippocampus.
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OBJECTIVE: To investigate the effect of the power-frequency electromagnetic field on antioxidant indexes in operation personnel. METHODS: By random sampling method,a total of 58 workers who work in 500 kV transformer substations for at least 5. 0 years were selected as the exposure group,and 60 administrative staffs in the same enterprise were included as the control group. The power frequency electromagnetic fields in the 2 groups were measured. The cumulative exposure dose of individual magnetic field was calculated. Peripheral venous blood was collected in these 2groups and was examined with the superoxide dismutase( SOD) activity,malondialdehyde( MDA) level and the relative gene expression level of manganese superoxide dismutase( MnSOD). RESULTS: There was no statistical significance in the SOD activity,MDA level and the relative gene expression level of MnSOD between the exposure group and the control group( P > 0. 05). The logistic regression analysis results indicated that cumulative exposure dose was not correlated with the SOD activity,MDA level and the relative gene expression level of MnSOD after adjusting confounding factors such as age,smoking,alcohol and tea drinking( P > 0. 05). CONCLUSION: Power-frequency electromagnetic field exposure has no significant effects on the SOD activity,MDA level and the relative gene expression level of MnSOD of operation workers.
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Aims: This study evaluated the effect of methanolic leaf extract of Magnifera indica on paracetamol-induced hepatic toxicity in rats. Study Design: Hepatic toxicity in rats was induced by oral administration of paracetamol followed by treatment with the leaf extract and evaluation of liver function parameters, lipid peroxidation activity and hematology. Place and Duration of Study: Department of Veterinary Physiology, Pharmacology and Biochemistry, Michael Okpara University of Agriculture, Umudike, Abia State, Nigeria/ One year. Methodology: Hepatic injury was achieved by oral administration of 2000mg/kg of paracetamol to rats. Three test doses (100, 200 and 300mg/kg) of Magnifera indica leaf extract (MILE) and a standard reference drug, silymarin (100mg/kg) were administered to the rats orally for ten days through gastric gavage. At the end of the treatment, blood was collected from the rats for liver function tests, hematology, malondiadehyde (MDA) levels and catalase activities. The effect of the extract was compared with silymarin and distilled water controls. Results: Liver function test showed that the extract and reference drug caused various levels of significant (P=0.02 to P=0.001) reduction of Aspartate aminotransferase (AST), Alanine aminotransferase (AST), Alkaline phosphatase (ALP) and total bilirubin when compared to negative control. Hematological analysis indicated various levels of significant increase in packed cell volume, hemoglobin concentration, Red blood cell count and White blood cell count (P=0.05-P<0.001). The MDA was also significantly (P=0.043) reduced by silymarin and MILE at the doses of 200 and 300mg/kg while there was no significant (P=0.24) changes in catalase activities of both treated and control rats. Conclusion: This study showed that Magnifera indica leaf extract ameliorated paracetamol-induced liver toxicity with optimum effect at 300mg/kg.
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Objective To observe the effects of exogenous sodium phosphocreatine (PCr) on cerebral repeffusion injury of rats after ischemia in order to explore the potential mechanism. Method Thirty-six healthy adult male Wistar rats with body weight 200- 220 g were randomly (random number) divided into sham operation group, ischemic reperfusion (I/R) group and PCr treatment group. The I/R model was established by using electro-cauterizing bilateral vertebral arteries and occluding bilateral common carotid arteries with atraumatic carotid clasps for 10 min, and then the clasps were released for 48 hours reperfusion. In sham operation group, bilateral common carotid arteries were exposed without occlusion. In PCr treatnent group, PCr in dose of 150 mg/kg was administered intravenously 60 min before the occlusion of bilateral common carotid arteries. Normal saline was administered intravenously instead of PCr into rats of I/R group. After reporfusion for 48 hours, the rats were sacrificed and brains removed for detections of neuron apoptosis by using TUNEL, malondialdebyde (MDA) level by using chromtometry and calmodulin (CaM) activity by using ELISA. Results Compared with sham operation group, TUNEL-positive cells, MDA level and CaM activity increased in I/R group and PGr treatment group ( P ＜0.01). Compared with I/R group, TUNEL-positive cells, MDA level and CaM activity were lower significantly in PCr treatment group ( P ＜ 0.01). Conclusions PCr can lessen cerebral ischemic reperfusion injury and neuron apoptosis, the mechanism maybe relates to the attenuation of abnormalities in calcium balance and reduction of oxygen free radicals by PCr.
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Objective To explore the prevention and treatment effect and its mechanism of Xuebijing injec-tion combined with dexamethasone on rats' paraqnat-induced acute and chronic pulmonary injury.Method One hundred and twenty of male Wistar rats were randomly divided into six groups:nomud group(A),administrated with saline;model group(B)and treatment groups(group C,D,E,F)were given 20%PQ(100 mg/kg.ip),and 2 hours later the normal and model groups were administrated with the same volume of saline for treatment,rats in group C and group D received 1.25 g/kg and 2.5 g/kg Xuebijing injection respectively.rdts in group E received 25,ng/kg dexamethasone,rats in group F receired 2.5 g/kg Xuebijing injection combined with 2.5 g/kg dexamethasone,one time per day till to be killed,while rats killed at 28 d were treated for 7 days.At 2 d,3 d,4 d after poisoned,five rats in each group were killed,serum SOD,MDA level and arterial gas(at 3 d)were measured.At 28 d,the rest of rats were killed,and serum TGF-β1,lung tissure HYP were measured.The pathology of the lung tissue was ob-served at 3 d and 28 d in guoup A,B,F.Results Compared with group B,poisoning symptoms in the treatment groups were milder and serum.SOD,MDA,TGV-β1,lung tissure HYP level were better,arterial oxygen content were higer.Among treatment groups,the treatment effects in group F were the best,SOD and MDA of 3 d,HYP and TGF-β1 of 28 d in group B and F were respectively(37.47±13.00,91.86±21.35)nmol/mL;(11.34±3.07,5.63±1.58)nmoL/mL;(2.54±0.63,1.32±0.07)mg/g;(484.13±63.79,202.22±49.83)pg/mL.The difference was significant(P＜0.05).The pathology of the lung tissue showed that acute lung hemorrhage,edema or chronic pulmonary fibrosis in group F were milder than that of group B.Conclusions In early stage,Xuebijing injection combined with dexamethasone has a stronger ability to clear out oxidized free radical and inhibit lipid super oxidized reaction.This may ameliorate acute pulmonary blooding and edema.In later stage,they could ameliorate chronic pulmonary fibrosis by inhibiting TGF-β1 secretion and HYP generation.
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Objective: To study the effect of seed oil of Hippophae rhamnoides L.(SOHR) on experimental hepatocirrhosis in mice. Methods: CCl_(4) was used in the experiment to form the model of experimental hepatocirrhosis in mice.In order to measure the possible changes of GPT and SOD in serum and SOD and MDA in tissues,we fed these mice with different concentration of SOHR for 45 days.The Does-Effect Curve was set up based on the data of this experiment. Results: SOHR could control the increase of GPT in serum and the decrease of SOD evidently,as well as the increase of MDA in tissues.The relationship of that the Hippophae rhamnoides dose with the decrease of GPT is significant. Conclusion: SOHR protects the experimental hepatacirrhosis in mice.
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AIM To evaluate the changes of serum and brain tissue endoxin in model of bilateral cerebral hemisphere ischemic reperfusion injury, and effect of anti digoxin antiserum (an antagonist of endoxin). METHODS The bilateral cerebral hemisphere ischemic model was prepared by ligating three vascular by Kameyama's manner. SD rats were randomly divided into 7 groups and each group had 8 rats. Sham group, ischemic reperfusion group, negative control group, nimodipine group, low concentration anti digoxin antiserum group, middle concentration anti digoxin antiserum group, high concentration anti digoxin antiserum group. The blood was collected at the end of reperfusion, meanwhile rats were killed, and the bilateral cerebral hemisphere were took out and used to prepare encephlon homogenate and made into samples of light microscope. RESULTS Compared with sham group, the serum CK content increased; Brain tissue SOD activity reduced and MDA content increased importantly in ischemia reperfusion group; The levels of serum and brain tissue endoxin in ischemia reperfusion group were significantly higher, while ATPase activity in brain tissue decreased; Mitochondrial Ca 2+ content in brain tissue increased significantly and Mg 2+ content decreased significantly. In brain tissue,there was some inflammatory change and local necrosis;The rank order and structure of cell wasn't clear;The morphology of pyramidal cell was abnormal. Compared with ischemic reperfusion group, Anti digoxin antiserum reduced serum CK content; It antagonized lowering of SOD activity and increase of MDA content in brain tissue; It remarkably reduced the level of brain tissue endoxin; It reduced abnormal ion content of brain tissue mitochondrion induced by cerebral ischemic reperfusion injury; The high and middle concentration anti digoxin antiserum had a significant effect on raising brain tissue ATPase activity. It reduced neuron denaturation. CONCLUSION Cerebral ischemic reperfusion can increase the level of brain tissue and serum endoxin and higher endoxin can promote brain injury. Endoxin is a major factor involved in cerebral ischemic reperfusion injury. Anti digoxin antiserum can reduce brain tissue injury and had a protective and treatment effect on cerebral ischemic reperfusion injury by antagonizing the effect of endoxin.
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Objective To explore the effects of intestinal trefoil factor (ITF) on interleukin-8(IL-8) and malondiadehyde (MDA) of neonatalrats' intestinal tissue post necrotizing enterocolitis(NEC), to investigate whether ITF has some protective effects on NEC.. Methods Thirty-two neonatal tats of NEC model were devided into four groups, (1)NEC+FTF 0.5 mg, (2) NEC+ITF 0.2 mg, (3) NEC, and (4) all others. After NEC model of neonatal rats was established and the ITF was treated, all the neonatal rats were returned to their mothers. In the 4th day, all the subjects were put to death. Intestinal tissue located at the boundary of ileum and cecum was obtained to observe hostological changes. Other intestinal sissue was removed to homogenate. Than the homogenate was centrifuged, supernates were used to determine the content of IL-8 and MDA. Results Content of IL-8 was dramatically less in group A and B than group C, respectively (29.722?7.134)、(30.512? 8.230)、(39.379 5?4.420) [pg/(mg?pro)](P0.05). Content of MDA was dramatically less in group A and B than group C, respectively(2.267?0.267)、(2.154?0.301)、(3.378?0.835)[nmol/(mg?pro)](P
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AIM: To study the effects of quateranary ammonium salt derivative (F2) of haloperidol on ischemia and reperfusion injury in rat hearts. METHODS: Ischemia and reperfusion injury in rat hearts was induced by occluding the left anterior descending coronary artery for 30 min and restoring blood reperfusion for 30 min. F2(1, 2, 4 mg·kg-1, respectively) was intravenously injected before heart ischemia. Plasma creatine kinase (CK), creatine kinase isoenzyme MB(CK-MB), lactate dehydrogenase(LDH), α-Hydroxybutyrate dehydrogenase (HBDH), grutamicoxalacetic transaminase(GOT), superoxide dismutase (SOD) activity and malondiadehyde (MDA) contents were measured. The pathologic changes of ischemia and reperfusion myocardium were observed on the transmission electron microscopy. RESULTS: F2 reduced the release of CK, CK-MB LDH, HBDH, GOT from I/R rat hearts, increased the activity of SOD and decreased the MDA contents. In F2(1mg·kg-1) group, the serum CK-MB LDH HBDH concentration was lowered significantly (vs I/R group P<0.01 or P<0.05). In F2(2 and 4 mg·kg-1) groups serum CK CK-MB LDH HBDH GOT concentration and MDA contents were decreased significantly (vs I/R group P<0.01), and SOD increased significantly (vs I/R group P<0.01). The decrease of CK, CK-MB, LDH, HBDH, MDA in F2(4 mg·kg-1) group was more remarkable than that in F2(2 mg·kg-1) group (P<0.01). CK-MB in F2(4 mg·kg-1) group was lowered than that in Verapamil (2 mg·kg-1) group (P<0.05). For morphology, myocytes of I/R heart showed intracellular edema, disarrangement and rapture of myocardial fiber, damaged mitochondria, marginated and concentrated nucleus. F2 modified these changes. CONCLUSION: F2 may play an apparent role against rat heart ischemia/reperfusion injury in dose-dependent manner.
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Objective To investigate the protective effect of Danxiong Recipe (DR) on brain in hypoxia mice.Methods Sixty mice were equally randomized to 6 groups:normal group,model group,propranolol group and low-,model- anti high-dose DR groups.Except the normal group,the mice in other groups were given the corresponding drug intra- gastrically according to the experimental design,once a day,for 7 days.After treatment,the survival time under nor- mobaric hypoxia condition in different groups was calculated.Meanwhile,the activities of superoxide dismutase(SOD) and nitric oxide synthase (NOS),and the contents of malondiadehyde (MDA) and lactic acid (LD) in the brain ho- mogenate were detected with test kit.Results The results showed that DR could prolong the survival time of the mice, inhibit obviously the abnormal increase of MDA and LD,reduce NOS activity,and enhance SOD activity in mice brain. Conclusion DR exerts protective effect on brain in hypoxia mice under normal pressure.
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AIM: To observe free radicals (MDA, NO) and iNOS of patients with severe acute respiratory syndrome (SARS) and to explore its significance. METHODS: MDA, NO_2~-/NO_3~- and iNOS were determined in SARS patients during the early, recovery and follow-up stage, front doctors and nurses (contact group) and health people (health control). RESULTS: The level of MDA during first stage was higher than that of recovery stage and the MDA level of recovery stage was higher than that of follow-up stage, contact group, and health control group (P0.05). CONCLUSION: The pathological injury in pathogenesis of SARS is related to free radicals. [
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Objective: To determine the mechanism of protective effects of lidocaine on brain during ischemia. Method: Wistar rats within 24h after birth were enrolled. The brain cortex cells were separated and then cutured under normal or anoxic condition. The OD value of these cells were detected with rapid colorimetric assay after they were cultured 24h and 48h. According to the above values, other cells were cultured in different condition and divided intc three groups: control group(N) cultured under normal condition (37℃, 5%CO_2+95%air); anoxic group(A) and anoxic+ lidoeaine group(L) cultured under anoxic condition(37℃, 5%CO_2+95%N_2). 6.9?10~(-5)mol/L lidocaine was added to the medium in group L. Cells of these three groups were cultured under different condition for 48h, then malondiadehyde and lactate levels of each group were measured. Result: The survival cells of anoxic group were significantly lower than that of control group after cultured for 48h, the malondiadehyde levels were as follows (nmol/ml): group N(4.93 ?0.43, n=12), group A(5.56?0.34, n=12), group L(4. 80?0.25, n=11); the lactate levels (mmol/L): group N(8.05?1.64, n=21), group A (11.86?2.58, n=22), group L(9.96?1.88, n=21), Conclusion: Lidocaine may protect brain from ischemia through inhibiting malondiadehyde and lactate production induced by anoxia.
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AIM To study the effects of quateranary ammonium salt derivative (F 2) of haloperidol on ischemia and reperfusion injury in rat hearts. METHODS Ischemia and reperfusion injury in rat hearts was induced by occluding the left anterior descending coronary artery for 30 min and restoring blood reperfusion for 30 min. F 2 (1, 2, 4 mg?kg -1 , respectively) was intravenously injected before heart ischemia. Plasma creatine kinase (CK), creatine kinase isoenzyme MB(CK MB), lactate dehydrogenase(LDH),? Hydroxybutyrate dehydrogenase (HBDH), grutamic oxalacetic transaminase(GOT), superoxide dismutase (SOD) activity and malondiadehyde (MDA) contents were measured. The pathologic changes of ischemia and reperfusion myocardium were observed on the transmission electron microscopy. RESULTS F 2 reduced the release of CK,CK MB LDH,HBDH,GOT from I/R rat hearts, increased the activity of SOD and decreased the MDA contents. In F 2 (1mg?kg -1 ) group, the serum CK MB LDH HBDH concentration was lowered significantly (vs I/R group P
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Effects of methylflavonolamine (MFA) on arachidonic acid(AA) metabolism pathway were studied. MFA (iv 40 mg ? kg-1) lightened the acute pulmonary thromboenblism signs in mice and reduced the mortality induced by AA. MFA(12. 5~200?mol ? L-1) in vitro dose-dependently inhibited rabbit platelet aggregation induced by AA. MFA(0.1~0. 4mmol ? L-1) in vitro dose - dependently inhibited rabbit platelet malondiadehyde(MDA) formation in-duced by AA. MFA(0. 4mmol?L-1) inhibited platelet MDA formation in rabbits induced by thrombin and AA. While propranolol inhibited MDA formation induced by thrombin but not by AA. MFA (0.4 mmol ? L-1) did not affect cAMP content in rabbit platelet. These results suggest that inhibitory effect of MFA on platelet AA metabolism may be one of the mechanism by which MFA inhibited platelet aggregation.
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AIM: To observe the effect of glycine on the myocardial ischemic injury in mice METHODS: Mice were supplied with 20% glycine twice daily (0 025 mL/g, ig), or 40% Injection salviae miltiorrhizae composita (ISMC, 0 025 mL/g, ig) One week later, 0 02 U/g pituitrin was injected intraperitoneally The electrocardiogram was recorded, and activities of nitric oxide synthase (NOS), superoxide dismutase (SOD) and the content of malondiadehyde (MDA) in the myocardium were examined RESULTS: Glycine reduced changes in J spot in electrocardiogram Both glycine and ISMC increased activities of SOD and NOS, inhibited increase in MDA content in the myocardium induced by pituitrin There was no difference in above parameters between glycine-treated and ISMC-treated mice. CONCLUSION: These results demonstrated that glycine can protect myocardium from ischemic injury, the mechanism may be related to increase in activities of NOS, SOD and supressing the lipid peroxidation.
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It was found that a large amount of malonyldialdehyde ( MDA ) was formed in the burnt skin after 20% TBSA full thickness burns was inflicted to rats. The re were 2 peaks of the increase of MDA on the 2nd and 7th day postburn in the skin respectively. The content of MDA in the plasma and erythrocytes also increased and reached the peak on the 3rd day after injury. The content of vitamin E in the plasma and erythrocytes decreased rapidly from the 2nd day postburn and reached the lowest point on the 3rd day- Hemolysis was found to be the severest on the 3rd day postbarn. After the relationship between the MDA levels in the burnt skin, plasma, and erythrocytes, the vitamin E levels in the plasma and ery-throcyles, and the severity of hemolysis was analyzed, it was found that there was different correlation rale between these parameters in different time-phases, but the general rule was that when MDA increased in the burnt skin, plasma and erythrocytes, vitamin E decreased in the plasma and erythrocytes and hemolysis became more severe. On the basis of these findings, the mechanism of erythrocyte damage after burn injury was discussed.