ABSTRACT
AIM To observe the oxidant stress and opoptotic effects of anisodine hydromide (AH) on chronic cerebral hypoperfusion (CCH) rats.METHODS In vivo CCH models were established in adult male SpragueDawley rats by permanent ligation of bilateral common carotid arteries [two-vessel occlusion (2-VO)] surgery.Rats were randomly divided into six groups,sham group,model group,positive group of n-butylphthalide and sodium chloride injection,and AH groups (1.2 mg/kg high-dose group,0.6 mg/kg medium-dose group,and 0.3 mg/kg low-dose group).Antioxidant indices including the activity of SOD,CAT,LDH and iNOS and the content of GSH and NO were measured.In the in vitro trial,PC12 cells were divided into control group,model group,positive group of n-butylphthalide,and AH groups (100 μmol/L high-dose group,50 μmol/L mediumdose group,and 25 μmol/L low-dose group),and the hypoxic models were established by treating PC12 cells with CoCl2.The cells had their release of NO and LDH detected,their cellular apoptosis determined by Hochest 33342 fluorescence staining,and the expression of P53 protein identified by IF (immunofluorescence) and Western blotting method.RESULTS The in vivo trial revealed AH's enhancement in serum SOD activity and inhibition in serum iNOS activityof the CCH rats,and its power in the cerebral GSH and LDH release reduction.The in vitro trial showed the resultant lower LDH and NO release,decreased number of neuro-apoptosis,and inhibited P53 pro tein expression after AH intervention.CONCLUSION The antioxidant and antiapoptotic effects of AH on CCH rats may be associated with down regulation of P53 protein.
ABSTRACT
OBJECTIVE:To observe the clinical efficacy and safety of beraprost combined with fibrinogenase in the treatment of lower extremity atherosclerotic occlusive disease(LEAOD).METHODS:A total of 82 LEAOD patients selected from our hospital dur-ing Jan. 2015-Jan. 2016 were divided into control group and observation group according to random number table,with 41 cases in each group.All patients received low salt and low fat diet on the basis of treatment for primary disease.Control group was additionally given Fibrinogenase injection 200 U,ivgtt,qd;observation group was additionally given Beraprost sodium tablets 40 μg,tid,after meal,on the basis of control group.Both groups were treated for 15 d.Clinical efficacies as well as hemorheological indexes,ankle-brachial indexes,pain scores,cold felling scores,intermittent claudication scores and serum oxidation stress indexes before and after treatment were compared between 2 groups. The occurrence of ADR was also recorded. RESULTS:Total response rate of observation group (90.24%)was significantly higher than that of control group(78.05%),with statistical significance(P<0.05). Before treatment, there was no statistical significance in above indexes between 2 groups(P>0.05).Compared to before treatment,whole blood high shear viscosity,plasma viscosity,hematocrit,fibrinogen contents,platelet adhesion rates,pain scores,cold feeling scores,intermit-tent claudication scores and serum MDA levels of 2 groups were decreased significantly after treatment;while ankle-brachial indexes, the serum levels of SOD,T-AOC and GSH-Px were increased;the indexes of observation group were better than those of control group,with statistical significance(P<0.05).There was no statistical significance in the incidence of ADR between 2 groups(P>0.05).CONCLUSIONS:Beraprost combined with fibrinogenase show good therapeutic efficacy for LEAOD,can effectively relieve clinical symptoms,promote local blood circulation and improve oxidant stress level with good safety.
ABSTRACT
OBJECTIVE:To investigate the clinical efficacy and safety of cilostazol combined with alprostadil in the treatment of peripheral arterial disease(PAD). METHODS:A total of 68 PAD patients in our hospital from Jan. 2015 to Jan. 2016 were di-vided into observation group(34 cases)and control group(34 cases)according to random number table. Control group was given basical treatment,and Alprostadil injection 2 mL+0.9% Sodium chloride injection 100 mL,ivgtt,qd. Observation group was addi-tionally given Cilostazol tablets 100 mg,po,bid,on the basis of control group. Both groups were treated for 30 days. Clinical effi-cacies of 2 groups were observed. The hemorheology indexes(hematocrit,whole blood high-shearing viscosity,erythrocyte aggre-gation index,erythrocyte deformation index,plasma viscosity),inflammatory factor indexes(TNF-α,IL-6,IL-8, hs-CRP),oxida-tion stress indexes(GSH-Px,SOD,T-Aoc,MDA),arteriosclerosis indexes(ABI,TBI,dorsalis pedis artery blood flow)were de-termined before and after treatment. The occurrence of ADR was recorded. RESULTS:Total response rate of observation group (91.18%)was significantly higher than that of control group(79.41%),with statistical significance(P0.05). After treatment,hematocrit,whole blood high-shearing viscosity,erythrocyte aggregation index,erythrocyte deformation index,plasma viscosity,the levels of TNF-α,IL-6,IL-8,hs-CRP and MDA in 2 groups were de-creased significantly;while the levels of GSH-Px,SOD,T-Aoc,ABI,TBI and dorsalis pedis artery blood flow were increased sig-nificantly;the improvement of above indexes in observation group was significantly better than control group,with statistical signif-icance(P0.05). CONCLUSIONS:For PAD,cilostazol combined with alprostadil can effectively improve hemorheolo-gy indexes,inflammatory factor indexes,oxidation stress indexes and arteriosclerosis indexes with good safety.
ABSTRACT
OBJECTIVE:To observe the clinical efficacy and safety of beraprost combined with fibrinogenase in the treatment of lower extremity atherosclerotic occlusive disease(LEAOD).METHODS:A total of 82 LEAOD patients selected from our hospital dur-ing Jan. 2015-Jan. 2016 were divided into control group and observation group according to random number table,with 41 cases in each group.All patients received low salt and low fat diet on the basis of treatment for primary disease.Control group was additionally given Fibrinogenase injection 200 U,ivgtt,qd;observation group was additionally given Beraprost sodium tablets 40 μg,tid,after meal,on the basis of control group.Both groups were treated for 15 d.Clinical efficacies as well as hemorheological indexes,ankle-brachial indexes,pain scores,cold felling scores,intermittent claudication scores and serum oxidation stress indexes before and after treatment were compared between 2 groups. The occurrence of ADR was also recorded. RESULTS:Total response rate of observation group (90.24%)was significantly higher than that of control group(78.05%),with statistical significance(P<0.05). Before treatment, there was no statistical significance in above indexes between 2 groups(P>0.05).Compared to before treatment,whole blood high shear viscosity,plasma viscosity,hematocrit,fibrinogen contents,platelet adhesion rates,pain scores,cold feeling scores,intermit-tent claudication scores and serum MDA levels of 2 groups were decreased significantly after treatment;while ankle-brachial indexes, the serum levels of SOD,T-AOC and GSH-Px were increased;the indexes of observation group were better than those of control group,with statistical significance(P<0.05).There was no statistical significance in the incidence of ADR between 2 groups(P>0.05).CONCLUSIONS:Beraprost combined with fibrinogenase show good therapeutic efficacy for LEAOD,can effectively relieve clinical symptoms,promote local blood circulation and improve oxidant stress level with good safety.
ABSTRACT
<p><b>OBJECTIVE</b>Anesthetic isoflurane plus surgery has been reported to induce cognitive impairment. The underlying mechanism and targeted intervention remain largely to be determined. Ginsenoside Rb1 was reported to be neuroprotective. We therefore set out to determine whether ginsenoside Rb1 can attenuate isoflurane/surgery-induced cognitive dysfunction via inhibiting neuroinflammation and oxidative stress.</p><p><b>METHODS</b>Five-months-old C57BL/6J female mice were treated with 1.4% isoflurane plus abdominal surgery for two hours. Sixty mg/kg ginsenoside Rb1 were given intraperitoneally from 7 days before surgery. Cognition of the mice were assessed by Barnes Maze. Levels of postsynaptic density-95 and synaptophysin in mice hippocampus were measured by Western blot. Levels of reactive oxygen species, tumor necrosis factor-α and interleukin-6 in mice hippocampus were measured by ELISA.</p><p><b>RESULTS</b>Here we show for the first time that the ginsenoside Rb1 treatment attenuated the isoflurane/surgery-induced cognitive impairment. Moreover, ginsenoside Rb1 attenuated the isoflurane/surgery-induced synapse dysfunction. Finally, ginsenoside Rb1 mitigated the isoflurane/surgery-induced elevation levels of reactive oxygen species, tumor necrosis factor-α and interleukin-6 in the mice hippocampus.</p><p><b>CONCLUSION</b>These results suggest that ginsenoside Rb1 may attenuate the isoflurane/surgery-induced cognitive impairment by inhibiting neuroinflammation and oxidative stress pending future studies.</p>
Subject(s)
Animals , Female , Mice , Anesthetics, Inhalation , Cognition , Cognitive Dysfunction , Ginsenosides , Pharmacology , Hippocampus , Inflammation , Isoflurane , Medicine, Chinese Traditional , Mice, Inbred C57BL , Oxidative Stress , Postoperative Complications , Random Allocation , Surgical Procedures, Operative , Synapses , MetabolismABSTRACT
Objective To investigate the effect and mechanism of thymoquinone on hepatic ischemia-reperfusion injury (IRI).Methods Thirty C57 mice were randomly divided into the sham operation (sham),IRI and thymoquinone (Thy)groups (n =1 0 in each group).At preoperative 1 h,thymoquinone at a dose of 40 ml/kg was administered via intraperitoneal injection in the Thy group.Absolute ethyl alcohol at the same dosage was given via intraperitoneal injection in the sham and IRI groups.Liver IRI mouse models were established in the IRI and Thy groups.Serum and liver specimens were collected at 4 h after reperfusion.Under light microscope,hepatic histopathological changes were observed and assessed by pathological injury grading.Reverse transcription polymerase chain reaction (RT-PCR)was performed to measure the messenger ribonucleic acid (mRNA)expression levels of tumor necrosis factor (TNF)-α,monocyte chemotactic protein (MCP)-1 and interleukin (IL)-6.The expression of TNF-α,MCP-1 and IL-6 proteins in the serum in the serum were assessed by ELISA.The content of malondialdehyde (MDA)in the liver tissue was detected by thiobarbituric acid (TBA).The activity of catalase (CAT),glutathioneperoxidase (GPx)and superoxide dismutase (SOD)in the liver tissue was determined by ELISA.The expression levels of Wnt,β-catenin and p53 proteins were measured by Western blot.Results Compared with the sham group,the liver injury was more severe and the hepatic injury grading was significantly enhanced in the IRI group (P <0.05),the expression of TNF-α,MCP-1 and IL-6 in the liver tissue and serum sample,and MDA, Wnt,β-catenin and p53 in the liver tissue was significantly up-regulated (P <0.05-0.001 ),whereas CAT,GPx and SOD activity in the liver tissue was dramatically reduced (all in P <0.001 ).Compared with the IRI group,the liver injury in the Thy group was slighter and the liver injury grading was significantly decreased (both in P <0.05).The expression levels of TNF-α,MCP-1 and IL-6 in the liver tissue and serum sample,MDA,Wnt,β-catenin and p53 in the liver tissue were significantly down-regulated (all in P <0.05),whereas CAT,GPx and SOD activity was considerably up-regulated in the liver tissue (all in P <0.05).Conclusions Thymoquinone can mitigate liver IRI through alleviating inflammatory response and oxidation stress.The underlying mechanism is correlated with inhibiting the activation of Wnt/β-catenin/p53 signaling pathway.
ABSTRACT
Objective To observe the effects of Hedan tablet on cytokines and oxidation factors in APOE-/-mouse, and to explore its effect on atherosclerosis and to explore its behind mechanism. Methods APOE-/-mice (n=50) were randomly divided into control group, model group, low dose Hedan tablet treatment group, high dose Hedan tablet treatment group and simvastatin treatment group. Mice in control group were given normal feed while mice in other groups were fed with high cho?lesterol diet. Hedan or Simvastatin was administrated intra-gastrically while normal saline was given to model group in the same route. After 12 weeks, mice were sacrificed to observe the mRNA level of tumor necrosis factor-α(TNF-αmRNA) in aorta by RT-PCR. Mean while, serum levels of interleukin-1 (IL-1), interleukin-10 (IL-10), malonaldehyde (MDA) and su?peroxide dismutase (SOD) were determined in different groups. Results Compared with control group, TNF-αmRNA tran?scription level as well as serum levels of IL-1 and MDA significantly increase while serum levels of IL-10 and SOD de?creased remarkably in model group, (P<0.01). Compared with model group, mRNA levels of TNF-αas well as serum levels of IL-1 and MDA were significantly decreased while serum levels of IL-10, SOD were greatly increased in low dose and high dose Hedan tablet treatment groups as well as in simvastatin treatment group (P<0.01). Conclusion Hedan tablet inhibit the formation of atherosclerosis through its anti-oxidation role and anti-inflammation role.
ABSTRACT
Cardiac contractile dysfunction and arrhythmic genesis are resulted from disturbed intracellular Na+and Ca2+ handling under condition of oxidation stress. Stress-induced intracellular signaling regulated mechanisms in which many activated stress kinases, such as cAMP-dependent protein kinase A, protein kinase C , Ca/calmodulin-dependent pro-tein kinaseⅡand classical pathways, are known to be involved. However, it is becoming increasingly evident that reactive oxygen species may directly oxidize these kinases, Na+and Ca2+channel protein and transporters, which lead to changing of intracellular Na+and Ca2+accumulation, and to trigger of arrhythmias.
ABSTRACT
Objective:To investigate the protective effect of ginkgetin from oxidative stress on immature testis induced by cyclophosphamide(CP) metabolite acrolein(ACR) in vitro.Methods:The sertoli cells were isolated from 7-days old SD rats' testes,culture and passage to F2 generations.Experiment groups were divided into: 1)Ginkgetin incubated for 12 hours and then treat with ACR 2) Ginkgetin and ACR add to cells at the same time 3) Ginkgetin and ACR were incubated for 12 hours,then add to cells.Control group include: 1) Vitamin E were incubated cells for 12 hours,then add ACR respectively 2) Added ACR only as the negative control group 3) Not add any factors as the positive control group.3 h later the viability of sertoli cell were determined by MTT.Protein concentration was determinate by Coomassie Brilliant Blue.Malondialdehyde(MDA),hydroxyl radical(OH ?),total antioxidant capacity(T-ACO),Superoxide dismutase(SOD) and glutathione reductase(GR) activity were tested.Results:1) Ginkgetin(add before ACR) can significantly raise the viability of the cells(P
ABSTRACT
Objective To measure the the expression of TNF-?、IL-6mRNA in liver of rats with alcohol fatty liver, and the amounts of TNF-?and IL-6, to observe the lesion of lipid superoxidation, to explore the pathogenesis of alcohol fatty liver. Methods 23 of SD rats were divided into the normal group(10) and the model group(13),all the rats in the model were given 50% alcohol by daily gavage, and drank 10% alcohol, after 14 weeks, all the rats were killed and the pathological change of liver were observed, the amounts of serum TG,TC,ALT,AST,FFA,MDA,SOD,GSH-PX,TNF-? and IL-6 were examined, the expression of TNF-?、IL-6mRNA was measured. Results In the model ,to different degree, there were some fatty steatosis , the amounts of TG、FFA、MDA、TNF-?and IL-6 were higher than that in the normal group, but the amounts of SOD and GSH-PX lower, in comparison with the normal, the expression of TNF-?mRNAand IL-6mRNA in liver of model were significantly increased. Conclusions long-term of ingestion of potation maybe cause the disorder of lipid metabolic system and alcohol fatty liver came into being. Simultaneously with the enhancement of oxidation stress/lipid superoxidation and abnormity of secretion of some cytokine such as TNF-?and IL-6.
ABSTRACT
Objective To study the change of oxidative stress in the formation of NASH in rats induced by high-fat diet,and observe the preventive and therapeutic effect of TFHL on NASH and explore its mechnism.Methods 110 rats were randomly divided into the normal group(40 rats),the model group(40 rats),the A.Nattermam group(10 rats) and high dosage and low dosage TFHL(10rats each).The normal rats were fed with the standard feedstuff the other rats fed with the high-fat diet.At the time of model-making,the rats in the A.Nattermam were fed the A.Nattermam suspension by daily gavage by 195.4mg/(kg?d),the rats in the high dosage and low dosage TFHL group were fed TFHL by daily gavage in 250、125mg/(kg?d),the rats in the normal and model groups were fed isometrical distilled water by daily gavage.At the ends of 2nd,4th,8th weeks of the experiment,10 rats in the nomal and model were killed respectively,at the end of experiment,all the rest were killed.pathological changes of liver tissues were observed,the levels of serum ALT,AST,the amount of TG,CHOL of livers tissue,the amount of MDA of serum and liver,the activity of OD、GSH-PX、T-AOC were measured.Results 1.the rats were fed with high-fat diet from 2 to 12w,the fatty degeneration of liver tissues were gradually serious,the amounts of TG,CHOL of livers were gradually increased.at 12th w the inflammatory cells in livers infiltrated obviously,the serum ALT,AST were obviously increased,it apeared a progressive process of NASH.2.from 4th w,after feeding with high-fat diet,the amounts of MDA of serum and liver were gradually decreased,the activity of SOD were gradually increased,the amount of T-AOC were gradually decreased as well and,increase or decrease with the development of inflammation.3.the inflammation degree of liver,the amount of liver CHOL and the serum ALT,AST in FMCL groups were lower than those in the corresponding model group;the amounts of MDA of serum and liver were decreased,the activity of SOD,GSH-PX and T-AOC were inceased than those in the corresponding model group,their oxidationresisting activity was better than those in the A.Nattermam group.Conclusions oxidation stress/Lipid Peroxidation plays an important role in the occurrence and development of NASH,TFHL can effectively treat and prevent the development of NASH,obviously ease oxidation stress,decrease Lipid Peroxidation of NASH,markedly enhance oxidationresisting abilily of body,which is the important mechanism of prevention and treatment for NASH.