Valsartan protects a rat model of adriamycin-induced dilated cardiomyopathy from left ventricular remodeling and failure

AIM: To investigate whether and how AT1 receptor blocker， valsartan， attenuates left ventricular remodeling and failure in a rat model of adriamycin（ADR）-induced dilated cardiomyopathy. METHODS: Weight-matched adult male Wistar rats were randomly divided into 3 groups as follows: 1) the ADR group, in which 2.5 mg/kg of ADR was weekly injected via a tail vein for 10 weeks (n=25); 2) concomitant AT1 receptor blocker valsartan and ADR, in which valsartan was administered by daily gavage at a dose of 30 mg·kg-1·d-1 (n=10); 3) control group (n=10). Hemodynamics and echocardiographic measurements were obtained at 12 weeks after treatment. Finally, left ventricle (LV) samples were collected at 12 weeks. The hydroxyproline content was determined by the methods of chloramines T. The expression of MMP-2, MMP-9 and tissue inhibitors of metalloproteinase-1 (TIMP-1) were measured by Western blotting. MMP-2 and -9 gelatinolytic activities were measured by gelatin zymography. RESULTS: Mortality was significantly lower in valsartan -treated rats than that in ADR rats (20% versus 40%, P<0.01). The dilatation of LV cavity was significantly attenuated in ADR-induced dilated cardiomyopathy rats given valsartan. Valsartan partially normalized LV contractile function, which was significantly reduced in ADR rats. The hydroxyproline content was increased in ADR-DCM group and significantly reduced by valsartan treatment (P<0.01). The protein levels of LV MMP-2 and MMP-9 were increased in ADR rats and attenuated by valsartan treatment (both P<0.01). However, no change in TIMP-1 was observed (P>0.05). The activities of LV myocardial MMP-2 and -9 gelatinolytic were increased significantly in ADR rats (both P<0.01) and attenuated by valsartan treatment (both P<0.01). CONCLUSION: Pretreatment with AT1 receptor blocker valsartan attenuates left ventricular remodeling and failure in a rat model of adriamycin-induced dilated cardiomyopathy.     

Changes of hydrogen sulfide content in plasma and tissues of rats with LPS-induced shock

AIM: To investigate the changes and significance of hydrogen sulfide (H2S) in both plasma and various tissues, including liver, kidney, heart, lung and arteriae aorta, in rats with LPS-induced shock. METHODS: A rat model of shock induced by injection of lipopolysaccharide (LPS) was developed. Male Wistar rats were divided into four groups: control group, LPS group, LPS+NaHS (H2S donor) group and LPS+ propargylglycine (PPG, metabolic enzyme inhibitor of H2S) group. The mean arterial pressure (MAP) of rats within 240 min was observed，and H2S contents were determined. The structures of various tissues were observed. RESULTS: Administration of LPS to male Wistar rats caused a sustained fall in MAP, various tissue injuries and a significant increase in H2S contents in plasma as well as liver, kidney, heart, lung and arteriae aorta within 240 min（all P<0.05）. Treatment with metabolic enzyme inhibitor of H2S, propargylglycine, was shown to reduce H2S content elevation in plasma as well as liver, kidney, heart, lung, and arteriae aorta, and ameliorate the hypotension and tissue injuries caused by LPS（all P<0.05）. However, treatment with H2S donor-NaHS was shown to increase H2S content elevation in plasma as well as liver, kidney, heart, lung and arteriae aorta, and aggravate the hypotension and tissue injuries caused by LPS（all P<0.05）. Endogenous H2S contents in both plasma and various tissues were negatively correlated with MAP（all P<0.05）.CONCLUSION: H2S may be a new endogenous mediator and play a role in the pathogenesis of endotoxic shock.     

Hydrogen sulfide regulates the expression of nitric oxide/nitric oxide synthase system during recurrent febrile seizures

AIM: To explore the effect of hydrogen sulfide (H2S) on nitric oxide (NO)/nitric oxide synthase (NOS) system during recurrent febrile seizures (FS). METHODS: Sprague-Dawley rats aged 21 days were randomly divided into four groups: control group (37.0 ℃ water, n=8); FS group (45.2 ℃ water, n=8); FS+NaHS group (45.2 ℃ water, n=8), FS+HA (hydroxylamine) group (45.2 ℃ water, n=8). FS in rats were induced ten times in a bath of warm water, once every 2 days. The plasma level of H2S and NO was detected by the spectrophotometer method. The expression of NOS mRNA was examined by in situ hybridization. The expression of nNOS protein was observed by immunohistochemistry. RESULTS: The plasma level of NO decreased significantly in FS+NaHS group while elevated obviously in FS+HA group compared with that in FS group. At the same time, the expression of nNOS down-regulated in FS+NaHS group while up-regulated in FS+HA group compared with that in FS group. CONCLUSION: H2S down-regulated the expression of NO/NOS system during recurrent FS.     

Protective effects of total saponins of panax notoginseng on myocardial hypertrophy and fibrosis induced by isoproterenol in rats

AIM: To investigate the protective effects of total saponins of panax notoginseng (PNS) on myocardial hypertrophy and fibrosis induced by isoproterenol (ISO) in rats.METHODS: Myocardial hypertrophy and fibrosis model of rats were induced by injection of ISO (5 mg·kg^-1·d^-1,sc) for 7 days.From day 2,the rats were administered with PNS at dose of 25 and 50 mg·kg^-1·d^-1,ip for 14 days,the control and ISO model group were received saline injection.Then,the heart-weight (HW),left ventricular weight (LVW),the ratio of HW/BW and LVW/BW (LVI) were measured;the hydroxyproline and malondialdehyde (MDA) and angiotensin (AngII) content of left ventricle.The level of nitric oxide (NO),nitric oxide synthase (NOS),superoxide disrnutase (SOD) and glutathione peroxidase (GSH-Px) activities in left ventricle were determined by spectrophotemetry and radioimmunoassay,respectively.RESULTS: Compared with NS control group,the ratio of HW/BW,LVW/BW and the content of hydroxyproline,AngII,MDA and iNOS activity in the left ventricle were significantly increased.The cNOS,SOD,GSH-Px activities and NO content were obriously decreased in the ISO model group.After treatment with PNS,the left ventricular NO content,cNOS,SOD and GSH-Px activities were markedly higher than those in ISO model group.The content of MDA,AngII and iNOS activities and the ratio of HW/BW,LVI were significantly lower than those in ISO model group.CONCLUSION: PNS reverses the myocardial hypertrophy and fibrosis induced by isoproterenol in rats.This effect may be related to eliminating the oxygen free radicals and raising NO level.     

Renoprotective effects of sesamin on renal hypertensive and hyperlipidemic rats

AIM: To investigate the effects of sesamin on progression of renal injury in renal hypertensive and hyperlipidemic rats (RHHR). METHODS: RHHR was induced by 2K1C and high lipid baitvessel. After 7 weeks of intragastric administration with sesamin, the contents of serum creatinine (Scr), blood urea nitrogen (BUN), 24 h urinary protein excretion (UPE) were measured. In addition, the activity of total antioxidative capacity (T-AOC), superoxide dismutase (SOD), the concentrations of malondialdehyde (MDA), hydrogen peroxide (H2O2), and the nitric oxide synthase (NOS) and nitric oxide (NO) levels in renal homogenate were measured. RESULTS: Compared with the model group, seasamin (in 100 mg·kg-1 and 33 mg·kg-1 groups) evidently decreased the contents of Scr, BUN, UP and the concentration of MDA, iNOS, H2O2 in renal tissure. It also improved the levels of NO, cNOS and activity of SOD, T-AOC in renal tissure. CONCLUSION: Sesamin ameliorates hypertensive and hyperlipidemic-induced renal injury, probably by enhancing antioxidative activity, scavenging hydroxyl radical and restraining iNOS level.     

Hydrogen sulfide inhibits inflammatory responses induced by acute myocardial ischemia in isolated rat hearts

AIM：To investigate whether hydrogen sulfide (H2S) protects the hearts against inflammatory responses induced by acute myocardial ischemia in isolated rat hearts. METHODS：Rat acute myocardial ischemia injury was induced by ligation of the left anterior descending coronary artery for 4 h, and the normal perfusate was replaced with NaHS (5 μmol/L, 10 μmol/L and 20 μmol/L) perfusate accordingly in NaHS groups 2 h after ischemia. The changes of cardiac function in the myocardial ischemic injury rats were observed. The mRNA expression of TNF-α, IL-1β, IL-6, IL-10 and ICAM-1 was detected by real-time PCR. The protein level of nuclear factor-κB (NF-κB) in the myocardial tissues was detected by Western blotting. RESULTS：The cardiac function in ischemia group was lower than that in sham group (P<0.01). Compared with ischemia group, perfusion of NaHS resulted in the improvement of the cardiac function (P<0.05 or P<0.01). Compared with sham group, the mRNA expression of TNF-α, IL-1β, IL-6 and ICAM-1 in the cardiac tissues was significantly increased, and the mRNA expression of IL-10 in the cardiac tissues was significantly decreased in ischemia group (P<0.01). Compared with ischemia group, the perfusion of NaHS significantly decreased the mRNA expression of TNF-α, IL-1β, IL-6 and ICAM-1 (P<0.05 or P<0.01). The perfusion of NaHS at concentrations of 10 μmol/L and 20 μmol/L significantly increased the mRNA expression of IL-10 (P<0.01). The protein level of NF-κB in ischemia group was markedly higher than that in sham group (P<0.01). Compared with ischemia group, the perfusion of NaHS at concentrations of 10 μmol/L and 20 μmol/L significantly decreased the expression of NF-κB (P<0.05 or P<0.01). CONCLUSION：H2S protects the hearts against acute ischemia injury through inhibition of NF-κB activation and subsequent down-regulation of NF-κB-dependent inflammatory gene expression.     

Effect of mesenteric lymph duct ligation on actue lung injury in rats

AIM：To explore the effect of mesenteric lymph duct ligation against actue lung injury (ALI) in rats.METHODS：45 Wistar rats were divided into three groups：the ligation group,the non-ligation group and sham operated group,and the two-hit model was established by hemorrhage and LPS injection.Mesenteric lymph was diverted by ligating mesenteric lymph duct in ligation group.All rats facilitated blood withdrawal for blood sample to arterial gas analysis after 24 hours.Then the WBC,NO,NOS,MDA,SOD and lung permeability index (LPI) were determined in bronchoalveolar lavage fluid (BALF),the MPO and ATPase activity were determined in lung homogenate.The ultrastructure was also observed.RESULTS：After two-hit,the PaCO2,the total cells and PMN,the NO2-/NO3-,NOS and MDA content in BALF and MPO activity in lung homogenate and LPI in non-ligation group were significantly increased than those in sham operated group.PaO2 and pH in arterial blood,SOD in BALF and the ATPase in lung homogenate were significantly lower (P<0.01 or P<0.05).The total cells and PMN,MDA,NO2-/NO3- in BALF,LPI in ligation group were significantly increased than those in sham operated group,and SOD in BALF was significantly lower (P<0.01 or P<0.05).The pH and PaO2 in arterial blood,the ATPase in lung homogenate in ligation group were significantly increased than those in non-ligation group,and the PaCO2,the total cells,PMN,NO2-/NO3-,NOS,MDA in BALF,LPI,and MPO in lung homogenate in ligation group were significantly lower than those in non-ligation group (P<0.01 or P<0.05).The injury of pulmonary vascular endothelium in ligation group was lighter than that in non-ligation group.CONCLUSION：The ligation of mesenteric lymph duct attenuates the ALI of rats.Mesenteric lymph might play an important role in the pathogenesis of ALI.     

Dexamethasone pretreatment attenuates reperfusion arrhythmia in rats

AIM: To investigate the effect of dexamethasone (DEX) preconditioning on reperfusion arrhythmia. METHODS: 46 Sprague-Dawley rats were divided randomly into DEX and control (CON) group, the rats were pretreated with DEX or sodium chloride before their hearts were separated for Langendorff perfusion and for ischemia/reperfusion. The reperfusion arrhythmias were observed dynamically after 60 min reperfusion following 30 min ischemia. The expression of HSP72 in myocardium was examined by Western blotting and immunohistochemistry at reperfusion 60 min. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and the activities of Na+-K+-ATP ase, Ca2+-Mg2+-ATPase on myocardial plasma membrane were detected. RESULTS: Compared with control group, the accumulated points and persistence time of ventricular arrhythmia were reduced significantly in DEX group (P<0.05), the expression of HSP72 was significant upregulated (P<0.05), the level of MDA was reduced significantly, the activities of SOD, CAT, GSH-Px and Na+-K+-ATPase were significantly higher (P<0.05). CONCLUSION: Dexamethasone pretreatment markedly reduces the reperfusion ventricular arrhythmias in rats, which may be attributed to upregulation of HSP72, SOD, CAT, GSH-Px , Na+-K+-ATPase and inhibition of lipid peroxidation.     

Effect of Auricularia auricular polysaccharide on ischemia myocardial injury

AIM: To investigate the protective effect of auricularia auricular polysaccharide (AAP) on the myocardial injury induced by ischemia and its underlying mechanism. METHODS: AAP was orally administrated to rats at the does of 50, 100 or 200 mg·kg-1·d-1 for 20 d. Myocardial injury was induced in anesthetized Sprague-Dawley rats by left anterior descending coronary artery ligation. Myocardial infarct size, the level of lactate dehydrogenase (LDH), the activity of superoxide dismutase (SOD), the production of lipid peroxidation malondialdehyde (MDA) and protein level of myocardial collagen of the heart were measured. RESULTS: The average myocardial infarct size in AAP groups was significantly smaller than that in ischemia group. The level of serum LDH induced by regional myocardial ischemia was significantly decreased in AAP group compared to ischemia group (P<0.01). AAP inhibited the production of MDA and increased the activity of SOD. Furthermore, AAP reduced the protein level of myocardial collagen after ischemia (P<0.01). CONCLUSION: AAP prevents myocardium from ischemia injury as an antioxidant.     

Impact of hydrogen sulfide donor on endothelin-1 and connective tissue growth factor expression in rats with pulmonary hypertension induced by high pulmonary blood flow

AIM: To explore the possible impact of hydrogen sulfide (H2S) donor-sodium hydrosulfide (NaHS) on endothelin-1 (ET-1) and connective tissue growth factor (CTGF) expressions in rats with pulmonary hypertension induced by high pulmonary blood flow. METHODS: Thirty-two male SD rats were randomly divided into 4 groups: shunt group, shunt+NaHS group, sham group and sham+NaHS group. Rats in shunt group and shunt+NaHS group were subjected to an abdominal aorta-inferior vena cava shunt to create an animal model of high pulmonary flow. After 11 weeks of experiment, rat systolic pulmonary artery pressure (SPAP), lung tissue H2S, plasma ET-1 concentration and lung tissue ET-1mRNA expression, as well as pulmonary artery CTGF protein expression were detected.RESULTS: After 11 weeks of experiment, SPAP, lung tissue ET-1mRNA, plasma ET-1 as well as pulmonary artery CTGF expressions were increased markedly, respectively, whereas H2S in lung tissue decreased significantly in rats of shunt group as compared with that in sham group (all P<0.05). After administration of NaHS for 11 weeks, H2S in lung tissue increased significantly, whereas SPAP, plasma ET-1 and lung tissue ET-1 mRNA expression as well as pulmonary artery CTGF protein expression decreased significantly, respectively, in rats of shunt+NaHS group as compared with that in shunt group (all P<0.05).CONCLUSION: NaHS might be involved in the development of pulmonary hypertension induced by high pulmonary blood flow by down-regulating vasoactive peptides ET-1 and CTGF expressions in lung tissues of rats.     

Effects of rhynchophylline on adriamycin-induced renal injury in rats

AIM: To explore the effects of rhynchophylline (RHL) on rat renal injury induced by adriamycin. METHODS: Fifty-two female SD rats were randomly divided into normal saline group (NSG, n=10), model group (MG, n=14), low-dose RHL treatment group (RHL-LG, n=14) and high-dose RHL treatment group (RHL-HG, n=14). The animals in the latter 3 groups were injected with adriamycin at a dose of 5 mg/kg through the tail vein. The animals in RHL-LG and RHL-HG were treated with RHL at doses of 5 mg/kg and 15 mg/kg, respectively, by intraperitoneal injection for 8 weeks. The animals in NSG and MG were treated with normal saline only. Urine and blood samples were collected to detect the urine protein, blood urea nitrogen (BUN) and serum creatinine (SCr). The renal tissues of the animals were collected for detection of malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, pathological changes and mRNA expression of angiotension Ⅱreceptors 1,2 (AT_1,2-R), angiotensin-converting enzyme (ACE) and angiotensinogen (AGT). RESULTS: The urine protein, BUN and SCr in RHL-LG were significantly lower than those in MG, but higher than those in RHL-HG (P<0.05). The SOD activity in MG was significantly lower than that in RHL-LG in the renal tissues. The SOD activity in RHL-LG was significantly lower than that in RHL-HG (P<0.05), but the content of MDA was on the contrary. The renal pathological damages in RHL-LG were weaker than that in MG, and that in RHL-HG were weaker than that in RHL-LG. The mRNA expression of AT₁-R, ACE and AGT in MG was significantly higher than that in RHL-LG in the renal tissues, and that in RHL-LG was higher than that in RHL-HG (P<0.05). The mRNA expression of AT₂-R in MG was significantly lower than that in RHL-LG, and that in RHL-LG was significantly lower than that in RHL-HG (P<0.05). CONCLUSION: RHL reduces adriamycin-induced renal injury in rats by attenuating the injury of lipid peroxidation in renal tissue, regulating the mRNA expression of AT_{1, 2}-R, ACE and AGT, and increasing renal blood flow.     

Effects of spermine on myocardial ischemia/ reperfusion injury in rats

AIM: To observe the effect of exogenous spermine (low concentration) on myocardial ischemia/reperfusion injury in rats.METHODS: 40 Wistar rats were randomly divided into 4 groups: sham- operation group (Sham), ischemic reperfusion group (I/R), spermine group (Sp) and natural saline group (NS). The model of ischemic/reperfusion injury was established by ligating rat coronary artery. In Sp group, spermine (0.5 mmol/L, 2 mL/kg) was injected slowly into rat vein. During the process, we recorded the electrocardiogram and the LV functional parameters, assayed the levels of SOD, LDH, NO and MDA in serum, and examined the ultrastructure of the myocardium. RESULTS: In I/R group, the incidence of arrhythmia was 90%, myocardial ultrastructure was injured seriously, values of LVSP and ±dp/dtmax decreased, levels of LDH, NO and MDA increased while SOD activity decreased (P<0.05 or P<0.01, compared with Sham group). Compared with I/R and NS group, all those indexes in Sp group changed significantly (P<0.05 or P<0.01). CONCLUSION: Exogenous spermine alleviates myocardial ischemia/ reperfusion injury in rats. The mechanism may be related to its antioxidant effect and relieving the injury caused by oxygen free radical.     

Effects of N-acetylcysteine combined with azithromycin on oxidative stress in rats with chronic obstructive pulmonary disease

AIM: To investigate the effects of N-acetylcysteine (NAC) combined with azithromycin (AZI) on oxidative stress in the rats with chronic obstructive pulmonary disease (COPD). METHODS: Male Wistar rats (n=60) were randomly divided into control group, model group, AZI intervention group,NAC intervention group and AZI+NAC group. The COPD model was established by passive smoking and intratracheal instillation of lipopolysaccharide. Each day 30 min prior to smoking, intragastric administration with AZI, NAC or combination of the 2 drugs was given for AZI, NAC, and AZI+NAC groups, respectively. On the 31st day, all rats were killed following lung function test. Cell counts of bronchoalveolar lavage fluid (BALF) were performed, and the contents of interleukin-8 (IL-8), interleukin-17 (IL-17) and tumor necrosis factor alpha (TNF-α) in BALF were measured by ELISA. The histopathology of the lung tissues was observed under light microscope, and the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in the lung homogenate were measured. RESULTS: Compared with control group, the other 4 groups showed decreased pulmonary function, and inflammatory cell infiltration and alveolar destruction in histopathology. Compared with control group, the other groups showed higher white blood cells, monocyte-macrophages, neutrophils and lymphocytes in the BALF (P<0.05). Compared with model group, AZI group and NAC group, lower white blood cells, neutrophils and lymphocytes in the BALF were observed in AZI+NAC group (P<0.05). Compared with model group, IL-8, IL-17, TNF-α and MDA in AZI group, NAC group and AZI+NAC group significantly decreased (P<0.05), while SOD and GSH-Px significantly increased (P<0.05). Compared with AZI or NAC group, IL-8, IL-17, TNF-α and MDA in AZI+NAC group significantly decreased (P<0.05), while SOD and GSH-Px increased significantly (P<0.05). CONCLUSION: Both NAC and AZI attenuate the lung inflammation and oxidative damage in COPD model rats. Combined medication exerts preferable anti-oxidation effects, which might be more suitable for the treatment of COPD.     

Effects of sodium hydrosulfide on cardiac function and activity of renin-angiotensin-aldosterone system in rats with chronic heart failure

AIM: To investigate the effect of sodium hydrosulfide (NaHS) on cardiac function and activity of renin-angiotensin (Ang)-aldosterone (ALD) system (RAAS) in the rats with chronic heart failure (CHF).METHODS: The CHF rat model was established by abdominal aortic coarctation. SD rats were randomly divided into sham operation group, model group, low dose of NaHS group and high dose of NaHS group (n=6). The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD) and left ventricular ejection fraction (LVEF) were measured before and after treatment by echocardiography in each group. The levels of renin, AngⅡ and ALD in the plasma were measured by ELISA. The expression of angiotensin-converting enzyme (ACE) and angiotensin Ⅱ type 1 receptor (AT1R) at mRNA and protein levels in the myocardium tissues was determined by qPCR and Western blot, respectively.RESULTS: After treatment with NaHS, compared with model group and before treatment, LVEDD and LVESD in low dose of NaHS group and high dose of NaHS group were decreased significantly, while LVEF was increased significantly (P<0.05). Compared with low dose of NaHS group, LVEDD and LVESD were decreased, while LVEF was increased in high dose of NaHS group (P<0.05). Compared with sham operation group, the levels of renin, AngⅡ and ALD in the plasma of model group were significantly increased (P<0.05), and the expression of ACE and AT1R at mRNA and protein levels in the myocardium tissues of model group were significantly increased (P<0.05). Compared with model group, the plasma levels of renin, AngⅡ and ALD in low dose of NaHS group and high dose of NaHS group were significantly decreased (P<0.05), and the myocardial expression of ACE and AT1R at mRNA and protein levels was significantly down-regulated (P<0.05). The plasma levels of renin, AngⅡ and ALD, and the myocardial expression of ACE and AT1R at mRNA and protein levels in high dose of NaHS group were significantly lower than those in low dose of NaHS group (P<0.05).CONCLUSION: NaHS inhibits the activation of RAAS, thus improving the cardiac function of CHF rats, and the effect of high-dose NaHS is better than that of low-dose NaHS.     

Antagonistic effect of bilirulin on acute lung injury induced by LPS in rats

AIM: To investigate the effect of bilirubin on acute lung injury (ALI) and the mechanism. METHODS: 30 male Wistar rats were divided into normal group, ALI group and bilirubin treatment group. Lung specimens were examined by histopathological technique. Lung index (LI) and lung permeability index (LPI) were measured. Moreover, white blood cell (WBC) count, neutrophil percentage (PMN%) and the content of protein (Pr) in the bronchoalveolar lavage fluid (BALF), as well as the contents of superoxide dismutase (SOD), malonaldehyde (MDA) and glutathione peroxidase (GSH-Px) in the lung homogenate were determined. RESULTS: (1) In ALI group: LI, WBC count, PMN%, Pr and LPI increased significantly compared with normal group (P<0.01). In bilirubin treatment group, all the values determined decreased compared with ALI group (P<0.01; P<0.05). No notable discrepancy between bilirubin treatment group and normal group (P>0.05) was observed. (2) In ALI group, the content of MDA was significantly higher (P<0.01), but the contents of SOD and GSH-Px were significantly lower than those in normal group (P<0.01). In bilirubin treatment group, the content of MDA decreased significantly (P<0.01) but the contents of SOD and GSH-Px increased significantly (P<0.01; P<0.05) compared with ALI group. No notable discrepancy between bilirubin treatment group and normal group was observed (P>0.05). CONCLUSION: Bilirubin relieves ALI induced by LPS in rats via antioxidation.     

香菇多糖对外周血肌酸激酶和尿素氮以及骨骼肌抗氧化能力影响

为探讨香菇多糖对大强度运动的大鼠外周血肌酸激酶、尿素氮及骨骼肌抗氧化能力的影响,筛选大鼠30只,分为安静组10只(A组)、运动组10只(B组)、运动给药组10只(C组)3组。运动给药组每天灌服香菇多糖剂量为30 mg·kg^-1d^-1,安静组、运动组按同样的方式给予同体积的蒸馏水。安静组不训练,运动组、运动给药组进行为期6周跑台练习,测定大鼠外周血肌酸激酶(CK)、尿素氮(BUN)含量,骨骼肌丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)测试盒、超氧化物歧化酶(SOD)活性。结果显示,运动组、运动给药组GSH-Px、SOD低于安静组(P<0.05),CK、BUN、MDA高于安静组(P<0.05);运动给药组CK、BUN、MDA低于运动组(P<0.05),GSH-Px、SOD高于运动组(P<0.05);表示香菇多糖能维持细胞正常生理功能运转,增加机体对运动负荷的承受力,提高骨骼肌组织抗氧化能力,具有抗疲劳功能。     

Effects of simvastatin on expression of Bcl-2 and Bax in myocardium of rats with renal ischemia-reperfusion injury

AIM: To observe the effect of simvastatin on myocardial tissue after renal ischemia-reperfusion injury and its mechanism. METHODS: A rat model of renal ischemia-reperfusion injury was prepared by clamping the bilateral renal arteries for 45 min. The rats (n=36) were randomly divided into sham operation group, renal ischemia-reperfusion (I/R) group and simvastatin group with 12 rats in each group. The content of serum creatinine (SCr), blood urea nitrogen (BUN) and myocardial tissue malondialdehyde (MDA), the myocardial activity of lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD), and the myocardial protein expression of Bcl-2 and Bax were detected. RESULTS: Compared with sham operation group, the content of SCr, BUN and myocardial MDA, and the myocardial activity of LDH and CK in I/R group were significantly increased (P<0.05), and the activity of SOD was significantly decreased (P<0.05). Compared with I/R group, the content of SCr, BUN and myocardial MDA, and the myocardial activity of LDH and CK in simvastatin group were significantly decreased (P<0.05), while SOD activity was enhanced (P<0.05). The protein expression of Bcl-2 and Bax in sham operation group was less than that in I/R group (P<0.05), and the protein level of Bax in simvastatin group was significantly lower than that in I/R group (P<0.05), while the protein level of Bcl-2 was increased (P<0.05). CONCLUSION: Simvastatin has a protective effect on the myocardium of the rats with renal ischemia-reperfusion injury, and the protective mechanism may be related to the elimination of free radicals by simvastatin, increase in the protein expression of Bcl-2 and decrease in the protein expression of Bax.     

Effect of glycine on cardiac injury induced by hypoxia-reoxygenation in isolated rat heart

AIM:To observe the effects of glycine on hypoxia-reoxygenation (H/R)-induced myocardial dysfunction, and to further clarify the protection of glycine (GLY) against myocardial ischemia/reperfusion injury and its mechanism. METHODS:A cardiac H/R model was established using a Langendorff isolated heart preparation. The left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), the maximum rising and dropping rates of left ventricular pressure (dp/dtmax and dp/dtmin) were observed. The coronary effluents at different time points were collected respectively to detect the concentration of superoxide dismutase (SOD) and malondialdehyde (MDA). RESULTS: The indexes of cardiac functions in H/R group were lower than those in other groups. After H/R, the indexes in GLY plus H/R group were higher than those in H/R group. Glycine inverted the effects of the decrease in SOD and the increase in MDA concentrations induced by H/R. CONCLUSION:Glycine ameliorates the cardiac functions under the condition of hypoxia-reoxygenation injury in isolated rat hearts. The mechanisms may be related to suppressing lipid peroxidation.     

Effects of bFGF on brain edema,nerve function injury and autophagy related protein in rats with traumatic brain injury

AIM:To study the effects of basic fibroblast growth factor (bFGF) on brain edema, nerve function damage and autophagy related proteins in rats with head injury. METHODS:The rat model of craniocerebral injury (CI) was constructed. The rats were divided into control group, CI group, and low-, middle-and high-dose bFGF groups (n=10). The CI model was established in CI group, while the rats in control group were not given epidural impact. The rats in low-dose, middle-dose and high-dose bFGF groups were given bFGF at 2, 4 and 6 μg, respectively, by intraperitoneal injection after 30 min. The neurological function in the rats was evaluated by improved neurological function scoring. The rat brain tissues were taken, and the water content was detected. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β in the brain tissue were measured by ELISA. The malondialdehyde (MDA) content was analyzed by thiobarbituric acid method. The activity of superoxide dismutase (SOD) was examined by WST-8 assay. The glutathine peroxidase (GSH-Px) activity was detected by colorimetric method. The protein levels of autophagy related proteins LC3-Ⅱ and beclin-1 in the brain tissues were determined by Western blot. RESULTS:The neurological function score was increased significantly of the rats in CI group. The rat model of craniocerebral injury was successfully constructed. Neurological function scores in the rats in low-dose, middle-dose and high-dose bFGF groups were reduced, the water content of the brain tissue was also reduced (P<0.05). The levels of TNF-α, IL-6 and IL-1 β were decreased in the brain tissues (P<0.05), the content of MDA was declined (P<0.05), the activities of SOD and GSH-Px were increased (P<0.05), the protein levels of LC3-Ⅱ and beclin-1 were decreased, compared with the untreated rats in CI group (P<0.05). CONCLUSION:bFGF improves the nerve function of the rats with craniocerebral injury, reduces the water content of the brain tissue, reduces the expression of autophagic protein LC3-Ⅱ and beclin-1.The mechanism is related to the inhibition of inflammatory reaction and oxidative damage.