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1.
自由基清除剂对几种蔬菜衰老种子活力的影响 总被引：2，自引：0，他引：2
用外源自由基清除剂ＳＢＮ（１、２ｍｍｏｌ／Ｌ）和ＧＳＨ（０．００１、０．００５ｋｇ／Ｌ）浸种西瓜、甜瓜和萝卜衰老种子能显著促进其萌发,而ＡｓＡ（５、１０、１５ｍｍｏｌ／Ｌ）浸种效果不明显,上述处理要不同程度地提高衰老种子中ＣＡＴ和ＳＯＤ活性,降低Ｏ２＾－产生速率,减轻膜脂过氧化作用。 相似文献
2.
AIM: To study whether the excitatory amino acids (EAAs)-triggered excitotoxicity contribute to the evolution of hyperbilirubinemia-associated brain injury. METHODS: Newborn rabbits with hyperbilirubinemia were decapitated and then, Na+-K+-ATPase activities, neurotransmitters and non-neurotransmitters concentration in brains were determined. RESULTS: It was found that the activities of Na+-K+-ATPase both in brains and cytomembrane and the amounts of glutamate (P<0.05) and aspartate (P＜0.01) in homogenated brains decreased significantly. But the amounts of GABA and non-neurotransmitters increased in model group. CONCLUSION: Extracellular abnormal accumulation of EAAs caused by bilirubin-induced energy failure in brain and the inhibition in Na+-K+-ATPase activity may result in excitotoxic neuronal death in newborn rabbits. 相似文献
3.
AIM: To observe the effect of rapamycin (Rapa) on human neuroblastoma SH-SY5Y cell injury induced by oxygen-glucose deprivation (OGD), and to explore the role of autophagy in this process. METHODS: The SH-SY5Y cells were randomly divided into 4 groups:normal control group:the cells were cultured without OGD treatment; Rapa group:the cells were pretreated with Rapa for 1 h; OGD group:the culture medium was replaced by glucose-free medium and the cells were transferred to a humidified incubation chamber flushed by a gas mixture of 1% O2, 94% N2 and 5% CO2 for 12 h; Rapa+OGD group:the cultured cells were treated with Rapa for 1 h, and then were given the same treatments as those in OGD group. The cell viability was assessed by MTT assay. The degree of the cell damage was evaluated by determining the leakage of lactate dehydrogenase (LDH). The enzyme activity of caspase-3 was detected. TUNEL staining were used to detect the variation of cell apoptosis. The protein levels of apoptosis-related proteins Bax and Bcl-2, autophagy-related protein beclin-1 and autophagy marker protein LC3B were determined by Western blot. RESULTS: Compared with OGD group, the viability of the SH-SY5Y cells was significantly increased, and the activity of caspase-3 was significantly reduced in Rapa+OGD group (P<0.05). The SH-SY5Y cell injury was apparent after OGD with a great increase in the apoptotic rate (P<0.05). Compared with OGD group, the apoptotic rate significantly decreased in Rapa+OGD group (P<0.05). Compared with control group, the protein level of Bcl-2 was significantly decreased (P<0.05) and the protein level of Bax was significantly increased in OGD group. Compared with OGD group, the levels of Bcl-2, beclin-1 and LC3B-Ⅱ were significantly increased and the protein level of Bax was significantly increased in Rapa+OGD group (P<0.05). CONCLUSION: Rapamycin has a protective effect on in vitro cultured SH-SY5Y cells injured by OGD. The mechanism may be related to the promotion of autophagy. 相似文献
4.
AIM: To explore the pathophysiological bases in the pathogenesis of the lasting emotional behavioral disorders following posttraumatic stress disorder(PTSD). METHODS: 240 male Wistar rats were divided randomly into 3 groups. Group SE(n =96) for rats with PTSD-like behavior by constant pulsating current of 100 μA with intratrain frequencies of 16 Hz, pulsating duration of 1 ms, train duration of 10 s and interstimulus interval of 7 min for 5 days with 8 times per day. Group CE(n =96) for control with electrode implanted in hippocampus without stimulation, and Group NC(n =48) for normal control. The activities of Na+-K+-ATPase and Ca2+ -ATPase, levels of intracellular calcium and free calmodulin(CaM), and the total CaM expression were detected in hippocampi of experimental rats. RESULTS: The activities of Na+-K+-ATPase and Ca2+ -ATPase in mitochondria of hippocampal cells in Group SE rats were significantly decreased at 48 h and 72 h after the last stimulation, respectively. The intracellular free calcium levels were increased, and the mean channel fluorescence of intracellular free CaM decreased remarkably at 72 h poststimulation, while the expression of total CaM was significantly elevated at 48 h after the last stimulation in hippocampi of Group SE rats. CONCLUSION: The lasting increased levels of intracellular free calcium and expression of Ca2+ -CaM in hippocampus, as well as the dysfunction of Na+-K+ pump and Ca2+ -ATPase in mitochondria may play important roles in the long-term neuropsychological sequelae in PTSD. 相似文献
5.
AIM:To reveal the pathogenesis of salt-induced hypertension.METHODS:Forty male SD rats were divided into five groups, which received on same chow but different drink. Control(NC)group: deionized water; High salt(HS)group: 1.5% NaCl solution; L-arginine(HS+Arg)group: L-arginine(4 g·kg-1·d-1)in 1.5% NaCl solution; Enalapril (HS+En) group: enalapril (30 mg·kg-1·d-1) in 1.5% NaCl solution; Terazozin(HS+Ter)group: terazozin(4 mg·kg-1·d-1)in 1.5% NaCl solution. At the end of 8 weeks, rats were anesthetized with pentobarbital sodium. Blood pressure(BP)were recorded and blood were drawn from inferior vena cava and kidneys, adrenals were removed. NO(x),ET and AngII, Na＋-K＋-ATPase and proscillaridin-like compound(PLC)were assayed.RESULTS:BP, PLC and ET in plasma and AngII in adrenal were increased, NO(x)and AngII in plasma and kidney were decreased in HS group compared with NC group.CONCLUSION:High salt intake may induce hypertension in SD rats. In addition to the Na＋-K＋-ATPase activity was inhibited by increased sodium-pump inhibitors, NO release decrease may also play an important role in the pathogenesis of hypertension. 相似文献
6.
AIM:To screen the proteins interacting with human augmenter of liver regeneration (hALR) by yeast two-hybrid system and to study the mechanism of hALR action. METHODS:hALR bait plasmid was constructed by ligating the gene of hALR into pGBKT7, then transformed into yeast AH109. The yeast strain AH109 containing pGBKT7-hALR was mated with yeast Y187 containing human liver cDNA library plasmid. Diploid yeast was plated on SD/-trp-leu-his-ade (QDO) for screening and on QDO containing X-α-gal for further selection.The AD/library inserts were amplified by PCR and the PCR products were characterized by digesting with Sau3AⅠ and HaeⅢ restriction enzyme to eliminate the duplicates. After sequencing, the positive clones were analysed by bioinformatics. RESULTS:Several positive clones were obtaind. The sequencing and analysis shown that one of them is 669 bp DNA fragment encoding β subunit of Na+, K+-ATPase. The 224 bp 3'terminal DNA fragment is non-encoder region, and the 445 bp 5'terminal DNA encodes C-terminal 147 amino acid residues of Na+, K+-ATPase β subunit. CONCLUSION:The results of screening proteins using yeast two-hybrid system showed that hALR could interact directly with Na+, K+-ATPase in the yeast cell. 相似文献
7.
AIM: To study mechanism of hepatocytic mitochondria damage following septic shock. METHODS: 30 SD rats were randomly divided into three groups: sham operation group, 12 h cecal ligation and puncture (CLP) group and 16 h CLP group. The model of septic shock was made by cecal ligation and puncture. The liver mitochondria respiratory control rate (RCR), phosphate/oxygen (P/O) and ATPase activities were assayed. RESULTS: In 12 h CLP group mean artery pressure (MAP) [(9.54±1.26)kPa] was significantly lower than sham operation group [(14.58±1.32)kPa,P<0.05]. However, mortality was obviously higher than sham operation group (P<0.05), the liver mitochondria respiratory control rate (1.27±0.25), phosphate/oxygen (1.67±0.34) and Na+-K+-ATPase (40.80±3.45), Ca2+-ATPase (58.00±2.43), Mg2+-ATPase (78.30±4.16), Ca2+-Mg2+-ATPase(2.70±2.25) activities decreased strikingly. The difference between 12 h CLP group and sham operation group was significant (P<0.05), 16 h CLP groups was more lower than 12 h CLP group. As RCR, P/O and ATPase activities were significantly reduced, mortality significantly increased. Futhermore, obvious positive correlation was showed between them (r=0.892,P<0.01;r=0.834,P<0.01). CONCLUSION: Liver mitochondria function of ingestion-oxygen and phosphorus-acidification are decreased and membrane fluxion is weaken. Energy metabolism is blocked and Ca2+-Mg2+ shows imbalanced. All of them cause hepatocytic mitochondria injury following septic shock. 相似文献
8.
AIM To investigate the effect of Panax notoginseng saponins (PNS) on pyroptosis of SH-SY5Y cells induced by oxygen-glucose deprivation/reoxygenation (OGD/R). METHODS The OGD/R was conducted to induce ischemia/reperfusion injury in SH-SY5Y cells. The effects of PNS on the viability (detected by CCK-8 assay) and membrane permeability [indicated by lactate dehydrogenase (LDH) leakage and propidium iodide (PI) staining positive cell proportion] of OGD/R-induced SH-SY5Y cells were observed. The protein levels of gasdermin D (GSDMD), GSDMD N-terminal fragment (GSDMD-N), caspase-1 and caspase-4, and the release of interleukin-1β (IL-1β) and IL-18 in the cells were also determined. RESULTS After exposure to OGD/R, the viability of SH-SY5Y cells dramatically decreased (P <0.01), while the LDH leakage, the PI staining positive cell proportion, the protein levels of GSDMD, GSDMD-N, caspase-1 and caspase-4, and the release of IL-1β and IL-18 were significantly increased (P <0.01). However, PNS treatment enhanced the viability of SH-SY5Y cells inhibited by OGD/R (P <0.01), but reduced the leakage of LDH and the percentage of PI staining positive cells (P <0.05 or P <0.01). Moreover, PNS reversed the increases in the protein levels of GSDMD, GSDMD-N, caspase-1 and caspase-4 and the release of IL-1β and IL-18 in OGD/R-induced SH-SY5Y cells (P <0.05 or P <0.01). CONCLUSION Treatment with PNS alleviates OGD/R-induced injury in SH-SY5Y cells. Its mechanism may be related to inhibition of SH-SY5Y cell pyroptosis induced by OGD/R. 相似文献
9.
LI Xiu-juan SHEN Hui WEI Lin-yu WANG Guo-hong ZHANG Li-bing LI Chao-kun LI Xin-juan WANG Lu ZHAO Hong-gang SONG Jing-gui LI Dong-liang 《园艺学报》2017,33(9):1587-1592
AIM: To investigate the neuroprotective effect of progesterone against adenosine triphosphate (ATP)-injured human neuroblastoma SH-SY5Y cells.METHODS: The SH-SY5Y cells in the logarithmic phase were divided into different groups according to the progesterone and ATP concentrations. The cell viability was measured by CCK-8 assay. The membrane permeability was detected using fluorescent dye YO-PRO-1. Cytosolic Ca2+ concentration was measured with fluorescent dye Fluo-3/AM. The expression of purinergic P2X7 receptor was assessed by Western blot.RESULTS: The viability of the SH-SY5Y cells was significantly decreased (P<0.05) and YO-PRO-1 uptake was obviously increased (P<0.05) in a concentration-dependent manner compared with control group when SH-SY5Y cells were treated with ATP at 1, 3, 5 and 7 mmol/L for 2 h. The viability reduction of the SH-SY5Y cells induced by ATP was obviously counteracted by treatment with progesterone at 3, 10 and 30 nmol/L for 30 min (P<0.05) as compared with ATP group. YO-PRO-1 fluorescence enhancement induced by ATP in SH-SY5Y cells was significantly reduced (P<0.05) by progesterone (30 nmol/L) or P2X7 receptor antagonist KN-62 (500 nmol/L) pretreatment for 30 min, and no obvious difference between treatments with progesterone and KN-62 was observed. Cytosolic Ca2+ fluorescence intensity in normal group was a little, but that in ATP group was increased (P<0.05). Progesterone or KN-62 pretreatment significantly decreased the cytosolic fluorescence intensity of Ca2+ induced by ATP (P<0.05). However, no obvious difference between treatments with progesterone and KN-62 was found. The expression of P2X7 receptor in ATP group was significantly higher than that in control group (P<0.05), and progesterone inhibited ATP-induced P2X7 receptor expression (P<0.05).CONCLUSION: Progesterone inhibits P2X7 receptor expression, membrane pore formation, intracellular Ca2+ increase and cell death induced by ATP, so progesterone may protect SH-SY5Y cells against ATP-induced injuries. 相似文献
10.
AIM: To study the effects of adiponectin on H2O2-induced cell injury and tau hyperphosphorylation in human neuroblastoma SH-SY5Y cells. METHODS: Cell viability was determined by MTT assay. H2O2-induced cell injury and morphological changes in the SH-SY5Y cells with or without adiponectin treatment were observed. The level of tau phosphorylation as well as the activities of protein phosphatase 2A(PP2A) and of glycogen synthase kinase-3β(GSK-3β) were examined by Western blotting. RESULTS: Adiponectin significantly attenuated H2O2-induced cell injury(P<0.01). Adiponectin upregulated the activity of PP2A and decreased phosphorylation levels of tau under the stimulation with H2O2 (P<0.01). Okadaic acid, a specific inhibitor of PP2A, blocked the protective effects of adiponectin(P<0.01). Adiponectin increased the phosphorylation level of GSK-3β at Ser9 site under H2O2 stimulation(P<0.01). CONCLUSION: Adiponectin protects SH-SY5Y cells against H2O2-induced cell injury and decreases tau hyperphosphorylation by activating PP2A and inactivating GSK-3β. 相似文献
11.
AIM: To evaluate the protective effect of rapid phase of ischemic preconditioning against spinal cord ischemic injury in rabbits. METHODS: Thirty six male New Zealands white rabbits were randomly assigned to 3 groups (12 in each group): ischemia and reperfusion injury group (IR group), ischemic preconditioning + IR group (IPC+IR group) and sham operation group (sham). In IR group, spinal cord ischemia was induced by an infrarenal aorta clamping for 20 min; The rabbits in IPC+IR group underwent a 6 min ischemic preconditioning followed by 30 min of reperfusion before the 20 min clamping; The rabbits in sham group underwent the same procedures as the IR group except for infrarental aortic unclamping. Neurologic status was scored at 8, 12, 24 and 48 h after reperfusion. All animals were sacrificed at 48 h after reperfusion and the spinal cords (L5-7) were removed for histopathologic study and determination of the activity of Na+, K+-ATPase. RESULTS: The neurologic function scores in sham group and IPC+IR group at each observation interval were higher than those in IR group (P＜0.01). Compared to IR group, there were more normal neurons in anterior horn of spinal cord in sham group and IPC+IR group (P＜0.01); the activity of Na+, K+-ATPase in sham group and IPC+IR group were higher than those in IR group (P＜0.01). CONCLUSION: The rapid phase of ischemic preconditioning has a protective effect against spinal cord ischemic injury in rabbits, and this neuroprotection may be related to the maintenance of Na+, K+-ATPase activity. 相似文献
12.
OUYANG Jing-ping LIU Yong-ming ZHENG Han-qiao WEI Lei TU Shu-zhen YANG Hai-lu CUI Ye-jian 《园艺学报》2000,16(1):70-73
AIM: The effects of BDM on isolated rat heart in cold cardioplegia were studied. METHODS: Rat heart were subjected to cold cardioplegia at 4℃ for 8, 18 and 24 h.Then each heart was perfused (90 cm H2O) in Langendorff model at 37℃ for 40 min. In the high K+ group(n=24) the hearts were preserved in St.Thomas cardioplegic solution, in BDM group(n=24) hearts were preserved in K-H solution with BDM 30 mmoL/L. RESULTS: After 18 h, heart rate and the coronary flow in BDM group were significantly higher than in high K+ group(P＜0.05). Activity of Na+-K+-ATPase in cell membrane and in mitochondrial membrane in the BDM group was significantly higher than high K+ group(P＜0.01). After 24 h, all hearts in high K+ group were dead, but were alive in BDM group. CONCLUSION: Under given experiment conditions, BDM did enhance the tolerance to cold ischemia significantly. The results showed that BDM may become a useful agent for prolong the storage period of heart in cold cardioglegia. 相似文献
13.
LI Jian-sheng ZHAO Jun-mei GUO Sheng-dian ZHANG Wei-hong ZHAO Jing GAO Ai-she LI Jian-guo 《园艺学报》2001,17(11):1052-1055
AIM: To study the mechanism of brain ischemia-reperfusion injury from ATPase activity and free radical metabolism in aged rats. METHODS: The young rats (5 months) and the aged rats (more than 20 months) were divided into young control group(YCG), young model group(YMG), aged control group(ACG) and aged model group(AMG). The ATPase and SOD activities and the contents of MDA, Ca2＋, Na＋ and K＋ were measured in the rats with 30 min brain ischemia followed by 60 min reperfusion. RESULTS: The Ca2＋content in the AMG was higher than that in the YMG and the ACG. The Na＋-K＋-ATPase activity in the ACG was lower than that in the YCG,was lower in the AMG than that in the YMG. The Ca2＋-ATPase activities in the YCG was higher than that in the ACG, was lower in the AMG than that in the YMG and was higher than the ACG's. The serum and brain tissue SOD activities in the ACG was lower than that in the YCG, was lower in the AMG than YMG 's. The serum and brain tissue MDA/SOD ratio in the AMG was higher than that in the ACG.CONCLUSION:The brain tissue ischemia-reperfusion injury was related with calcium overload and free radical injury.The pathological changes were obvious and had some characteristics in the aged rats compared with the young rats because of the brain t issue aging changes in ATPase,calcium content and free radical metabolism in the aged rats. 相似文献
14.
AIM: Studying the mechanism of protective role of metallothionein(MT) in hypoxic preconditioning(HPC) of cultivated rat cardiomyocytes. METHODS:Using the model of hypoxia/reoxygenation of cultivated rat cardiomyocytes. Determining the contents of MT, malonyldialdehyde (MDA)-metabolism product of lipid peroxidation and the activities of Na+-K+ATPase, Ca2+-Mg2+ATPase of cardiomyocytes 24h after HPC, also determining the relevant changes after using MT antibody. RESULTS: After 24 h in HPC, the contents of MT and activities of Na+-K+ATPase, Ca2+-Mg2+ATPase were obviously higher than those in the control and hypoxia/reoxygenation(P＜0.05), and the contents of MDA were decreased remarkedly (P＜0.01). Then after using MT antibody, the activities of two enzyme were progressively decreased and the contents of MDA were significantly higher than those in the control and MT antibody-free groups(P＜0.01). CONCLUSION: HPC may induce excessive synthesis of MT, and MT can protect myocardial reoxygenation injury by eliminating lipid peroxidation and rising the activities of Na+-K+ATPase and Ca2+-Mg2+ATPase. 相似文献
15.
AIM: To investigate the role of zerumbone (ZER) in 1-methyl-4-phenylpyridinium (MPP+)-induced cytotoxicity of human neuroblastoma SH-SY5Y cells. METHODS: Human neuroblastoma SH-SY5Y cells were cultured in vitro and the protective effect of ZER against MPP+-induced cytotoxicity was measured by CCK-8 assay. Flow cytometry was used to determine the apoptosis and reactive oxygen species (ROS). The expression of Parkinson disease protein 7 (PARK7) was knocked-down by using PARK7-specific short hairpin RNA (shRNA). The protein levels of PARK7, nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were determined by Western blot. RESULTS: MMP+ remarkably reduced the cell viability in a dose-dependent and time-dependent manner. The SH-SY5Y cell injury model was established by treatment with MPP+ at 600 μmol/L for 24 h. ZER up-regulated the protein levels of PARK7 and Nrf2 (P<0.05), alleviated apoptosis (P<0.05), and reduced ROS production (P<0.05) in the SH-SY5Y cell injury model. Meanwhile, N-acetyl-L-cysteine (NAC) had the similar functions. Moreover, significant reductions in the protein levels of Nrf2 and HO-1 (P<0.05), and obvious increases in apoptosis (P<0.05) and ROS level (P<0.05) were demonstrated in PARK7-knockdown cells. CONCLUSION: ZER protects SH-SY5Y cells against MPP+-induced cytotoxi-city, which may be related to activation of PARK7/Nrf2/HO-1 pathway, and subsequent attenuation of oxidative stress and apoptosis. 相似文献
16.
AIM: To explore whether the damage of neurons induced by amyloid β-protein (Aβ) is related to the regulation of autophagy and its mechanism based on Akt/mTOR pathway. METHODS: SH-SY5Y cells were incubated with Aβ25-35 (5 μmol/L, 10 μmol/L, 15 μmol/L, 20 μmol/L and 25 μmol/L) for 24 h, and the cell viability was measured by MTT assay. The protein levels of LC3-I, LC3-II, Akt, p-Akt, mTOR and p-mTOR in the SH-SY5Y cells were determined by Western blot. After the SH-5Y5Y cells were incubated with autophagy inducer rapamycin (Rapa) or autophagy inhibitor 3-methyladenine (3-MA) combined with Aβ25-35 for 24 h, the cell viability and related protein expression were detected by the same methods above mentioned. RESULTS: Each concentration of Aβ25-35 damaged SH-SY5Y cells and decreased the viability of SH-SY5Y cells. Aβ25-35 increased the expression of autophagy marker protein LC3-II, increased the level of LC3-II/LC3-I, and down-regulated the phosphorylation level of Akt and mTOR proteins (P<0.05). When combined with autophagy inducer Rapa, the cell viability was not significantly affected, the expression of LC3-II protein was increased, LC3-II/LC3-I was increased significantly, and p-mTOR/mTOR level was decreased (P<0.05). When combined with autophagy inhibitor 3-MA, the protein expression of LC3-II and the level of LC3-II/LC3-I showed a downward trend, while the level of p-Akt/Akt was decreased (P<0.05). CONCLUSION: Aβ25-35 may induce SH-SY5Y cell autophagy and injury by down-regulating phosphorylation levels of Akt and mTOR proteins. 相似文献
17.
AIM: To investigate the effects of salidroside on intracellular free calcium concentration [Ca2+]i, apoptosis, mitochondrial membrane potential (MMP) and activity during injury induced by hypoxia/hypoglycemia in cultured SH-SY5Y cells. METHODS: Mitochondrial activity was measured by methylthiazolyl tetrazolium test. MMP,[Ca2+]i and apoptosis were measured by flow cytometry. RESULTS: SH-SY5Y cells were cultured in a hypoxia/hypoglycemia condition for 2, 4, 6 and 12 h,[Ca2+]i and apoptosis rate significantly increased compared with control group (P<0.01). After hypoxia /hypoglycemia cultures, MMP and mitochondrial activity declined 29.17% (P<0.01) and 38.80% (P<0.01) at 2 h, 56.72% (P<0.01) and 63.58% (P<0.01) at 12 h, were lower than that in control group (P<0.01). Salidroside significantly decreased [Ca2+]i and apoptosis rate, and increased MMP and mitochondrial activity in hypoxia /hypoglycemia-treated SH-SY5Y cells. CONCLUSIONS: Salidroside might inhibit the decline in MMP and mitochondrial activity induced by hypoxia /hypoglycemia, and has an inhibitory effects on neuronal apoptosis. The mechanism might be related to inhibiting intracellular calcium overload. 相似文献
18.
AIM:To evaluate the effects of different doses of valsartan alone or with concomitant be-nazepril on blood pressure,left ventricular hypertrophy,RAASfunction and endoxi nlevel in spontaneously hy-pertensive rats(SHR).METHODS:Thirty SHR(fourteen-week-old,male)were divi ded into five groups(six rats in each group):SHR control group:fed with normal saline;benazepril group:fed with 1 mg·kg-1·d-1benazepril);low dose valsartan group:fed with 8 mg·kg-1·d-1valsartan;high dose valsartan group:fed with 24 mg·kg-1·d-1valsartan;combination drug therapy group:fed with valsartan(8 mg·kg-1·d-1)and benazepril(1 mg·kg-1·d-1),all for 8 weeks.WKY control group(n=6):fed with normal saline for 8 weeks.RESULTS:SBP,LVM/BW,TDMof SHR were remarkably lower than those of control after drug i n-tervene,and effect on SBP was most remarkable in high dose valsartan group and i nthe combi nation drug ther-apy group;effect on LVM/BW,TDM were most remarkable in combination drug therapy group.Renin activi-ties in plasma and myocardiumwere remarkably i ncreased in drug i ntervene groups.The levels of AngⅡi nplasma and myocardiumwere remarkably increased in two different dose of valsartan treati ng group,and thelarger dose of valsartan were,the higher levels of AngⅡin plasma and myocardium were;decreased in be-nazepril treati ng group and combination drug therapy group.Na+-K+-ATPase activities in myocardi umwere remarkably i ncreased and the level of endoxi n i n myocardium were remarkably decreased as SBP de-creased after drug intervene.CONCLUSION:Different dose of valsartan alone or combi ned with benazeprilcan decrease SBP of SHR,have the effect of inhibiti ng progression of ventricular hypertrophy.The effect ofcombination drug therapy group was most remarkable among five groups and can avoi d the si de effect of highAngⅡin plasma and myocardiumduri ng long-termuse of valsartan alone. 相似文献
19.
JIAO Ya-nan YAO Ying-jia KONG Liang LI Shao-heng TAO Zhen-yu YAN Yu-hui YANG Jing-xian 《园艺学报》2015,31(11):2053-2058
AIM: To explore the protective effect of osthole on the SH-SY5Y cells transfected with APP595/596 gene, and to investigate the molecular mechanism. METHODS: The SH-SY5Y cells were transfected with APP595/596 gene in vitro for establishing a cell model to study the pathogenic role of amyloid β-protein (Aβ). The cell viability was detected by CCK-8 assay. The release of lactate dehydrogenase (LDH) was determined by the colour reaction of diaphorase-INT. The cell apoptotic rate was analyzed by flow cytometry. The expression of β-site APP cleaving enzyme 1(BACE1) at mRNA and protein levels was detected by RT-PCR and Western blot. The expression of Aβ was measured by the technique of immunofluorescence cytochemistry and Western blot. RESULTS: Treatment with osthole inhibited the LDH release, and increased the viability of the cells. The percentage of apoptotic cells was also significantly decreased. Osthole also inhibited the expression of BACE1 at mRNA and protein levels and the protein expression of Aβ. CONCLUSION: Osthole has protective effect on SH-SY5Y cells transfected with APP595/596 gene. The mechanism may be association with inhibiting the mRNA and protein expression of BACE1. 相似文献
20.
AIM: To observe the effect of Shenmai injection on the acute myocardial ischemia/ reperfusion injury in rats. METHODS: The left-anterior coronary artery was ligated for 10 minutes and then loosed for 15 minutes to establish the animal model of acute myocardial ischemia/reperfusion injury. During the process, electrocardiogram was traced continuously to observe the arrhythmia caused by reperfusion. The levels of SOD, MDA, Na+, K+-ATPase and Ca2+ -ATPase in ventricular myocardium were measured. The mitochondria was observed through electron microscope. RESULTS: Shenmai injection decreased the incidence of arrhythmia caused by reperfusion and shortened its duration. Shenmai injection improved the activity of SOD, Na+, K+-ATPase and Ca2+ -ATPase, decreased the content of MDA in myocardium and relieved the injury of mitochondria. CONCLUSION: Shenmai injection had a protective effect on acute myocardial ischemia/reperfusion injury in rats. The mechanism may be related to relieving the injury caused by oxygen free radical and calcium overload. 相似文献