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Objective To observe the antihypertensive effect of compound Yibazhen granules on spontaneous hypertensive rats ( SHR) . Methods Wistar rats were served as normal control group. Sixty SHR were randomly divided into model control group,captopril group,Jane chrysanthemum antihypertension tablet group and compound high dose group,middle dose group and low dose group ( n = 10 each group ) by digital table method. Captopril group was given captopril 30 mg.kg-1 .d-1 ,and Jane chrysanthemum antihypertension tablet group was treated with Jane chrysanthemum antihypertension tablet ( 0. 6 tablet per kg ) , compound Yibazhen granules high dose group, middle dose group and low dose group received compound of 13.18,6.59 and 3.3 mg.kg-1 .d-1 ,respectively. Normal control group and model control group were intragastrically administered with 0.9% sodium chloride solution for 8 weeks. Changes of systolic and diastolic blood pressure of rats and blood urea,creatinine,nitric oxide (NO),nitric oxide synthase (NOS) and angiotensin Ⅱ (Ang Ⅱ) were observed. Results Diastolic pressure of rats in compound Yibazhen granules high dose group, middle dose group and low dose group decreased significantly in 2 weeks. Systolic blood pressure and diastolic blood pressure of compound Yibazhen granules high dose group decreased significantly in 4 weeks,compared with the model control group (P<0.05). Compared with the model control group, concentration of urea and crea in compound Yibazhen granules high dose group, middle dose group and low dose group were significantly lower( P<0.05) . The content of NOS and AngⅡ in rats of compound Yibazhen granules high dose group decreased significantly and the contents of NO increased, which were compared with the model control group ( P<0. 05, P<0. 01 ) . Conclusion The protective effect of compound Yibazhen granules in treating early renal damage in SHR is related to decreasing diastolic blood pressure,concentration of urea,crea and AngⅡ and regulating the levels of NOS and NO.
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Objective To explore the effect of total flavonoids of astragalus (TFA) on the apoptosis of endothelial cells induced by serum of uremia patient .Methods The serum of 22 healthy volunteers and 25 uremia patients receiving regularly hemodialysis were enrolled in the study .HUVECs were used as research objects ,which were divided into control group(adding serum of healthy people when cell synchronized) and uremia group (adding serum of uremia patient when cell synchronized ) .Low dose ,moderate dose and high dose group were prepared by adding 0 .5 ,1 .0 ,2 .0 mg/mL TFA respectively 6 h before cell synchronization .After 24 hours′culture since the serum were added ,the morphological change of endothelial cells were observed by microscopy ,proliferation activities were tested by using MTT ,SOD activities were tested by using xanthine oxidase method ,NO levels were measured by u-sing nitrate reductase colorimetric method ,DNA damage was detected by using comet assay ,the morphological change of apoptosis was observed by using TUNEL method .Results Compared with the control group ,the proliferation activity ,SOD activity ,NO lev-els were lower in uremia group(P< 0 .01) ,DNA tailing rate ,apoptosis index(AI) significantly increased (P<0 .01) .Compared with cells of uremia group ,cell proliferation activity of all the TFA intervention groups increased (P<0 .05) ,NO levels also in-creased (P<0 .01) .Compared with uremia group ,moderate and high dose group′s SOD activity increased (P<0 .05) ,DNA damage tailing rate decreased (P<0 .05) .Conclusion Total flavonoids of astragalus reduces apoptosis of HUVECs induced by serum of uremia patient ,the possible mechanism is associated with the decrease of oxidative stress .
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Objective To study in vitro the inhibitory effects and mechanisms of N-butanol extract of Potentilla anserine L.(NP)against hypoxia-induced nitric oxide(NO)in hippocampus neuron of rats. Methods The models of hippocampus neurons hypoxia injury of Sprague-Dawley(SD)neonatal rats were cultured in vitro. The cultured hippocampus neurons were divided randomly into blank control group, hypoxia injury model group, nimodipine group(2 μmol/L)and NP high(250.0 mg/L),middle(62.5 mg/L),low(15.6 mg/L)dose groups. The activities of hippocampus neurons were examined by methyl thiazolyl tetrazolium(MTT)assay,and meanwhile their contents of nitrogen monoxidum(NO)were detected. Half quantity reverse transcription-polymerase chain reaction(RT-PCR)and Western blotting were used to detect neuronal nitric oxide synthetase(nNOS)mRNA and protein expression levels respectively in each group,immunocytochemistry stain was used to detect protein positive rate. Results Compared with blank control group,the activity of neuron〔absorbance(A)value〕was significantly decreased(0.0826±0.0095 vs. 0.3315±0.0105),content of NO(μmol/g:0.0509±0.0027 vs. 0.0291±0.0032), the expression levels of nNOS mRNA (0.1463±0.0081 vs. 0.0801±0.0058), the positive rate of nNOS〔(74.4238±3.9423)%vs.(28.3714±4.1361)%〕,the expression levels of nNOS protein(A value:1.9130±0.0471 vs. 0.5068±0.0368)were all significantly increased in the hypoxia injury model group(all P0.05). Conclusions NP can ameliorate the injury of rat hippocampus neurons induced by hypoxia in vitro. The possible mechanisms might be related to the effective inhibition of the synthesis of nNOS and NO excessive generation.
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Objective To investigate the effect of sodium ozagrel injection on hemorheology, endothelin (ET) and nitrogen monoxidum (NO) of patients with non-ST segment elevation myocardial infarction (NSEMI). Methods A total of 81 NSEMI patients were divided randomly into two groups: control group and experimental group. Isosorbide mononitrate, low molecular heparin and simvastatin were administered in the control group while sodium ozagrel was added to the experimental group apart from the above-mentioned drugs. The clinical effect of sodium ozagrel was observed. The changes in the indexes of hemorheology, ET and NO were analyzed. Results The clinical effect was significantly better in the experimental group than in the control group (P<0.05). The level of ET was obviously lower after treatment than that in the experimental group and the control group before treatment (P<0.05). The level of NO was obviously higher after treatment than that in the experimental group and the control group before treatment (P<0.05). The changes of ET and NO in the experimental group post-treatment were more significant than those in the control group after-treatment (P<0.05). The level of hemorheology index after treatment was lower than that before treatment in the experimental group (P<0.05). High-shear rate of whole blood viscosity, platelet adherence rate, and fibrin as hemorheology indexes were lower after-treatment than those pretherapy in the control group (P<0.05). Conclusion Sodium ozagrel injection could affect hemorheology,ET and NO of patients with non-ST segment elevation myocardial infarction. Thefore, the therapeutic efficacy can be better if sodium ozagrel is added to the conventional therapy.
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Abdominal aortic aneurysm is one kind of common disease in clinic. For the disruption and followed high mortality, it has already caused people's deep concern. For the past few years, nitricoxide syn-thase has played an important role in the processes and development of abdominal aortic aneurysm. This arti-cle gave an overview of the subject.
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OBJECTIVE:To study the pharmacological action and mechanism of Cynanchum auriculatum(CYA)on the gastrointestinal tract.METHODS:Using atropine sulfate to inhibit mice's intestinal propulsive activity and the effect of CYA on the intestinal propulsive activity of mice was observed.Using clipping tail stimulation method to induce functional dyspepsia model in rats and the effect of CYA on nitrogen monoxidum(NO)level in gastric mucous membrane of the model rats was observed.Using cold and bitter rhubarb lax method to induce rat spleen-deficiency diarrhea model and the effect of CYA on levels of gastrin(GAS)and motilin(MTL)in the model rats was observed.RESULTS:CYA can apparently increase the intestinal propulsive activity of mice,markedly decrease the level of NO in gastric mucous membrane of functional dyspepsia model rats,and markedly increase levels of GAS in serum and MTL in plasma of spleen-deficiency diarrhea model rats.CONCLUSION:CYA can improve intestinal propulsive activity,which might be attributed to the decreased NO level in gastric mucous membrane and the elevated levels of GAS in serum and MTL in plasma.
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Expression of endogenous ouabain in placenta and the concentrations of serum ET-1 and NO were examined in 30 patients with hypertensive disorder complicating pregnancy (HDCP) and 30 healthy pregnant women to investigate the effect of endogenous ouabain on HDCP. Compared with the healthy pregnant group, the expression of endogenous ouabain dramatically increased in the HDCP groups (P<0.01). There was a significantly positive correlation between the expression of en- dogenous ouabain with ET-1 (r=0.5567, P<0.01), while the correlation of endogenous ouabain and NO was significantly negative (r=-0.6895, P<0.01). As expected, the correlation between ET-1 and NO was negative (r=-0.7796, P<0.01). ET-1 concentrations of maternal and cord sera in HDCP groups were significantly higher in comparison with healthy pregnant group (P<0.01). On the con- trast, NO concentrations were much lower in the maternal and cord sera of HDCP groups as com- pared with healthy pregnant group (P<0.01). Our data suggest that endogenous ouabain is directly involved in the nosogenesis of HDCP, with accompanying decreased NO and the elevated of ET-1.
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6.66 kPa),30 cases of light degree pulmonary artery hypertension group (3.99 kPa
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Aim To observe the influences of ginsenoside Rg1 on the spontaneous contraction of small intestine smooth muscle of rabbits in vitro and explore the mechanism.Methods With the isothermal perfusion of small intestine in vitro,the influences of ginsenoside Rg1 on the spontaneous contraction of small intestine was observed and the mechanism of ginsenoside Rg1 was studied.Results Ginsenoside Rg1 reduced the amplitude of contraction of small intestine smooth muscle in rabbits in a dose-depended manner.Bay K8644 and nitro-L-arginine methylester(L-NAME)could completely block the inhibition of ginsenoside Rg1 on the contraction of small intestine smooth muscle.Ginsenoside Rg1 inhibited the intracellular calcium-depended contraction induced by rynodine in the Ca2+ free Tyrode's solution.Conclusions Ginsenoside Rg1 inhibits the contraction of small intestine smooth muscle of rabbits in vitro.The mechanism may be related to increase NO concentration in small intestine smooth muscle so that it inhibits extracellular Ca2+ inflowing via cell membrane and intracellular Ca2+ releasing via sarcoplasmic reticulum.
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AIM: To research the protective effects of crocetin on cerebral ischemia-reperfusion(CIR) injury in mice.METHODS: The effects of crocetin on brain edema,brain capillary permeability,the activities of lactate dehydrogenase(LDH),superoxide dismutase(SOD),glutathione peroxidase(GSH-Px) in brains and the contents of malondialdehyde(MDA) and nitric oxide(NO) in CIR model mice were observed.RESULTS: Compared with the CIR group,crocetin(50,100 mg/kg i.g.for 5 d) decreased the content of water,Evans blue,MDA and NO in mice brain tissue,and increased LDH、SOD and GSH-Px activity in brains of CIR mice,with statistical significance.CONCLUSION: Crocetin has protective effects on cerebral ischemia-reperfusion injury in mice,the mechanism may be related to its anti-oxidative activity and inhibition of NO overproduction.
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OBJECTIVE:To investigate the effect of the active site F 022 of Radix Isatidix antiendotoxin on the LPS-stimulated release of inflammatory cell factors in monocytes of mice.METHODS:Monocytes samples taken from the abdominal cavities of BALB/C mice were divided into6groups,the trial group were divided into1%,0.5%,0.25%and0.125%4groups,which added with Radix Isatidis F 022 sample solution and LPS solution;The positive group were treated with LPS solution;The negative group were added with1%F 022 solution.Thereafter the levels of TNF-?,IL-6and NO of the3kinds of inflammatory cell factors cultured in the clear supernatant liquid were determined.RESULTS:LPS could stimulate monocytes of mice to excessively release inflammatory cell factors including TNF-?,IL-6and NO.Compared with the positive group,the levels of inflammatory cell factors in the trial group reduced and which was dose dependent.CONCLU-SION:The active site F 022 of Radix Isatidix antiendotoxin has inhibitory action on LPS-stimulated excessive release of in-flammatory cell factors of in monocytes of mice.
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Objective To investigate the protective effects of felodipine on mRNA levels of endothelial nitricoxide synthase (eNOS) and inducible nitricoxide synthase (iNOS) as well as the level of nitrogen monoxidum (NO) from human umbilical vein endothelial cells (HUVECs) injuryed by oxidized low density lipoprotein (ox-LDL). Methods Isolated HUVECs were divided into blank control group,ox-LDL injury group treated with ox-LDL of different concentrations (6,12.5 and 25 mg/L),and intervention group of felodipine (0.1,1.0 and 10 ?mol/L)+ox-LDL (25 mg/L). Then eNOS and iNOS expressions were measured by real time-polymerase chain reaction and the level of NO in the supernatants of the cultures was assayed by nitrate reductase method. Results The mRNA expressions of eNOS and iNOS in HUVECs and NO level in the supernatants during treatment with different ox-LDL concentrations were higher than those in control group. However,felodipine significantly down-regulated the expression of iNOS in HUVECs injured by ox-LDL and inceased NO generation. Conclusion Felodipine has protective effects on endothelial cells. The mechanism may be related to its lowering the mRNA expression of iNOS induced by low ox-LDL concentration and increasing NO production.