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OBJECTIVE@#To reveal the neuroprotective effect and the underlying mechanisms of a mixture of the main components of Panax notoginseng saponins (TSPN) on cerebral ischemia-reperfusion injury and oxygen-glucose deprivation/reoxygenation (OGD/R) of cultured cortical neurons.@*METHODS@#The neuroprotective effect of TSPN was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, flow cytometry and live/dead cell assays. The morphology of dendrites was detected by immunofluorescence. Middle cerebral artery occlusion (MCAO) was developed in rats as a model of cerebral ischemia-reperfusion. The neuroprotective effect of TSPN was evaluated by neurological scoring, tail suspension test, 2,3,5-triphenyltetrazolium chloride (TTC) and Nissl stainings. Western blot analysis, immunohistochemistry and immunofluorescence were used to measure the changes in the Akt/mammalian target of rapamycin (mTOR) signaling pathway.@*RESULTS@#MTT showed that TSPN (50, 25 and 12.5 µ g/mL) protected cortical neurons after OGD/R treatment (P<0.01 or P<0.05). Flow cytometry and live/dead cell assays indicated that 25 µ g/mL TSPN decreased neuronal apoptosis (P<0.05), and immunofluorescence showed that 25 µ g/mL TSPN restored the dendritic morphology of damaged neurons (P<0.05). Moreover, 12.5 µ g/mL TSPN downregulated the expression of Beclin-1, Cleaved-caspase 3 and LC3B-II/LC3B-I, and upregulated the levels of phosphorylated (p)-Akt and p-mTOR (P<0.01 or P<0.05). In the MCAO model, 50 µ g/mL TSPN improved defective neurological behavior and reduced infarct volume (P<0.05). Moreover, the expression of Beclin-1 and LC3B in cerebral ischemic penumbra was downregulated after 50 µ g/mL TSPN treatment, whereas the p-mTOR level was upregulated (P<0.05 or P<0.01).@*CONCLUSION@#TSPN promoted neuronal survival and protected dendrite integrity after OGD/R and had a potential therapeutic effect by alleviating neurological deficits and reversing neuronal loss. TSPN promoted p-mTOR and inhibited Beclin-1 to alleviate ischemic damage, which may be the mechanism that underlies the neuroprotective activity of TSPN.
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Animals , Rats , Beclin-1 , Brain Ischemia/metabolism , Glucose , Infarction, Middle Cerebral Artery/drug therapy , Mammals/metabolism , Neuroprotection , Neuroprotective Agents/therapeutic use , Oxygen , Panax notoginseng , Proto-Oncogene Proteins c-akt/metabolism , Reperfusion Injury/metabolism , Saponins/therapeutic use , TOR Serine-Threonine Kinases/metabolismABSTRACT
Objective To explore the effect of the total saponins of panax notoginseng ( TSPN) on depression-like behavior following global cerebral ischemia depression in rats and its mechanism. Method-s Using four-vessel occlusion method to build the global cerebral ischemia model,then the cerebral ischemi-a rats were given solitary breeding with chronic unpredictable mild stress ( CUMS) to prepare depression model. Seventy rats were divided into sham group (n=10),model group ( n=20),PSD group ( n=20) and TSPN group (n=20). The rats in the TSPN group were administered TSPN intraperitoneally 30 min post-brain ischemia. The dose of TSPN (75mg/kg) was suspended in 0. 9% saline 10g/L,once per day for 30 days after reperfusion. While rats in the vehicle group and PSD group was treated with equal volume of 0. 9% saline,one injection per day until the rats were sacrificed at 30 days after brain ischemia. The BrdU,dou-blecortin (DCX) expression in the hippocampus was assessed by immunohistochemistry. Results In com-parison with the model group,the sucrose preference percentage in the PSD group was significantly lower ((46. 2±9. 2)%,(61. 2±7. 6)%;t=3. 18,P<0. 05),then the PSD rats were administered TSPN intraperito-neally,the sucrose preference percentage increased significantly ((62. 4±3. 4)%,(46. 2±9. 2)%;t=3. 43, P<0. 05). During the forced swimming test,the immobility time of PSD group was significantly increased compared with the model group ((119. 4±9. 7)s,(88. 0±15. 6)s ;t=4. 30,P<0. 01),while after PSD rats administering TSPN intraperitoneally,the immobility time was shorten remarkably ((97. 4±6. 7)s,(119. 4± 9. 7)s;t=3. 01,P<0. 05). Compared with the Model group( BrdU+:( 12. 6± 2. 2)/mm2,DCX+:( 38. 6± 4. 2)/mm2),the number of BrdU+ and DCX+ cells in the SGZ of hippocampus in PSD group decreased (BrdU+:(8. 8±1. 5)/mm2,DCX+:(27. 2±2. 8)/mm2;t=3. 25,4. 29,both P<0. 01). And compared with PSD group,the number of BrdU+ and DCX+ cells in the SGZ of hippocampus in TSPN group increased sig-nificantly (BrdU+:(14. 8±2. 8)/mm2,DCX+:(37. 0±3. 3)/mm2;t=4. 68,3. 69,both P<0. 05). Conclu-sion TSPN can improve the depression-like behavior of rats following global cerebral ischemia,which may be related with promoting hippocampal nerve regeneration.
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Objective: To explore the effect of the total saponins of Panax notoginseng (TSPN) on learning and memory of global cerebral ischemia rats and its mechanism. Methods: Using four-vessel occlusion method to establish the global cerebral ischemia model. Rats were divided into sham group, vehicle group, and TSPN group. The rats in the TSPN group were administered TSPN intraperitoneally 30 min post-brain ischemia. The dose of TSPN (75 mg/kg) was suspended in 0.9% saline 10 g/L, once per day for 14 d after reperfusion. Rats in the vehicle group were treated with equal volume of 0.9% saline, one injection per day for 14 d. The Morris Water Maze was performed to test the learning and memory of rats and doublecortin (DCX) and NeuN expression in the hippocampus was assessed by immunohistochemistry. Furthermore, immunoblotting was adopted to test the protein level of DCX in the CA1 subfield of hippocampus. Results: The escape latency in the vehicle group was longer than that in the TSPN group (P < 0.05). The times across the platform were less in the vehicle group than that in the TSPN group (P < 0.05). In comparison with the vehicle group, the number of the NeuN+ cells in the CA1 subfield and DCX+ cells in the SGZ of the TSPN group were significantly increased (P < 0.01); Moreover, the result of immunoblotting demonstrated that the protein level of DCX in the CA1 subfield of hippocampus of the TSPN group was significantly higher than that in the vehicle group (P < 0.01). Conclusion: TSPN could improve the learning and memory of global cerebral ischemia rats and its mechanism may be related to the promotion of hippocampus neurogenesis.
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Objective To investigate the degradation of three kinds of saponins (notoginseng saponin R1, ginsenoside Rg1, and ginsenoside Rb1) from total saponins of Panax notoginseng (tPNS) by intestinal flora in male and female rats in vitro. Methods tPNS were incubated for 24 h with male and female rats intestinal flora separately in vitro under anaerobic environment. The content of three kinds of saponins was measured at different treatment time. Results The results showed that the intestinal flora both in male and female rats all had the degradation action against ginsenosides Rb1, in which the degradation of male rats was slightly faster than that of female rats. But the intestinal flora both in male and female rats had no obvious degradation to notoginseng saponin R1 and ginsenoside Rg1. Conclusion Under the condition of in vitro, tPNS can be degraded by rats intestinal flora, of which Rb1 was degraded most, while notoginseng saponin R1 and ginsenoside Rg1 were more stable.
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Aim To investigate the therapeutic effects of total saponins of Panax notoginseng( PNS) on ather-osclerosis( AS) in ApoE knockout mice. Methods According to TC level, ApoE knockout mice were ran-domly assigned into six groups. Control group was fed with normal diet, and the other groups were fed with high-fat diet. After 16 weeks, mouse serum and aortas were harvested. The formation of atherosclerotic plaque was analyzed by oil red staining, the proportion of pathological lesion and the apoptosis of endothelial cells in left ventricular outflow tract were analyzed by HE staining and TUNEL. The serum level of lipids profiles, oxLDL-C were detected, and the mRNA ex-pressions of ICAM-1, VCAM-1, iNOS, eNOS, IL-1, IL-6 and TNF-α were detected by qPCR. Results In model group, the serum content of TC, LDL-C and HDL-C significantly increased(P<0.01); the area of atherosclerotic plaque significantly increased ( P <0.01) ; and the apoptosis of endothelial cells and the proportion of pathological lesion of left ventricular out- flow tract significantly increased(P<0.01). Also, the mRNA expression of ICAM-1, VCAM-1, iNOS, IL-1, IL-6 and TNF-α in model group increased. Compared with model group, the serum content of TC, LDL-C and HDL-C decreased after administration of PNS. The serum content of oxLDL-C was significantly reduced in PNS groups( P <0.01, P <0.05 ) . The apoptosis of endothelial cells significantly declined as well ( P <0.01, P <0.05 ) . The area of atherosclerotic plaque decreased after administration of PNS. The mRNA ex-pression of ICAM-1, VCAM-1, iNOS, IL-1, IL-6 and TNF-α in PNS groups were down-regulated. Conclu-sions In ApoE-KO mouse model, PNS plays a role in the therapy of AS, which may be due to its modulating lipid metabolism, protecting vascular endothelium, de-creasing inflammation and inhibiting adhesion of im-mune cells.
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Objective To explore the effect of the total saponins of Panax notoginseng (TSPN) on the expression of GFAP in hippocampus and brain water content in rats subjected global cerebral ischemia injury. Methods Using four-vessel occlusion method built the global cerebral ischemia model. Rats were divided into Sham group, vehicle group, and TSPN group. The rats in the TSPN group were administered TSPN intraperitoneally 30 min post-brain ischemia. The dose of TSPN (75 mg/kg) was suspended in 0.9% saline, once per day for days 1, 3, 7, and 14 after reperfusion. While rats in the vehicle group was treated with equal volume of 0.9% saline, one injection per day until the rats were sacrificed at either days 1, 3, 7, and 14 after brain ischemia. The brain water contentwas detected by dry-wet technique and GFAP expression in the dentate subgranular zone (SGZ) was assessed by immunohistochemistry. Moreover, immunofluorescence was applied to detect the GFAP/DCX in the SGZ, and western-blot was adopted to test the protein level of GFAP. Results The brain water content in the TSPN group was significantly lower than the vehicle group (P < 0.05); There was statistical difference in the GFAP+ cells density in SGZ at the 3th, 7th, 14th day in two groups (P < 0.05). Furthermore, compared with the vehicle group, the ratio of the GFAP/DCX to DCX in the SGZ at 7th, 14th d of TSPN group was significantly different (P < 0.05), and the protein level of GFAP on days 3, 7, 14 in the TSPN group was higher (P < 0.05). Conclusion TSPN could play a neuroprotective effect through promoting gliosis, neuroregeneration in the SGZ, and alleviating brain water content of rats following global cerebral ischemia.
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To investigate the protective effect of Panax notoginseng saponins combined with total flavonoids of epimedium on D-gal-induced senescence of H9c2 cells and explore its underlying mechanisms. The 50 mol•L⁻¹ D-gal was used to induce H9c2 cells senescence. Different concentrations of TPNS, TFE, and TPNS combined with TFE were used for 4 hours for pre-treatment. D-gal was used to stimulate H9c2 cardiac muscle cells for 24 h. Then in order to determine the best combined scheme, MTT was used to detect cell viability. Cell senescence was identified by β-galactosidase staining. Levels of reactive oxygen species(ROS) was observed by DCFH-DA detection. The changes of mitochondrial membrane potential were identified by JC-1 detection. Protein levels of silentmating type information regulation 2 Homolog-1(SIRT1), peroxisomal proliferator-activated receptor-coactivator 1α(PGC-1α) and silentmating type information regulation 2 Homolog-3(SIRT3) were detected by western blot analysis. The results showed that TPNS(5 mg•L⁻¹) combined with TFE(5 mg•L⁻¹) had significant synergistic effect on H9c2 myocardial cell proliferation(Q=1.154), so 5 mg•L-1TPNS combined with 5 mg•L⁻¹ TFE was determined as the best scheme. The quantity of β-galactosidase staining and the fluorescence intensity of ROS were apparently decreased in 5 mg•L⁻¹ TPNS combined with 5 mg•L⁻¹ TFE scheme. Meanwhile, it markedly increased the florescence intensity of mitochondrial membrane potential and enhanced the protein expression of SIRT1, PGC-1α and SIRT3. TPNS combined with TFE could protect H9c2 cells from D-gal-induced senescence. The mechanism might be related to adjusting the signal pathways of SIRT1/PGC-1α, SIRT3, adjusting the structure and function of mitochondria and reducing oxidative stress injury.
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Objective: To explore whether total saponins of Panax notoginseng (TSPN) can protect hippocampal CA1 subfield neurons against apoptosis following global cerebral ischemia via up-regulating the Bcl-2/Bax ratio and preventing Caspase-3 activation. Methods: Using four-vessel occlusion method to build the global cerebral ischemia model and the ischemia time was 30 min. All rats were divided into Sham group, vehicle group, and different doses (25, 50, 75, and 100 mg/kg) of TSPN groups. The rats in TSPN groups were ip administered with TSPN. The dose of TSPN was suspended in 0.9% saline (10 g/L), while rats in vehicle group were treated with equal volume of 0.9% saline, one injection per day. Compared the survival rate and hippocampal CA1 subfield neuronal density by Nissl staining after reperfusion of 14 d to make sure the best dose of TSPN for neuroprotection. Then to evaluate the neurological score and investigate the expression level of the Caspase-3, Bcl-2, and Bax in the hippocampus CA1 region at days 1, 3, 7, and 14 post-ischemia by immunohistochemistry; In addition, the Western-blotting was adopted to test the protein level of these three proteins. Results: The survival rate of the rats in 75 mg/kg TSPN groups was 100%, and its neuronal density was significantly higher than that in vehicle group and other doses of TSPN groups (P < 0.05); The neurological score in TSPN group was significantly less than that in vehicle group (P < 0.01); The Caspase-3 neuronal density in the CA1 subfield of TSPN group on days 7 and 14 was significantly less than that in vehicle group (P < 0.001); The statistical meaning existed about the protein level of Caspase-3 with molecular weight of 20 000 on days 3, 7, and 14 and 17 000 on days 7 and 14 in two groups (P < 0.001). The neuronal density of Bcl-2 cells in the CA1 subfield and Bcl-2 protein level in the hippocampus of TSPN group at days 7 and 14 was significantly higher than that in vehicle group (P < 0.001); Besides, the Bax neuronal density at days 7 and 14 was significantly lower than that in vehicle group (P < 0.001); And its protein level of the hippocampus was less than that in vehicle group at days 3, 7 and 14 (P < 0.001). The results of ratio of Bcl-2/Bax from not only the neuronal density but also the protein expression demonstrated that the Bcl-2/Bax ratio in TSPN group was significantly higher than that in vehicle groups on days 7 and 14 (P < 0.001). Conclusion: TSPN can protect the hippocampal CA1 subfield neurons against apoptosis following global cerebral ischemia in adult rats via up-regulating the Bcl-2/Bax ratio and preventing Caspase-3 activation.
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Objective: To explore the effect of total saponins of Panax notoginseng (TSPN) on the neuroregeneration in subventricle zone (SVZ) in rats with global cerebral ischemia. Methods: Using four-vessel occlusion method to build the global cerebral ischemia model. Rats were divided into Sham group, vehicle group, and TSPN group. The rats in TSPN group were ip administered with TSPN 30 min post-brain ischemia. The dose of TSPN (75 mg/kg) was suspended in 0.9% saline (10 g/L), once per day for 1, 3, 7, 14 days after reperfusion. While rats in the vehicle group were treated with equal volume of 0.9% saline, one injection per day until the rats were sacrificed at either 1, 3, 7, and 14 days after brain ischemia. The BrdU and Doublecortin (DCX) expression in SVZ was assessed by immunohistochemistry and applying the immunofluorescence double-labelling to detect the BrdU/DCX, DCX/Ki67, and GFAP/DCX in SVZ. Results: In comparison with the vehicle group, the number of BrdU+ cells in SVZ of TSPN group was significantly higher on days 7 and 14 (P < 0.01, 0.001); Statistical meaning existed in two groups on days 7 and 14 about the mean optical density of DCX+ cells in SVZ (P < 0.01, 0.001). In comparison with the vehicle group, the number of the BrdU-labeled cells co-expressing DCX in the SVZ on day 14t of TSPN group was significantly different (P < 0.01, 0.001). There was statistical meaning in comparison of the number of colocalization of DCX with Ki67 on days 7 and 14 in SVZ between the TSPN group and vehicle group (P < 0.01, 0.001). The ratio of GFAP/DCX to DCX in SVZ of two groups were statistically different on days 2, 7, and 14 (P < 0.05, 0.001). Conclusion: TSPN could promote the neuroregeneration, drive the proliferation and differentiation of neural progenitor cells, and enhance the differentiation of gliosis into newborn immature neurons in SVZ of rats with global cerebral ischemia.
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Objective: To investigate the effect of Xueshuantong Injection (lyophilized, main constituents are total saponins of Panax notoginseng with content of 95%) on the platelet function of rabbits with hyperlipemia. Methods: The model was made by giving the food with high fat to rabbits for 2 weeks, then Xueshuantong Injection (6.25, 12.50, and 25.00 mg/kg) was iv given once daily for 14 d and the function of platelet was tested after preparing serum and plasma by taking blood form carotid artery. Results: Xueshuantong Injection could reduce blood lipid levels, inhibit the platelet aggregation induced by ADP, AA, & COLL, and reduce the aggregation curve slope & the aggregation delay; lower the expression levels of VCAM-1, PF4, and P-selectin; prolong the APTT, and decrease the level of FIB. Conclusion: Xueshuantong injection (lyophilized) has the anti-aggregation function.
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To establish the uncertainty evaluation for the quantitative analysis on Xuesaitong Injection by near infrared (NIR) spectroscopy based on β-content tolerance interval (β-CTI). The data of NIR calibration and validation sets were obtained by " I × J × K" full factorial experimental design. The NIR quantification model was established through the PLS algorithm. Based on the validation data, the β-CTI was introduced to estimate the quantitative analysys on uncertainty of NIR, which was compared with the regular β-expectation tolerance interval (β-ETI). Among the seven designed concentration levels, the uncertainty values estimated by the β-ETI are smaller than that estimated by the β-CTI, except for the concentration level of 1.485 mg/mL. Then, the relationship between the relative expanded uncertainty (U) and corresponding concentration (Y) was fitted by lnU= a + b lnY model. When the uncertainty acceptance limit (λ) was set to 20% and the decision profile of uncertainty was plotted, the critical concentration for β-ETI and β-CTI with the acceptable uncertainty could be read as 4.867 and 5.686 mg/mL, respectively. This study has proved that β-CTI can be used to adequately estimate the uncertainty of quantitative analysis by NIR, which provides a new potential tool for the assessment of the accuracy and reliability of NIR spectroscopy.
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Objective:To study the preparation of total leaves saponins of panax notoginseng liposomal gels and evaluate the quali-ty. Methods:The total leaves saponins of panax notoginseng liposomes were prepared by the film-dispersion method, and the formula was optimized by the orthogonal experimental design. A high-speed centrifugation method was applied to determine the encapsulation efficiency used as the evaluation index for the optimization of the preparation process. Then the gels were prepared and an HPLC meth-od was used to determine the content of ginsenoside Rb3 . The stability was preliminarily studied as well. Results:The preparation was semi-solid, and viscous gels with low skin irritation and good stability. The quality was accordance with the relevant provisions in Chi-nese Pharmacopoeia (2010 edition). Conclusion: The gels are with the properties of simple preparation process, reliable detection methods and stable and controllable quality.
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Objective: To study the effects of Xueshuantong injection (lyophilized, main component of Panax Notoginsenosidum, total content of 95%) on platelet aggregation induced by adenosine diphosphate (ADP), arachidonic acid (AA), and platelet-activating factor (PAF) in rabbits. Methods: Using the Born method, the platelet aggregation induced by ADP, AA, and PAF was detected. Results: Compared with the control group, Xueshuantong injection (7.2 and 14.4 mg/mL) could significantly inhibit the platelet aggregation rate induced by ADP, AA, and PAF (P < 0.01), Xueshuantong injection (3.6 mg/mL) could significantly inhibit the platelet aggregation rate induced by ADP (P < 0.01). Conclusion: Xueshuantong injection could inhibit the in vitro platelet aggregation of rabbits.
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OBJECTIVE:To study the general pattern and characteristics of the ADRs associated with Saponins of panax notoginseng(SPN)injection to guide rational administration of this drug.METHODS:ADR cases induced by SPN injection that retrieved from domestic medical journals between 1994 and 2006 were analyzed statistically.RESULTS:Of the total 81 ADR cases induced by SPN injection,females showing higher percentage than males,and the ADRs were more often seen in aged group.The ADRs usually occurred following second time injection or repeated injections.The clinical manifestations of ADRs varied and could involve multiple organs and systems,which were characterized predominantly by damages of skin and its appendages.CONCLUSION:Doctors and pharmacists should master the pattern and characteristics of ADRs and strengthen ADR monitoring so as to reduce the incidence of ADRs.
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Objective To study the effects of total saponins of panax notoginseng on the proliferation of bone marrow strowal cells during differentiating into neuron-like Cells in vitro. Methods BMSCs were isolated from femur and tibia of rats and cultured in basal medium(Control),dimethylsulfoxide(DMSO) and butylated hydroxyanisole(BHA) in basal medium as induction group and containing PNS 100mg/L induction medium as PNS group. The morphological changes were observed under inverted microscope.The differentiated BMSCs were detected by immunohistochemistry,and the proliferation were evaluated by MTT assay.Results During induction differentiation,nestin was expressed by all BMSCs with ball-like shape and short process.The nestin expression of PNS group increased as compared with induction group(P
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Objective To investigate the effect of total saponins of panax notoginseng(PNS)on the production of collagen Ⅰ,Ⅲ and TGF-?1 in rats with experimental fibrosis.Methods Experimental fibrosis model was copied by intracutaneous injection of BSA and rats feeding on diet rich in lipid.From the 1st day after BSA injection,SPN(60 or 30 mg/kg)or Colchicine were given intracutaneously once a day for 42 days.All animals were sacrificed on the 43rd day.Their hepatic function was evaluated by determining the levels of ALT,AST,ALB in serum.The progression of hepatic fibrosis was confirmed by pathological analysis.Then type collagenⅠ,Ⅲ and TGF-?1 were observed with immunohistochemical method.Results The BSA injection significantly elevated the levels of ALT and AST,while SPN treatment significantly down-regulated them.But the level of ALB was opposite to that of ALT or AST in SPN treatment group.The positive staining of the collagenⅠ,Ⅲ and TGF-?1 was stronger in hepatic fibrosis model group than in SPN treatment group.The contents of the collagen were identical to the immunohistochemical results.Conclusion SPN has the protective effect against liver fibrosis.
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Aim To investigate the antagonistic action o f total saponins of panaxnotoginseng(PNS) on cardiac hypertrophy and its nervous mechanism.Methods (1)cardiac hypertrophy of rats due to pressure overload was induced by constricting of abdominal aorta. There were five groups in the experiments. The rats in Group A(control group)were sham operated . Group B was aorta-constricted group.The rats in Group C,D,E were given ip PNS 50,100,150 mg?kg?d -1 for three weeks respectively. Three weeks later, We measured the heart-weight(HW),left ventricular weight(LVW), the ratio of HW/BW,LVW/BW (LVI) and the cardiomyocyte diameters(MD) after dyeing by HE color.(2)The effects of PNS on the fast excitatory postsynaptic potential(f-EPSP),membrane depolarization induced by application of acetylcholine (ACh),membrane potential and membrane resistance of the isolated Stellate ganglion(SG)of the rats were investigated by means of intracellular recording techniques. Results (1)HW/BW, LVI and MD of Group E were significantly lower than that of Group B(P0.05).(2)At the concentration of 0.10 ～0.16 g?L -1, PNS reversibly depressed the amplitude of f-EPSP, but the ACh depolarization,membrane potential and membrane resistance were not significantly altered by PNS. Conclusion PNS can prevent cardiac hypertrophy due to pressure overload in rats and this action may underline its inhibitory action on presyn aptic effect of regulating calcium influx.
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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.
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OBJECTIVE: To investigate the effect of PNS on experimental atherosclerosis in rabbits, including the serum levels of TG, TC, LDL-C, level of MDA, activity of SOD and plaque area. METHODS: White Japanese rabbits were divided into normal control group, AS model group, low dose PNS group and high dose PNS group. Administration was for 12 consecutive weeks. The serum levels of TG, TC, LDL-C, MDA and activity of SOD were determined before experiment and at the end of the 12th week, respectively. RESULTS: The serum levels of TG, TC and LDL-C in AS model group were significantly higher than that in control group ( P
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Aim To study the relationship between theeffects of saponins of panax notoginseng(PNS)on fir-ing frequency and hyperpolarization potential in neu-rons.Methods Applieation of a depolarizing currentpulse to stellate ganglion(SG) neurons of rat evokedaction potentials(AP).These neurons were classifiedas phasic or tonic neurons on the basis of their firingpatterns.Then we investigated the effects of PNS on fir-ing pattern and frequency,after hyperpolarization po-tential(AHP) and fastexcitatory postsynaptic potential(f-EPSP) in high Ca2 +Krebs’solution of SG neuronsin rat.Results The firing frequency of tonic neuronswas reduced by PNS.At the concentration of0.12 ~0.16 g.L-1,PNS reversibly depressed AHP in a dosedependentmanner.And the aggrandizing action of highCa2 +on f-EPSP was antagonized by PNS.Conclusion PNS can reduce the firing frequency of rat SG neu-rons,but this action was not caused by reinforcement ofAHP potential.The restraining regulation of excitabili-ty of neurons by PNS may underlie its inhibitory actionon calcium influx.