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Objective To establish a method to analyze the composition and content of monoses in the garlic polysaccharide by ion chromatography. Methods The monoses in the solution of garlic polysaccharide hydrolysised by trifluoroacetic acid were determined by amino PAC column, eluted by gradient hydroxide sodium and identified by ampere detector (AU as working electrode, Ag/AgCl as reference electrode). Results The garlic polysaccharide was mainly composed by arabinose, galactose, glucose, xylose and fructose. Good resolution could be achieved among the above mentioned five kinds of monoses. Their linear correlations over the investigated concentration were above 0.998, while the average recovery rates were in the range of 95%-105%. Conclusion The ion chromatography method is fast, accurate, simple and reliable, and can be applied in the content determination and quality control of garlic polysaccharide.
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Objective To study the protective effects of garlic polysaecharide on L02 from oxidative injury.Methods Cultured L02 were injured by ethanol.Various concentrations of GP(10、20、40、80 mg/L) were added into culture medium.Then the cellular MDA,SOD,and GSH-Px were determined in order to observe the protection of curcumin and the time-dose-response effects.Meanwhile,HO-1 mRNA was detected by RT-PCR method after ethanol exposure.The expressions of HO- 1 proteins were detected by Western blotling.Results GP (10、20、40、80 mg/L) could reduce oxidative injury induced by ethanol in L02 cells.Liver cells were 100 mmol/L alcohol after 8h exposure,SOD[(3.65±0.42) NU/mg,(4.11±0.16) NU/mg,(4.61 ±0.23)NU/mg],GSH-Px [ (75.96 ± 8.96) mg/mg,(81.83±5.70) mg/mg,(89.32±6.35) mg/mg respectively],GSH-Px[(75.96±8.96),(81.83±5.70),(89.32±6.35) respectively]activity,MDA[(1.05±0.16) nmol/mg,(0.99± 0.12) nmol/mg; (0.78± 0.11) nmol/mg respectively]levels compared with the control group [ (2.35 ±0.28) NU/mg,(54.41 ±8.17) mg/mg,(1.58±0.23) nmol/mg respectively],there was a significant difference (P＜ 0.05 ); HO-1 mRNA expression was in a concentration- dependent effect.Conclusion GP had protective effects on L02 from oxidative injury probably by reducing GSH consumption,improving antioxidant enzyme activity and inhibiting lipid peroxidation reaction at dose-dependent manner.GP could promote expression of HO-1 mRNA co-coordinating role in protecting liver cells from oxidative injury.
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Aim: To study the inhibitory effects and its mechanisms of Garlic Polysaccharide (GP) on adriamycin(ADR)-induced cardiotoxicity in mice. Mehtod: ADR was injected intraperitoneally to induce myocardium injury model in mice. The activities of several serum and heart tissue enzymes were measured. With scanning electron microscope, the cardiac ultrastructural changes were examined. Results: ADR (3 mg· kg-1 ip, qod x 7) induced severe myocardial damages with the increasing activities of creatine kinase (CK), lactate dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT) and inducible nitric oxide synthase (iNOS) (P < 0.01). ADR increased myocardial malondialdehyde (MDA) content, while decreased the superoxide dismutase (SOD) activities (P < 0.01). It also caused mitochondrion edema at ultrastructural levels. GP (0.75-3.0 g·kg-1 ig, qd x 15) relieved these damages. GP decreased the activities of serum CK, LDH, GOT and iNOS. It also increased SOD activities and depressed MDA content in a dose-dependent manner. Especially, the extent of ADR-induced myocardial damage was markedly reduced by high dose of GP (P < 0.05 or P < 0.01). The changes of myocardial pathological and ultrastructural damages were improved by GP. Conclusion: These observations highlight the antioxidative property of GP and its cytoprotective action against ADR-induced cardiotoxity.
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Aim: To study the inhibitory effects and its mechanisms of Garlic Polysaccharide (GP) on adriamycin(ADR)-induced cardiotoxicity in mice. Mehtod: ADR was injected intraperitoneally to induce myocardium injury model in mice. The activities of several serum and heart tissue enzymes were measured. With scanning electron microscope, the cardiac ultrastructural changes were examined. Results: ADR (3 mg· kg-1 ip, qod x 7) induced severe myocardial damages with the increasing activities of creatine kinase (CK), lactate dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT) and inducible nitric oxide synthase (iNOS) (P < 0.01). ADR increased myocardial malondialdehyde (MDA) content, while decreased the superoxide dismutase (SOD) activities (P < 0.01). It also caused mitochondrion edema at ultrastructural levels. GP (0.75-3.0 g·kg-1 ig, qd x 15) relieved these damages. GP decreased the activities of serum CK, LDH, GOT and iNOS. It also increased SOD activities and depressed MDA content in a dose-dependent manner. Especially, the extent of ADR-induced myocardial damage was markedly reduced by high dose of GP (P < 0.05 or P < 0.01). The changes of myocardial pathological and ultrastructural damages were improved by GP. Conclusion: These observations highlight the antioxidative property of GP and its cytoprotective action against ADR-induced cardiotoxity.
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Aim To observe the protective effects and its mechanisms of Garlic Polysaccharide(GP) on toxic cardiac myocyte induced by adriamycin (ADR). Methods Primary culture neonatal SD rat cardiac myocyte and ADR injury model were established. The activities of several superior fluid and cells enzymes were measured. Using MTT assay and flow cytometry, the apoptotic cardiac myocyte was shown. Results ADR increased the superior fluid creatine kinase (CK), lactate dehydrogenase(LDH), glutamic oxaloacetic transaminase (GOT), and augmented myocardial malondialdehyde (MDA) content, while decreased the superoxide dismutase (SOD) activities (P
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Aim To study the inhibitory effects and its mechanis ms of Garlic Polysaccharide (GP) on adriamycin(ADR)-induced cardiotoxicity in mic e.Mehtod ADR was injected intraperitoneally to induce myocardiu m injury model in mice. The activities of several serum and heart tissue enzymes were measured. With scanning electron microscope, the cardiac ultrastructural c hanges were examined.Results ADR (3 mg?kg -1 ip, qod?7) induced severe myocardial damages with the increasing activities of creatine kin ase (CK), lactate dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT) a nd inducible nitric oxide synthase (iNOS) (P