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Objective To observe the effects of hedysari polysaccharide (HPS) on myocardial fibrosis and the expression of MMP-2/TIMP-2 in model mice of diabetic cardiomyopathy; To discuss the mechanism of action of prevention and treatment of myocardial fibrosis in diabetes.Methods Sixty mice were randomly divided into model group, rosiglitazone group and HPS high-, mediume- and low-dose groups. The normal group was 12 non-transgenic male BKS.Cg-Dock7m+/+Leprdb/JNjumice with the same age. Each group was given relevant medicine for gavage, for 8 weeks. Blood glucose of mice before and after medication 2, 4, 6, and 8 weeks was detected. The levels of MMP-2, MMP-2 and MMP-9 in myocardium were measured by Masson staining. The protein expressions of MMP-2 and TIMP-1 in myocardium were detected by Western blot.Results Compared with the model group, the blood glucose of HPS (high- and medium dose) groups and rosiglitazone group decreased significantly. Masson staining showed that the green fibers in the model group significantly increased and rosiglitazone group and HPS high-dose group decreased compared with the model group. Western blot showed that the expressions of MMP-2 in model group and MMP-2/TIMP-2 ratio were declined significantly, while the expression of MMP-2 was increased and TIMP-2 was decreased significantly, and the ratio of MMP-2/TIMP-2 increased in rosiglitazone group and HPS high- and medium-dose group.Conclusion HPS may reduce the degree of myocardial fibrosis in model mice with diabetic cardiomyopathy. The therapeutic effect of HPS may be to relieve myocardial fibrosis in model mice by increasing the ratio of MMP-2/TIMP-2.
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Objective To observe the effects of Hedysari Polysaccharide (HPS) on the expressions of TSP-1 and PDGF-B in the retina of diabetic rats;To discuss the protective effect and possible mechanism on diabetic retinopathy. Methods The diabetic model was established by intraperitoneal injection of streptozotocin. 50 male SPF Wistar rats were randomly divided into 5 groups:model group, calcium dobesilate group, and HPS high-, medium-, and low-dose group, extra 10 rats were set as the normal group, 10 rats in each group. Each administration group was given relevant medicine for gavage, while model group and normal control group were given same amount NS for gavage, once a day for 8 weeks. The mRNA and protein expression of TSP-1 and PDGF-B were detected by qRT-PCR and immunohistochemistry. The retinal structure was observed by HE staining. Results HE staining showed that each layer of the retina of the model group was clear and complete, but the outer nucleus layer became looser, thinner and more disorderly, and the number of ganglion cells decreased slightly; the administration groups were improved markedly compared with the model group. Compared with the normal control group, the mRNA level and protein expression of retina TSP-1 on the model group dramatically dropped (P<0.01), and those of PDGF-B strikingly increased (P<0.01);Compared with the model group, the mRNA level and protein expression of retina TSP-1 on alladministration groups rose (P<0.05, P<0.01), and those of PDGF-B went down (P<0.01); Compared with all other administration groups, there was statistical significance in the mRNA level and protein expression of retina TSP-1 and PDGF-B on HPS high-dose group (P<0.05, P<0.01). Conclusion HPS may prevent the angiogenesis and proliferation in diabetic retinopathy process through adjusting the content of TSP-1 and PDGF-B in retina of diabetic rats so as to protect the retina.
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OBJECTIVE: To isolate and purify radix hedysari polysaccharide 3 (HPS-3) and determine the monosaccharide composition and the contents of polysaccharide in its four components. METHODS: Radix Hedysari polysaccharide was extracted by water, precipitated with ethanol, treated with Sevag method, decolored with H2O2, then precipitated with ethanol and dialyzed. By using DEAE-cellulose 52 and Sephadex G-100, HPS-3-A, HPS-3-B, HPS-3-C and HPS-3-D were purified. Their purity were determined by high performance gel permeation chromatography (HPGPC). By TLC and GC, the monosaccharide composition of four components was analyzed, and then the modified phenol sulfuric acid method was used to determine the content of polysaccharide of the four fractions. RESULTS: HPS-3-A was composed mainly of glucose, and the content of polysaccharide was 99.2%. But HPS-3-B, HPS-3-C and HPS-3-D were all composed mainly of arabinose and galactose. The contents of polysaccharide of them were 96.5%, 95.3% and 95.2%, respectively. CONCLUSION: This study provides the foundation for the research of structure-function relationship of Radix Hedysari polysaccharide 3. Copyright 2012 by the Chinese Pharmaceutical Association.
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Hedysari polysaccharide (HPS) is the main component of hedysarum polybotrys. HPS can inhibit tumor cell proliferation, block the cell cycle in the G2-M period, modulate apoptosis via the mitochon drial pathway, and improve the red blood cell innate immunity and T lymphocyte immune function. HPS can relieve low immunity caused by chemotherapeutics.HPS plays anti-tumor effects by these ways mentioned above.
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AIM: To study effects and mechanisms of total hedysari polysaccharide(THPS)inducing apoptosis of S180 tumor. METHODS: 60 Kunming mice were divided into 5 groups randomly after inoculating S180 tumor.Sample group(S) and cyclophosphamide group(CY) were injected intraperitoneally with normal sodium and cyclophosphamide respectively.Low dose THPS group(H100),moderate dose THPS group(H200),and high dose THPS group(H400) were injected intraperitoneally with low,moderate,and high dose THPS respectively.The mice were killed after being treated for 14 days.Appearance of tumor was observed by electron microscope,and DNA,RNA,intracellular (Ca~(2+)),free radicals,mitochondrial membrane potential of tumor were determined by laser scanning confocal microscope. RESULTS: Moderate dose THPS raised intracellular Ca~(2+),free radicals and reduced mitochondrial membrane potential and DNA,RNA of tumor. CONCLUSION: Moderate dose THPS induces apoptosis of S180 tumor through raising intracellular Ca~(2+),free radicals and reducing mitochondrial membrane potential.