Effect Of Polysaccharide Peptide Research Articles

Potent protective effects of polysaccharide peptide on vascular endothelium and cardiac remodelling in post myocardial infarction patients: A prospective double-blind randomized controlled trial

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Indonesia"s Ministry of Research and Technology/National Research and Innovation Agency grants Background Inflammation and oxidative stress contribute to endothelial dysfunction leading to progression of atherosclerosis and myocardial infarction (MI). Purpose To evaluate the effect of polysaccharide peptide of Ganoderma lucidum mycelium extracts (β-1,3/1,6-D-Glucan) as protective vascular endothelium and cardiac reverse remodelling in post MI. Methods This is a prospective, randomized double-blind clinical trial in 45 post MI patients. Treated group (TG) was given 3 divided dose of 540 mg β-1,3/1,6-D-Glucan daily for 90 days, and control group (CG) received placebo. Variable measured were EPC,CEC,IL-1,IL-6,TNF-α,hsCRP,NO,SOD,MDA and echocardiography parameters. Results β-1,3/1,6-D-Glucan administration significantly increased EPCs (P = 0.000), but not significantly reduced CECs (P = 0.069). Significant suppression was found in IL-1, IL-6 and TNF-α (all P < 0.05), but not in hsCRP (P = 0.064). TG exhibited significant elevation of NO (P = 0.02) and SOD (P = 0.023), and reduction of MDA (P = 0.001). TG revealed significant improvement of LVEF, LVMI, LVIDd, RWT, RWMA and LV diastolic dysfunction (all P < 0.05); but not in FS and TAPSE (P = 0.24, P = 0.20; respectively). Conclusions Polysaccharide peptide exhibits potent protective vascular endothelium and cardiac reverse remodelling in post MI patients, hence promising as add-on medication on top of standard medical regiment. Result comparison between study groupsVariableMeanPretestMean Difference Post-testP valuePolysaccharide peptide (β-1,3/1,6-D-Glucan)PlaceboVascular Endothelium BiomarkersCECsEPCs87.99 ± 76.7398.32 ± 44.52-48.01 ± 64.0714.90 ± 24.05-13.84 ± 58.67-17.65 ± 27.870.0690.000Oxidative Stress MarkersSODMDANitric Oxide2.93 ± 0.5419.68 ± 9.9737.98 ± 14.440.26 ± 0.74-5.52 ± 10.756.04 ± 9.27-0.23 ± 0.685.75 ± 10.29-0.62 ± 3.300.0230.0010.02Proinflammatory BiomarkershsCRPTNF-αIL-1IL-62512.90 ± 1332.11348.58 ± 85.0392.14 ± 29.62259.40 ± 125.52-6.78 ± 1099.60-44.98 ± 100.94-15.77 ± 27.06-29.63 ± 104.30-1.42 ± 795.35-1.34 ± 104.893.42 ± 33.1475.77 ± 130.830.0640.0060.0420.005Echocardiographic ParametersLVEFFSLVMITAPSELVIDdRWT57.20 ± 11.3930.85 ± 7.07114.07 ± 59.612.14 ± 0.354.86 ± 0.820.54 ± 0.352.30 ± 9.770.73 ± 7.59-4.55 ± 14.460.99 ± 0.49-0.49 ± 0.45-0.14 ± 0.29-2.08 ± 3.353.74 ± 9.2711.48 ± 23.94-0.17 ± 0.340.23 ± 0.430.03 ± 0.040.0080.2480.0430.2020.0000.017Abstract Figure. Comparison among pre- and post-treatment

Polysaccharide Peptide: A promising Anti Inflammation and Anti Oxidant in Atherosclerosis

Background : Heart disease is the leading cause of death for both men and women, but heart disease is preventable and controllable. Ganoderma lucidum is widely used as traditional medicine for centuries particularly in China, Japan, and Korea. Previous study showed antioxidative activity of polysaccharide peptide (PsP) from Genoderma lucidum.Objective : This study was aimed to evaluate anti-inflammatory and antioxidant effect of polysaccharide peptide (PsP) from Ganoderma lucidum in atherosclerotic rats.Methods : The atherosclerotic rats were randomly divided into four groups (5 rats each group) : atherosclerotic model with high-fat diet, low dose PsP treated group (50 mg/kgBW), medium dose PsP treated group (150 mg/kgBW), high dose PsP treated group (300 mg/kgBW), with normal mice used as a control group. Parameters measured were the level of MDA, SOD, IL - 6 , IL - 10, hsCRP, TNF - ?, lipid profile and foam cell.Results : After PsP therapy for 5 weeks, the levels of MDA (p=0.01), hsCRP (p=0.018) in rats model of atherosclerosis decrease significantly. PsSP can reduce levels of IL - 6 (p=0.933) and increase levels of SOD (p=0.28) descriptively at PsP doses 150 mg/kgBW. While the levels of TNF-? (p=0.894) and IL-10 (p=0.98) was not affected by administration of PsP. PsP improve the lipid profile by increasing HDL (p=0.002) and lowering total cholesterol (p=0.04). The formation of foam cells (p=0.024) as a marker of atherogenesis significantly decreased by administration of PsP .Conclusion : PSP can be useful to reduce inflammatory processes and oxidative stress to prevent the process of atherogenesis.

Effects of polysaccharide peptides from COV-1 strain of Coriolus versicolor on glutathione and glutathione-related enzymes in the mouse

The effects of polysaccharide peptide (PSP), an immunomodulator isolated from Coriolus versicolor COV-1, on glutathione (GSH) and GSH-related enzymes was investigated in C57 mouse. Administration of PSP (1–4 μmole/kg, i.p.) produced a transient, dose-dependent depletion (10–37%) of hepatic GSH, with no effect on serum glutamic–pyruvic transaminase (SGPT) activity. Blood GSH was depleted (6–25%) at 3 h, followed by a rebound increase above the control GSH level (20%) at 18 h. The GSSG/GSH ratio, a measure of oxidative stress, was increased 3 h after PSP treatment but returned to normal levels at 24 h. Sub-chronic treatment of PSP (1–4 μmole/kg/day, i.p.) for seven days did not produce any significant changes in hepatic GSH levels and the GSSG/GSH ratio when measured 24 h after the final dose of PSP. PSP had little effect on glutathione transferase (GST), glutathione reductase (GSSG reductase) and glutathione peroxidase (GPX) activities in the liver. However, a dose-dependent increase in blood GPX activity (30–48%) was observed at 3 h, which coincided with the increase in the GSSG/GSH ratio. The increase in blood GPX activity may be a responsive measure to deal with the transient oxidative stress induced by PSP treatment. The results showed that PSP only caused a transient perturbation on hepatic glutathione without affecting the GSH-related enzymes such as GST, GSSG reductase and GPX. The observed changes in blood GSH simply reflected the intra-organ translocation of glutathione, as the glutathione-related enzymes were not significantly affected by PSP treatment.

Effects of polysaccharide peptide (PSP) from Coriolus versicolor on the pharmacokinetics of cyclophosphamide in the rat and cytotoxicity in HepG2 cells

Polysaccharide peptide (PSP), isolated from Coriolus versicolor COV-1, has been shown to restore the immunological effects against cyclophosphamide-induced immuno-suppression, although the mechanism(s) involved remain uncertain. This study investigated the PSP-cyclophosphamide interaction by studying the effects of PSP on the pharmacokinetic of cyclophosphamide in the rat and the effect of PSP on the cytotoxic effects of cyclophosphamide on a cancer cell line (HepG2 cells). In the pharmacokinetic studies in the rat, acute pre-treatment of PSP (4 μmol/kg/day, i.p.) decreased the clearance (CL) of cyclophosphamide by 31%, with a concomitant increase in the area under concentration–time curve (AUC) by 44%, and prolongation of the plasma half-life ( T 1/2) by 43%. Sub-chronic pre-treatment of PSP (2 μmol/kg/day, i.p., 3 days) decreased the CL of cyclophosphamide by 33%, with a concomitant increase in the AUC by 50%, and prolongation of the plasma T 1/2 by 34%. In cytotoxicity studies using HepG2 cells, non-toxic dose of PSP (1–10 μM) enhanced the cytotoxicity of cyclophosphamide. PSP at 10 μM further decreased HepG2 cell viability by 22% compared to when cyclophosphamide was present alone. In summary, PSP enhanced the cytotoxic effect of cyclophosphamide on a cancer cell line in vitro and altered the pharmacokinetics of cyclophosphamide in vivo in the rat. Both of these effects may be beneficial in the use of PSP as an adjunct to cyclophosphamide treatment.

Effect of polysaccharide peptide (PSP) on in vivo sulphation and glucuronidation of paracetamol in the rat.

The effect of polysaccharide peptide (PSP), an immunomodulator isolated from Coriolus versicolor COV-1, on the disposition of paracetamol was investigated in the rat. PSP (100 and 200 mg/kg, i.v.) was administered 30 min before a moderate dose (100 mg/kg, i.v.) of paracetamol was given. Plasma and bile concentrations of paracetamol, paracetamol glucuronide and paracetamol sulphate were measured by high performance liquid chromatography. The pharmacokinetics of paracetamol (100 mg/kg) alone was consistent with those reported previously, using a one-compartment model. PSP (200 mg/kg) significantly (P < 0.05) increased the clearance (controls, 19.06 +/- 2.74 ml/min/kg: PSP treated, 26.22 +/- 0.84 ml/min/kg) and volume of distribution (controls, 1.35 +/- 0.11 l/kg: PSP treated, 1.61 +/- 0.04 l/kg) of paracetamol by 37% and 21%, respectively. These changes were associated with concomitant increases in the glucuronide and sulphate metabolites in plasma, with significant increases in the Cmax and Tmax for both metabolites. The biliary excretion rate of paracetamol glucuronide and paracetamol sulphate were also measured. The Cmax values of paracetamol sulphate were significantly (P < 0.01) increased by 2.4-fold from 907.8 +/- 157.7 micrograms/ml (controls) to 3061 +/- 331 micrograms/ml after PSP treatment. The lower dose of PSP (100 mg/kg) had no significant effect on the disposition of paracetamol in this study, which agreed with previous reports that a low dose of PSP (100-200 mg/kg, i.p.) was less effective in the protection against paracetamol-induced hepatotoxicity. The time course of the increase in paracetamol sulphate in plasma and bile in this study coincided with the transient perturbation of glutathione (GSH) turnover by a similar dose range of PSP previously described, such that more cysteine was available for oxidation to inorganic sulphate. This increase in sulphate conjugation by PSP would, in part, contribute to the increase in disposition of paracetamol and may be related to the ability of PSP to decrease the covalent binding of paracetamol to microsomal proteins previously reported. Further studies are necessary to understand the mechanism(s) involved in the PSP-induced increases in paracetamol glucuronide and paracetamol sulphate formation and biliary excretion.