As a strategy to prevent the well-known immunosuppressant effects of cyclophosphamide (Cyp), the immunomodulatory effects of the polysaccharide extract of the fruit of Schisandra chinensis (Turcz.) Baill. were investigated in the present study. The crude Schisandra polysaccharide (SCP) was obtained by water extraction and alcohol precipitation methods. The total carbohydrate, uronic acid and protein contents were determined using the phenol-sulfuric acid, m-hydroxydiphenyl and Bradford method, respectively. The monosaccharide composition of SCP was determined by high-performance liquid chromatography. ICR mice were randomly divided into control, model, low-dose SCP (0.4 mg/10 g), medium-dose SCP (0.8 mg/10 g) and high-dose SCP (1.6 mg/10 g) groups. The mice in the SCP groups were intragastrically administered SCP once a day for 21 days and those from the control and model groups were administered the same volume of distilled water. Subsequently, the mice in the model and SCP groups were intraperitoneally injected with Cyp (20 mg/kg) once a day for 5 days. The mouse leukocyte count in the peripheral blood as well as thymus and spleen indexes were determined, and the phagocytic function of macrophages was estimated using a carbon clearance test. The thymus and spleen were histomorphologically observed. The levels of tumor necrosis factor-α and interferon-γ were measured by ELISA. Furthermore, antibody formation and spleen lymphocyte proliferation were measured by the serum hemolysin and the MTT method, respectively. The apoptotic rate of splenic lymphocytes was determined by flow cytometric analysis. The results indicated that SCP prevents Cyp-induced impairment of the cellular, humoral and non-specific immunity, and may be an auxiliary immune enhancer for the prevention of immune hypofunction.
Danshen was able to reduce the risk of the patients with coronary heart disease (CHD), but the mechanism is still widely unknown. Biochemical indices (lipid profile, markers of renal and liver function, and homocysteine (Hcy)) are closely associated with CHD risk. We aimed to investigate whether the medicine reduces CHD risk by improving these biochemical indices. The patients received 10 Danshen pills (27 mg/pill) in Dashen group, while the control patients received placebo pills, three times daily. The duration of follow-up was three months. The serum biochemical indices were measured, including lipid profiles (LDL cholesterol (LDL-C), HDL-C, total cholesterol (TC), triglycerides (TG), apolipoprotein (Apo) A, ApoB, ApoE, and lipoprotein (a) (Lp(a))); markers of liver function (gamma-glutamyl transpeptidase (GGT), total bilirubin (TBil), indirect bilirubin (IBil), and direct bilirubin (DBil)); marker of renal function (uric acid (UA)) and Hcy. After three-month follow-up, Danshen treatment reduced the levels of TG, TC, LDL-C, Lp(a), GGT, DBil, UA, and Hcy (P < 0.05). In contrast, the treatment increased the levels of HDL-C, ApoA, ApoB, ApoE, TBil, and IBil (P < 0.05). Conclusion. Danshen can reduce the CHD risk by improving the biochemical indices of CHD patients.
BackgroundSchisandra, a globally distributed plant, has been widely applied for the treatment of diseases such as hyperlipidemia, fatty liver and obesity in China. In the present work, a rapid resolution liquid chromatography coupled with quadruple-time-of-flight mass spectrometry (RRLC-Q-TOF-MS)-based metabolomics was conducted to investigate the intervention effect of Schisandra chinensis lignans (SCL) on hyperlipidemia mice induced by high-fat diet (HFD).MethodsHyperlipidemia mice were orally administered with SCL (100 mg/kg) once a day for 4 weeks. Serum biochemistry assay of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) was conducted to confirm the treatment of SCL on lipid regulation. Metabolomics analysis on serum samples was carried out, and principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) were carried out for the pattern recognition and characteristic metabolites identification. The relative levels of critical regulatory factors of liver lipid metabolism, sterol regulatory element-binding proteins (SREBPs) and its related gene expressions were measured by quantitative real-time polymerase chain reaction (RT-PCR) for investigating the underlying mechanism.ResultsOral administration of SCL significantly decreased the serum levels of TC, TG and LDL-c and increased the serum level of HDL-c in the hyperlipidemia mice, and no effect of SCL on blood lipid levels was observed in control mice. Serum samples were scattered in the PCA scores plots in response to the control, HFD and SCL group. Totally, thirteen biomarkers were identified and nine of them were recovered to the normal levels after SCL treatment. Based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analysis, the anti-hyperlipidemia mechanisms of SCL may be involved in the following metabolic pathways: tricarboxylic acid (TCA) cycle, synthesis of ketone body and cholesterol, choline metabolism and fatty acid metabolism. Meanwhile, SCL significantly inhibited the mRNA expression level of hepatic lipogenesis genes such as SREBP-1c, fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), and decreased the mRNA expression of liver X receptor α (LXRα). Moreover, SCL also significantly decreased the expression level of SREBP-2 and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) in the liver of hyperlipidemia mice.ConclusionAnti-hyperlipidemia effect of SCL was confirmed by both serum biochemistry and metabolomics analysis. The mechanism may be related to the down-regulation of LXRα/SREBP-1c/FAS/ACC and SREBP2/HMGCR signaling pathways.
1. Schizandrol A is an active component in schisandra, also the representative component for the identification of schisandra. 2. A rapid resolution liquid chromatography coupled with quadruple-time-of-flight mass spectrometry (RRLC-QTOF/MS) was developed to investigate the pharmacokinetics of schizandrol A after itsintragastric administration (50 mg/kg) in rats. 3. Schizandrol A was rapidly absorbed (T=2.07 h), with a longer duration (t=9.48 h) and larger apparent volume of distribution (Vz/F = 111.81 L/kg) in rats. Schizandrol A can be detected in main organs and the order of its distribution was in the liver > kidney > heart > spleen > brain, particularly higher in the liver. 4. Five schizandrol A metabolites were identified, including 2-demethyl-8(R)-hydroxyl-schizandrin, 3-demethyl-8(R)-hydroxyl-schizandrin, hydroxyl-schizandrin, demethoxy-schizandrin, 2, 3-demethyl-8(R) -hydroxyl-schizandrin, indicating that the hydroxylation and demethylation may be the major metabolic way of schizandrol A. 5. This study defined the pharmacokinetic characteristics of schizandrol A in vivo, and the RRLC-QTOF/MS is more sensitive and less limited by conditions, and needs less samples, which may be a useful resource for the further research and development of schisandrol A.
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