Chengyi Zhang

Immunomodulatory effect of Schisandra polysaccharides in cyclophosphamide‑induced immunocompromised mice

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.

Metabolomics study of the therapeutic mechanism of Schisandra chinensis lignans on aging rats induced by D-galactose

Objective The aim of this study was to evaluate the antiaging effect of Schisandra chinensis lignans (SCL) by analyzing the characteristics in the serum of d-galactose (d-gal)-induced rats. Methods Forty male Wistar rats were randomly divided into control group, d-gal model group, low-dose SCL group (50 mg/kg/d), medium-dose SCL group (100 mg/kg/d), and high-dose SCL group (200 mg/kg/d). A serum metabolomics analysis method based on rapid resolution liquid chromatography coupled with quadruple-time-of-flight mass spectrometry was carried out to study the characteristics of d-gal-induced aging rats and evaluate the antiaging effects of SCL, and multivariate statistical analysis was performed for pattern recognition and characteristic metabolites identification. The relative levels of p19, p53, and p21 genes in the brain tissue were measured by quantitative real-time polymerase chain reaction for investigating the underlying mechanism. Results Metabolomics analysis showed that 15 biomarkers were identified and 13 of them recovered to the normal levels after the administration of SCL. Based on the pathway analysis, the antiaging mechanisms of SCL might be involved in the following metabolic pathways: energy, amino acid, lipid, and phospholipid metabolism. Furthermore, SCL significantly inhibited the mRNA expression level of p19, p53, and p21 in the brain of aging rats induced by d-gal. Conclusion These results suggest that SCL can delay rat aging induced by d-gal through multiple pathways.

Pharmacokinetics and distribution of schisandrol A and its major metabolites in rats

Abstract 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 its intragastric administration (50 mg/kg) in rats. 3. Schizandrol A was rapidly absorbed (T max = 2.07 h), with a longer duration (t 1/2 = 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.