ABSTRACT
Cynomorium songaricum Rupr is widely known in China as a traditional herbal medicine. In this study, single-factor experiments and response surface methodology were used to optimize the extraction of Cynomorium songaricum Rupr glycoprotein (CSG). The results show that a maximum glycoprotein yield of 6.39 ± 0.32% was achieved at a ratio of solid to liquid 32:1 for 4.2 H at 52 °C. Then, the IR, monosaccharide composition, amino acid composition, type of glycopeptide linkage, and average molecular weight of CSG-1 purified from CSG were characterized. The results indicate that CSG-1 presented the characteristic absorption peak of polysaccharide and protein, including four monosaccharides and 17 amino acids, had O-linked glycopeptide bonds, Mw , Wn , Mw /Mn , Mp , and the z-average were 5.343 × 106 , 3.203 × 106 , 1.668, 8.911 × 106 , and 6.948 × 106 , respectively. Besides, CSG-1 solution was described by the Herschel-Bulkley model and it behaved as a shear-thinning fluid. Also, under a frequency sweep the moduli G' and Gâ³ both increased with increasing CSG-1 concentration and the CSG-1 dispersions had weak thermal stability over the temperature sweep. These results provide a scientific basis for the further study of Cynomorium songaricum Rupr.
Subject(s)
Cynomorium/chemistry , Glycoproteins , Plant Proteins , Glycoproteins/chemistry , Glycoproteins/isolation & purification , Plant Proteins/chemistry , Plant Proteins/isolation & purification , RheologyABSTRACT
High altitude cerebral edema (HACE) is a high altitude malady caused by acute hypobaric hypoxia (AHH), in which pathogenesis is associated with oxidative stress and inflammatory cytokines. Potentilla anserina L is mainly distributed in Tibetan Plateau, and its polysaccharide possesses many physiological and pharmacological properties. In the present study, the protective effect and potential treatment mechanism of Potentilla anserina L polysaccharide (PAP) in HACE were explored. First, we measured the brain water content and observed the pathological changes in brain tissues, furthermore, malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), and glutathione (GSH) were evaluated by kits. Finally, the protein contents and mRNA expressions of pro-inflammatory (IL-1ß, IL-6, TNF-α, vascular endothelial cell growth factor [VEGF], NF-κB, and hypoxia inducible factor-1 α [HIF-1α]) were detected by ELISA kits, RT-PCR, and western blotting. The results demonstrated that PAP reduced the brain water content, alleviated brain tissue injury, reduce the levels of MDA and NO, and increased the activity of SOD and GSH level. In addition, PAP blocking the NF-κB and HIF-1α signaling pathway activation inhibited the generation of downstream pro-inflammatory cytokines (IL-1ß, IL-6, TNF-α, and VEGF). Therefore, PAP has a potential to treat and prevent of HACE by suppression of oxidative stress and inflammatory response.
Subject(s)
Brain Edema/drug therapy , Brain/drug effects , Cell Hypoxia/drug effects , Polysaccharides/therapeutic use , Potentilla/chemistry , Signal Transduction/drug effects , Animals , Brain/pathology , Male , Mice , Polysaccharides/pharmacology , Rats , Rats, WistarABSTRACT
OBJECTIVES: Bronchopulmonary dysplasia is the most common chronic lung disease of infancy and is associated with pulmonary hypertension (PH). Inhibition of glycogen synthase kinase (GSK)-3 ß has been shown to attenuate lung injury and PH in hyperoxia-exposed newborn rats. Genipin has been widely used for the treatment of inflammatory diseases. The aim of this study was to show that genipin decreased the expression of GSK-3 ß in lung tissues of hyperoxia-exposed rat pups. METHODS: We established models of hyperoxia-exposed rat pups, evaluated lung injury and pulmonary hypertension and detected the mRNA and protein expression of key molecules. RESULTS: Hyperoxia resulted in the reduction of survival rate and histologic injury of lung tissues; an increase of the messenger RNA (mRNA) expression of transforming growth factor-ß1, extracellular matrix proteins collagen-I and fibronectin, and α-smooth muscle actin; an increase of right ventricular (RV) systolic pressure and the weight ratio of RV to left ventriclar (LV) plus septum (S) (RV/LVâ¯+â¯S) were inhibited by genipin. Genipin also decreased the levels of tumor necrosis factor-α, interleukin-1 ß, and interleukin-6 in both bronchoalveolar lavage fluid and lung tissues after hyperoxia exposure. In addition, genipin inhibited p65 nuclear factor-κB nuclear translocation and matrix metalloproteinase-2 and -9 expression. Moreover, hyperoxia resulted in an increase of methane dicarboxylic aldehyde content and a decrease of superoxide dismutase activity, catalytic subunit of glutamate-cysteine ligase, modified subunit of glutamate-cysteine ligase, and nuclear factor erythroid 2-related factor 2 expression were inhibited by genipin. All these effects induced by genipin were blocked by upregulation of GSK-3 ß. Genipin downregulated GSK-3 ß expression, decreased nuclear factor-κB translocation, increased nuclear factor erythroid 2-related factor 2 expression, attenuated inflammation and oxidative stress, leading to amelioration of lung injury and PH in hyperoxia-exposed rat pups. CONCLUSION: Overall, genipin may provide a novel therapeutic option for preventing and treating infants with bronchopulmonary dysplasia.