Research on the structural characteristics of a novel Chinese Iron Yam polysaccharide and its gastroprotection mechanism against ethanol-induced gastric mucosal lesion in a BALB/c mouse model

Abstract

In this study, a triple-helix Chinese Iron Yam polysaccharide (CIYP) with a molecular weight of 1.67 × 10³ kDa was obtained. The CIYP was extracted with deionized water followed by deproteination, decoloration and purification using anion-exchange chromatography and size exclusion chromatography. Its structural characteristics and micromorphology were investigated by GC-MS, periodate oxidation and Smith degradation, FT-IR, NMR spectroscopy, SEM and AFM. The results showed that CIYP is a catenarian polysaccharide composed of rhamnose, arabinose, mannose, glucose, galactose and galacturonic acid in the ratio of 1 : 1.33 : 8.31 : 2.83 : 1.12 : 2.62. Meanwhile, the gastric mucosa protective effect of CIYP on an ethanol-injured BALB/c mouse model was investigated. It was found that the preventive CIYP-treatment groups (200 and 400 mg kg⁻¹ d⁻¹) showed gastric mucosa protective effects on the BALB/c mouse model. The lesion index and lesion inhibition rate of the CIYP and cimetidine treatment groups were significantly altered compared with the ethanol-induced gastric mucosal lesion (GML) group. Moreover, the administration of CIYP showed definite effects of increasing the NO, PGE2 and EGF levels, and SOD activities, and reducing the MDA levels of gastric mucosa tissues to prevent gastric oxidative stress. Histopathological analysis indicated that the microscopic morphology of gastric mucosal tissues was changed after being damaged by ethanol and the damage was significantly reduced after CIYP administration. Finally, the western blot and quantitative real-time polymerase chain reaction (qRT-PCR) results provided comprehensive evidence that the CIYP could repress gastric inflammation through the reduction of IL-1β, TNF-α and IL-6, prevent gastric oxidative stress through the inhibition of lipid peroxides, and favor cell survival via downregulating the TAK1, MKK3, P-p38 and Bax levels and upregulating the protein expression levels, compared with the CIM group.