We herein report a food-derived polysaccharide (EJP) with the effect of relieving myocardial ischemia reperfusion injury (MIRI). This novel polysaccharide was isolated from the leaf of Eriobotrya japonica, and we first found its myocardium protective effects in vitro. Then, we firstly characterized EJP with a series of analytical technologies and further tested its effect on myocardial ischemia reperfusion injury (MIRI) with the illustration of the potential mechanisms in vivo. Interestingly, in the murine model of MIRI, administration of EJP effectively improved post-I/R heart contraction and limited the infarct size. Moreover, EJP significantly attenuated IR-induced oxidative damage and inflammatory reaction, as evidenced by decreasing MDA, IL-6, and TNF-α contents and increasing SOD activity and GSH-Px expression. In addition, we proved that EJP not only had no nephrotoxicity but also demonstrated a protective effect on the kidneys through HE staining and biochemical analysis. In sum, EJP, with a significant protective effect against myocardial I/R injury by showing anti-inflammatory and anti-oxidative activities, may become a meaningful drug candidate for the treatment of myocardial I/R injury.
Berberidis radix polysaccharide (BRP) extracted as capping agents was applied to prepare BRP-selenium nanoparticles (BRP-SeNPs) in the redox reaction system of sodium selenite and ascorbic acid. The stability and characterization of BRP-SeNPs were investigated by physical analysis method. The results revealed that BRP were tightly wrapped on the surface of SeNPs by forming C-O⋯Se bonds or hydrogen bonding interaction (O-H⋯Se). BRP-SeNPs presented irregular, fragmented and smooth surface morphology and polycrystalline nanoring structure, and its particle size was 89.4 nm in the optimal preparation condition. The pharmacologic functions of BRP-SeNPs were explored in vitro and in vivo. The results showed that BRP-SeNPs could heighten the cell viabilities and the enzyme activity of GSH-Px and decrease the content of MDA on H2O2-induced AML-12 cells injury model. In vivo tests, the results displayed that BRP-SeNPs could increase the body weight of mice, promote the enzyme activity like SOD and GSH-Px, decrease the liver organ index and the hepatic function index such as ALT, AST, CYP2E1, reduce the content of MDA, and relieve the proinflammation factors of NO, IL-1β and TNF-α in CCl4-induced mice injury model. Liver tissue histopathological studies corroborated the improvement of BRP-SeNPs on liver of CCl4-induced mice. The results of Western blot showed that BRP-SeNPs could attenuate oxidant stress by the Nrf2/Keap1/MKP1/JNK pathways, and downregulate the proinflammatory factors by TLR4/MAPK pathway. These findings suggested that BRP-SeNPs possess the hepatoprotection and have the potential to be a green liver-protecting and auxiliary liver inflammation drugs.