Helenalin from Centipeda minima ameliorates acute hepatic injury by protecting mitochondria function, activating Nrf2 pathway and inhibiting NF-κB activation.

Acute liver injury is a life-threatening syndrome that often caused by hepatocyte damage and is characterized by inflammatory and oxidative responses. Helenalin isolated from Centipeda minima (HCM) has been found to have anti-inflammatory and anti-oxidative effects. Here, this study aimed to investigate the effects and underlying mechanisms of HCM on Lipopolysaccharide/D-Galactosamine (LPS/D-GalN)-induced acute liver injury. Mice were intragastrically administered with various dose of HCM for 10 days; 2 h after the final treatment, the mice were injected with 50 µg/kg LPS and 800 mg/kg D-GalN. The histopathological changes, hepatocyte apoptosis, serum cytokines, oxidative stress and inflammatory cytokines were assessed. The results showed that HCM significantly ameliorated the hepatic injury, as evidenced by the attenuation of histopathological changes and the decrease in serum aminotransferase and total bilirubin activities. HCM markedly decreased hepatocyte apoptosis by modulating the mitochondria-dependent pathway, including the increase in the Bcl-2/Bax ratio, the inhibition of caspase-3, -8 and -9, and the inhibition of cytochrome C release. Moreover, HCM strongly alleviated oxidative stress, lipid peroxidation and reactive oxygen species (ROS) generation by activating the Nrf2 signaling pathway. In addition, HCM significantly attenuated inflammatory cytokines including TNF-α, IL6 and IL-1ß as well as NO production by inhibiting TLR4 signaling transduction and NF-κB activation. In conclusion, HCM protects hepatocytes from damage induced by LPS/D-GalN, which may contribute to its ability to alleviate hepatocyte apoptosis by protecting the mitochondrial function, inhibit oxidative stress by activating the Nrf2 pathway, and attenuate inflammation by inhibiting NF-κB activation. This study demonstrates that HCM may be developed as a potential agent for the treatment of acute liver failure.

Functionalizing bottom ash from biomass power plant for removing methylene blue from aqueous solution.

In order to seek a possible path for utilization bottom ash, the solid waste from biomass incineration for power generation, its basic characteristics were investigated, and removing methylene blue (MB) from aqueous solution was attempted as well. Results indicated bottom ash dominantly contained Si and Ca-related minerals with >35 mineral elements, meanwhile, it was typically characterized by alkalinity (pH of 9.5) and low specific surface area (14.5m2/g). As the only bottom ash was employed for removing MB, removal efficiency was lower than 44%, however, it was greatly improved to 100% as hydrogen peroxide was supplemented (final concentration of 4.0%). Based on the elucidated mechanisms, Fenton-like reaction was triggered by bottom ash, which was dominantly responsible for removing MB, rather than the adsorption by bottom ash. Besides, increasing reaction temperature and duration dramatically promoted MB removal by bottom ash with the aid of hydrogen peroxide (HBA). A great promotion on MB removal from 92.3mg/g to 143.9mg/g was achieved as pH was adjusted from 2.0 to 5.0, indicating MB removal was pH-dependent. The maximum removal of 260.9mg/g was achieved by HBA at a relatively high initial MB concentration of 2000.0mg/L, suggesting a great potential in treating dye wastewater by functionalizing bottom ash with the aid of hydrogen peroxide. Moreover, the released heavy metals and derived by-products from MB removal were acceptable in consideration of their potential environmental risks. Thus, the current work offers a new path to valorize the solid waste in biomass electricity generation plant.

Effect of Astragalus polysaccharides on expression of TNF-α, IL-1ß and NFATc4 in a rat model of experimental colitis.

AIM: Astragalus membranaceus is a Chinese medicinal herb and has been shown to improve hapten-induced experimental colitis. One of its major components is polysaccharides. We investigated the effect of Astragalus polysaccharides (APS) on expression of TNF-α, IL-1ß and NFATc4 in a rat model of experimental colitis. METHODS: The experimental colitis model was induced by TNBS. Forty five rats were divided into five groups (n=9): Normal control group, receiving ethanol vehicle with no TNBS during induction and IP saline injection during treatment; TNBS colitis model group (TNBS+IP saline), receiving only IP saline vehicle treatment; APS low dose group (TNBS+L-APS), receiving APS 100mg/kg; APS high dose group (TNBS+H-APS), receiving APS 200mg/kg; and positive control group (TNBS+Dexm), receiving dexamethasone 0.3mg/kg. The clinical features, macroscopic and microscopic scores were assessed. The expressions of TNF-α, IL-1ß and NFATc4 were measured by real-time PCR and ELISA assays. RESULTS: Compared to normal control rats, TNBS+IP saline had significant weight loss, increased macroscopic and microscopic scores, higher disease activity index (DAI) up-regulation of TNF-α, IL-1ß and NFATc4 mRNA expression and up-regulation of TNF-α and IL-1ß protein expression. Compared to TNBS+IP saline, treatment with APS or dexamethasone significantly reduced DAI, partially but significantly prevented TNBS colitis-induced weight loss and improved both macroscopic and microscopic scores; high dose APS or dexamethasone significantly down-regulated TNF-α and IL-1ß expressions (both mRNA and protein) and up-regulated NFATc4 mRNA and protein expression. The effect of high dose APS and dexamethasone is comparable. CONCLUSIONS: APS significantly improved experimental TNBS-induced colitis in rats through regulation of TNF-α, IL-1ß and NFATc4 expression.