No abstract

Microglia mediate multiple facets of neuroinflammation. They can be phenotypically divided into a classical phenotype (pro-inflammatory, M1) or an alternative phenotype (anti-inflammatory, M2) with different physiological characteristics and biological functions in the inflammatory process. Betaine has been shown to exert anti-inflammatory effects. In this study, we aimed to verify the anti-inflammatory effects of betaine and elucidate its possible molecular mechanisms of action in vitro. Lipopolysaccharide (LPS)-activated microglial cells were used as an inflammatory model to study the anti-inflammatory efficacy of betaine and explore its mechanism of regulating microglial polarisation by investigating the morphological changes and associated inflammatory changes. Cytokine and inflammatory mediator expression was also measured by ELISA, flow cytometry, immunofluorescence, and western blot analysis. Toll-like receptor (TLR)-myeloid differentiation factor 88 (Myd88)-nuclear factor-kappa B (NF-κB) p65, p-NF-κB p65, IκB, p-IκB, IκB kinase (IKK), and p-IKK expression was determined by western blot analysis. Betaine significantly mitigated the production of pro-inflammatory cytokines and increased the release of anti-inflammatory cytokines. It promoted the conversion of the microglia from M1 to M2 phenotype by decreasing the expression of inducible nitric oxide synthase and CD16/32 and by increasing that of CD206 and arginase-1. Betaine treatment inhibited the TLR4/NF-κB pathways by attenuating the expression of TLR4-Myd88 and blocking the phosphorylation of IκB and IKK. In conclusion, betaine could significantly alleviate LPS-induced inflammation by regulating the polarisation of microglial phenotype; thus, it might be an effective therapeutic agent for neurological disorders.

Radix Astragali (RA) is one of the most widely used Chinese herbs prescribed in many Chinese formulas to reinforce 'Qi' and treat vital energy deficiency. This study combined fingerprinting with quantitative analysis multi-components by a single marker (QAMS) to improve the quality control standard for RA on the basis of existing quality control methods of traditional Chinese medicinal materials. UPLC-ESI-TOF-MS technique was used to evaluate the quality of RA by fingerprinting and QAMS. Using the anti-inflammatory, anti-oxidation and anti-anoxic activities to screen characteristic components of RA, the calycosin-7-O-β-d-glucoside (CG), ononin, astragaloside IV, astragaloside II, calycosin and astrageloside I significantly inhibited ear edema in mice, the calycosin and CG had good antioxidant activity and the astragaloside I had a significant anti-hypoxia activity. Astragaloside I, astragaloside II, astragaloside IV, ononin, calycosin and CG had significant pharmacological actions. These components were comprehensively used as the indicative components for the quality control of RA. Astragaloside I was used as the internal standard of the relative correction factors of CG (13.45), ononin (0.51), calycosin (12.08), astragaloside IV (0.73) and astragaloside II (0.81). Astragaloside I and CG were used as internal standards of the relative correction factors of the flavonoids and saponins of ononin (1.11), calycosin (0.04), astragaloside IV (0.73) and astragaloside II (0.81). The study combined fingerprinting with QAMS to improve the quality control standard for RA.

No abstract

Fulminant hepatic failure (FHF), associated with high mortality, is characterized by extensive death of hepatocytes and hepatic dysfunction. There is no effective treatment for FHF. Several studies have indicated that flavonoids can protect the liver from different factor-induced injury. Previously, we found that the extracts of Elaeagnus mollis leaves had favorable protective effects on acute liver injury. However, the role and mechanisms behind that was elusive. This study examined the hepatoprotective mechanisms of kaempferol-3-O-α-l-arabinopyranosyl-7-O-α-l-rhamnopyra-noside (KAR), a major flavonol glycoside of E. mollis, against d-galactosamine (GalN) and lipopolysaccharide (LPS)-induced hepatic failure. KAR reduces the mouse mortality, protects the normal liver structure, inhibits the serum aspartate aminotransferase (AST) and alamine aminotransferase (ALT) activity and decreases the production of malondialdehyde (MDA) and reactive oxygen species (ROS) and inflammatory cytokines, TNF-α, IL-6, and IL-1β. Furthermore, KAR inhibits the apoptosis of hepatocytes and reduces the expression of TLR4 and NF-κB signaling pathway-related proteins induced by GalN/LPS treatment. These findings suggest that the anti-oxidative, anti-inflammatory, and anti-apoptotic effects of KAR on GalN/LPS-induced acute liver injury were performed through down-regulating the activity of the TLR4 and NF-κB signaling pathways.