The effect of lipid metabolism regulator anthocyanins from Aronia melanocarpa on 3T3-L1 preadipocytes and C57BL/6 mice via activating AMPK signaling and gut microbiota.

This study investigated lipid metabolism regulation by anthocyanins from Aronia melanocarpa (AAM) in 3T3-L1 preadipocytes and high fat diet (HFD) mice. Ultra-performance liquid chromatography/ion mobility quadrupole time-of-flight mass spectrometry analysis identified the constituents of AAM, which decreased lipid content and inflammation in 3T3-L1 cells without cytotoxicity. Meanwhile, taking normal diet and orlistat mice as references, AAM supplementation improved blood lipid levels and adipocyte degeneration, promoted beneficial gut microbial growth, and maintained lipid metabolism in HFD mice. Furthermore, AAM activated the AMP-activated protein kinase (AMPK) signaling pathway, accompanied by the regulation of adipogenic transcription factors and their target genes in vitro and in vivo. Collectively, our data demonstrated that AAM exhibits anti-adipogenic activities that were partially mediated by the AMPK pathway and gut microbiota regulation. This study provides new insight into the regulation of lipid metabolism by AAM and suggests that AAM has potential therapeutic effects on hyperlipidemia.

Protective effects of oxymatrine against lipopolysaccharide/D­galactosamine­induced acute liver failure through oxidative damage, via activation of Nrf2/HO­1 and modulation of inflammatory TLR4­signaling pathways.

Oxymatrine has a variety of pharmacological functions, including anti-viral, anti-liver fibrotic, anti-cancer, anti­bacterial, anti­epidemic, analgesic, anti­allergy and anti­inflammatory properties. The present study aimed to investigate the protective effects of oxymatrine against lipopolysaccharide (LPS)/D­galactosamine (D­GalN)­induced acute liver failure and the associated underlying mechanisms. Mice were administrated 4 mg/kg LPS and 600 mg/kg D­GalN. Then, mice in the Oxymatrine group were treated with 120 mg/kg of oxymatrine for 4 weeks. Oxymatrine treatment increased survival rate, decreased plasma aspartate transaminase and alanine aminotransferase activity, increased superoxide dismutase and glutathione peroxidase and decreased malondialdehyde, tumor necrosis factor­ and myeloperoxidase activities in mice with LPS/D­GalN­induced liver failure. Furthermore, Oxymatrine activated nuclear factor erythroid 2­related factor (Nrf) 2 and heme oxygenase (HO)­1 protein expression, and suppressed Toll like receptor (TLR)4, myeloid differentiation primary response 88 and nuclear factor­κB protein expression in mice LPS/D­GalN mice. Overall, the present study suggests that oxymatrine effectively attenuates LPS/D­GalN­induced acute liver failure by oxidative damage via activation of Nrf2/HO­1 and modulation of TLR4­dependent inflammatory signaling pathways.