Autophagy: a promising process for the treatment of acetaminophen-induced liver injury.

Toxicity from drugs has become an important cause of acute liver failure. Acetaminophen, a commonly used analgesic, can cause severe acute liver injury that can worsen into acute liver failure. Autophagy, a protective cell programme, has been reported to have protective effects in a variety of diseases such as cancer, immune diseases, neurodegenerative diseases, and inflammatory diseases. In this review, we describe how an excess of acetaminophen causes liver injury step by step, from the formation of the initial protein adduct to the final hepatocyte necrosis, as well as the induction of autophagy and its beneficial effects on diseases. Emphasis is placed on the potential effect of autophagy on improving the damage of acetaminophen to hepatocytes. Finally, we are committed to providing insights into the treatment of acute liver failure through the mechanism of acetaminophen induced liver injury, the mechanism of autophagy, and the link between autophagy and liver injury.

Galacto-Oligosaccharide Alleviates Alcohol-Induced Liver Injury by Inhibiting Oxidative Stress and Inflammation.

Alcoholic liver disease (ALD) is a primary cause of mortality and morbidity worldwide. Oxidative stress and inflammation are important pathogenic factors contributing to ALD. We investigated the protective mechanism of galacto-oligosaccharide (GOS) against ALD through their antioxidant and anti-inflammatory activities by performing in vivo and in vitro experiments. Western blot and RT‒PCR results indicated that the expression of cytochrome P450 protein 2E1 (CYP2E1) in liver tissues and L02 cells was reduced in the GOS-treated mice compared with the model group. In addition, GOS prominently reduced the expression of Kelch-like ECH-associated protein 1 (Keap1), increased the expression of the nuclear factor erythroid-2-related factor 2 (Nrf2) and haem oxygenase-1 (HO-1) proteins, and enhanced the antioxidant capacity. In addition, GOS decreased inflammation by reducing inflammatory factor levels and inhibiting the mitogen-activated protein kinase (MAPK)/nuclear factor kappa B (NF-κB) pathway. Based on these results, GOS may be a prospective functional food for the prevention and treatment of ALD.

Nondigestible Oligosaccharides with Anti-Obesity Effects.

Obesity has an important influence on health conditions, causing a multitude of complications and comorbidities, and drug therapy is considered to be one of the treatment strategies. Nowadays, there is increasing interest in the study of intestinal microbiota regulation of obesity; also, an increasing number of agricultural and sideline products have been found to have anti-obesity potential. In the present review, we summarize an overview of current known and potential anti-obesity oligosaccharides and their molecular structures. We describe their anti-obesity potential activity and the molecular structure associated with this activity, the regulation of intestinal microbiota composition and its mechanism of action, including regulation of the short-chain fatty acid (SCFA) pathway and altering bile acid (BA) pathway. This review will provide new ideas for us to develop new anti-obesity functional foods.

Kupffer Cells in Non-alcoholic Fatty Liver Disease: Friend or Foe?

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing all around the world and it may become the primary cause of terminal liver disease in adults and children in the next few decades. However, the pathogenesis of NAFLD is complex, and the Food and Drug Administration (FDA) has not approved any drugs for its treatment. Kupffer cells are the key cells regulating immunity in the liver, and the effect of their unique polarization on NAFLD has received increasing attention. Kupffer cells mainly reside in the lumen of hepatic sinusoids and account for 80% to 90% of colonized macrophages in the human body. They are phagocytic cells with the capacity for self-renewal that rarely migrate from their niche in the liver, and play a crucial role in regulating and maintaining homeostasis. Upon liver damage, Kupffer cells will be activated, releasing a good deal of inflammatory cytokines and chemokines. This review summarizes the multiple roles of Kupffer cells in the pathogenesis of NAFLD, the role of infiltrating macrophages in the pathogenesis of NAFLD is also briefly discussed, and aims to provide a theoretical basis for designing an NAFLD treatment strategy with Kupffer cells as the therapeutic target.