The Edible Insect Gryllus bimaculatus Protects against Gut-Derived Inflammatory Responses and Liver Damage in Mice after Acute Alcohol Exposure.

Accumulation of reactive oxygen species (ROS) in response to excess alcohol exposure is a major cause of gut barrier disruption and lipopolysaccharide (LPS)-induced hepatic inflammation, as well as liver steatosis and apoptosis. This study was designed to investigate protective effects of the cricket Gryllus bimaculatus, an edible insect recognized by the Korea Food and Drug Administration, against acute alcoholic liver damage in mice. Administration of G. bimaculatus extracts (GBE) attenuated alcohol-induced steatosis and apoptotic responses in the liver and intestinal permeability to bacterial endotoxin. These protective effects were associated with suppression of ROS-mediated oxidative stress in both the liver and small intestine. Furthermore, in vivo and in vitro studies revealed that GBE inhibits LPS-induced Kupffer cell activation and subsequent inflammatory signaling. Importantly, the protective effects of GBE were more potent than those of silymarin, a known therapeutic agent for alcoholic liver diseases.

LB-9, Novel Probiotic Lactic Acid Bacteria, Ameliorates Dextran Sodium Sulfate-Induced Colitis in Mice by Inhibiting TNF-α-Mediated Apoptosis of Intestinal Epithelial Cells.

Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease, is a group of chronic and relapsing inflammatory conditions within the gastrointestinal tract. An increase in intestinal epithelial cell (IEC) apoptosis is a major characteristic of UC. Tumor necrosis factor-α (TNF-α) plays an essential role in the regulation of apoptosis. Aberrant activation of the immune response to resident microflora contributes to overproduction of TNF-α in the mucosal tissue of the gastrointestinal tract; a hallmark of UC. There are no curative medications for IBD. Thus, establishment of novel strategies for the treatment of this disease is imperative. Lactic acid bacteria (LAB) have been characterized as probiotics that can alleviate imbalances in indigenous microflora in UC, exhibiting beneficial effects for the treatment and prevention of IBD. In this study, we elucidate the potential of LB-9, a novel probiotic LAB, to protect against colitis development using a dextran sodium sulfate (DSS)-induced mouse model of UC. Treatment using LB-9 reduced clinical symptoms of colitis. In addition, both colitis-induced and NF-κB-mediated IEC apoptosis was markedly reduced in mice treated with LB-9. Moreover, these results were closely associated with reduced TNF-α levels. Our study demonstrates that the LB-9 probiotic exhibits therapeutic potential for UC through suppression of TNF-α-mediated IEC apoptosis in a murine DSS-induced colitis model, with important biological implications for treatment of IBD in humans.