Inhibitory effect of tumor necrosis factor-α on the basolateral Kir4.1/Kir5.1 channels in the thick ascending limb during diabetes.

Diabetic nephropathy is a major contributor to the morbidity and mortality of patients with diabetes. TNF-α expression is elevated during diabetes and is implicated in the pathogenesis of diabetic nephropathy; however, its underlying molecular mechanisms remain unclear. The present study aimed to investigate the effect and molecular mechanism of TNF-α on the basolateral inwardly rectifying potassium (Kir)4.1/Kir5.1 channels in the thick ascending limb (TAL) of rat kidneys using western blotting and the patch clamp technique to provide a theoretical basis for the cause of the decrease in kidney concentrating capacity during diabetes. The results demonstrated that urinary TNF-α excretion and protein TNF-α expression in the TAL increased and basolateral Kir4.1/Kir5.1 channel activity decreased during diabetes; however, diabetic rats exhibited amelioration of Kir4.1/Kir5.1 activity with a soluble TNF-α antagonist, TNF receptor fusion protein (TNFR:Fc). These results suggested that TNF-α inhibited the activity of the basolateral Kir4.1/Kir5.1 channel in the TAL of rat kidneys during diabetes. In addition, the protein expression levels of phospholipase A2 (PLA2) and cyclooxygenase-2 (COX2) increased in diabetic rats, the effects of which deceased following treatment with TNFR:Fc compared with the diabetic group. Furthermore, an agonist of PLA2 (melittin) and COX2 production [prostaglandin E2 (PGE2)] inhibited the basolateral Kir4.1/Kir5.1 channels. Taken together, the results of the present study suggested that the inhibitory effect of TNF-α on the basolateral Kir4.1/Kir5.1 channels in the TAL during diabetes is mediated by the PLA2/COX2/PGE2 signaling pathway.

The Interaction Between Viruses and Intestinal Microbiota: A Review.

As the main pathogen threatening human and animal health, viruses can affect the immunity and metabolism of bodies. There are innate microbial barriers in the digestive tract of the body to preserve the homeostasis of the animal body, which directly or indirectly influences the host defence against viral infection. Understanding the interaction between viruses and intestinal microbiota or probiotics is helpful to study the pathogenesis of diseases. Here, we review recent studies on the interaction mechanism between intestinal microbiota and viruses. The interaction can be divided into two aspects: inhibition of viral infection by microbiota and promotion of viral infection by microbiota. The treatment of viral infection by probiotics is summarized.

Bacillus amyloliquefaciens B10 inhibits aflatoxin B1-induced cecal inflammation in mice by regulating their intestinal flora.

Aflatoxin B1 is a mycotoxin that widely exists in feed and has a great impact on human and animal health. This study aimed to examine whether Bacillus amyloliquefaciens B10 protected against aflatoxin B1-induced cecal inflammation in mice. It was found that Bacillus amyloliquefaciens B10 could significantly improve the effects of AFB1 on body weight and intestinal inflammation of mice and enhance the expression of tight-junction protein. Compared with the CON group, the combination of AFB1 and B10 significantly increased the abundance of Actinobacteria and Bacilli in a collaborative manner, and significantly reduced the abundance of Ruminococcae, Lactobacillaceae and Clostridia. Meanwhile, the results showed that the abundance of Bacterides and Bacterdia in AFB1 + B10 group was significantly lower than that of AFB1 group, and the Firmicutes increased significantly. Bacillus amyloliquefaciens B10 can be used as a feed additive and alleviate cecal inflammation induced by AFB1 in mice by regulating intestinal flora.

Bacillus amyloliquefaciens B10 can alleviate liver apoptosis and oxidative stress induced by aflatoxin B1.

Aflatoxin B1 (AFB1) is a mycotoxin often found in food and livestock feed. It can affect human and animal health and is especially damaging to the liver. This study aims to evaluate whether Bacillus amyloliquefaciens (hereafter referred to as B. amyloliquefaciens) B10 can alleviate the toxic effects of AFB1 and, if so, what mechanism is responsible for its action. Specific pathogen-free (SPF) Kunming mice (5-6 weeks old) were divided into four groups (Control, AFB1, B10 strain, and AFB1 + B10 strain) and conducted continuously via gavage for 28 days. Oxidation indices (MDA, T-AOC, SOD, GSH-Px, and CAT) were then measured using their liver tissues and liver coefficient were calculated. Apoptosis was determined using the TUNEL method. Gene expression was determined for Bax, Bcl-2, BIP, CHOP, JNK, Caspase-12, Caspase-9, and Caspase-3, and protein expression was detected for Bax, Bcl-2, and Caspase-3. Our results showed that AFB1 induced the oxidative damage and apoptosis in the livers of mice. However, for mice given B. amyloliquefaciens B10, the biochemical indices, pathological changes, the expressions of genes and proteins related to oxidative stress and apoptosis were significantly reversed. The results indicate that B. amyloliquefaciens B10 antagonizes oxidative damage and apoptosis induced by AFB1 in the livers of mice. The results of this study are of significance for the future use of this strain to reduce the harm of AFB1 to human health and animal reproductive performance.