Egg matrices alleviate long-term florfenicol-induced behavioral alterations the gut microbiota and host metabolism in mice.

Florfenicol (FFC) is a broad-spectrum antibiotic that is commonly detected as a residue in livestock products, such as eggs. Although the adverse effects of FFC have been widely reported, the combined influence of the food matrix with FFC exposure on the gut microenvironment and the short-term self-recovery dynamics after FFC discontinuation remain unclear. Therefore, this study has comprehensively evaluated the effects of FFC residues in eggs on the gut microbiota and metabolism in a mouse model, and the self-recovery situation was also determined.

MiR-34a-5p/Sirt1 axis: A novel pathway for puerarin-mediated hepatoprotection against benzo(a)pyrene.

Benzo[a]pyrene (BaP) as a carcinogen induces oxidative stress and inflammation, causing health problems including liver damage. Puerarin (a natural flavonoid) is traditionally used to provide hepatoprotective effects. This research was established to meet the rising demand for effective therapies/treatments against hepatic diseases and investigate the mechanism underlying the protective actions of puerarin against BaP-induced liver damage.

Secoisolariciresinol diglucoside mitigates benzo[a]pyrene-induced liver and kidney toxicity in mice via miR-101a/MKP-1-mediated p38 and ERK pathway.

Benzo[a]pyrene (BaP) can cause hepatorenal toxicity. Secoisolariciresinol diglucoside (SDG), a polyphenolic compound present in flaxseed, has shown a variety of biological activities including antioxidant, anti-inflammatory, anti-apoptotic effects. This study aimed to investigate the protective effects and working mechanisms of SDG against BaP-induced hepatorenal injury.

Cadmium induces ferroptosis and apoptosis by modulating miR-34a-5p/Sirt1axis in PC12 cells.

Cadmium (Cd) is a potent neurotoxic metal present in the environment and food. In this study, CdCl (2 or 4 μM) induced cytotoxicity and neurotoxicity in PC12 cells, causing decreases in cell viability and NEP protein expression and increase in p-tau protein expression. For the first time, CdCl -initiated injury was found to result from the induction of not only apoptosis but also ferroptosis, as evidenced by the increased iron content, ROS production, and mitochondrial membrane potential along with changes in the expressions of iron death-related genes (FTH1, GPX4, ASCL4, PTGS2, and NOX1) and levels of caspase9, Bax, and Bcl-2 proteins.

Caffeic acid phenethyl ester mitigates cadmium-induced hepatotoxicity in mice: Role of miR-182-5p/TLR4 axis.

Cadmium (Cd), an environmental pollutant, is evidenced to cause hepatotoxicity. In this study, the potential protective effect of caffeic acid phenethyl ester (CAPE) on cadmium-induced liver damage was investigated. Forty male mice were treated daily with either CdCl (1.