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Zearalenone (ZEN) is a non-steroidal estrogen mycotoxin produced by Fusarium fungi, which inevitably exists in human and animal food or feed. Previous studies indicated that apoptosis seems to be a key determinant of ZEN-induced toxicity. This experiment aimed to investigate the protective effects of Glutamine (Gln) on ZEN-induced cytotoxicity in IPEC-J2 cells. The experimental results showed that Gln was able to alleviate the decline of cell viability and reduce the production of reactive oxygen species and calcium (Ca 2+ ) induced by ZEN. Meanwhile, the mRNA expression of antioxidant enzymes such as glutathione reductase, glutathione peroxidase, and catalase was up-regulated after Gln addition. Subsequently, Gln supplementation resulted in the nuclear fission and Bad-fluorescence distribution of apoptotic cells were weakened, and the mRNA expression and protein expression of pro-apoptotic genes and apoptotic rates were significantly reduced. Moreover, ZEN reduced the phosphorylation Akt, decreased the expression of Bcl-2, and increased the expression of Bax. Gln alleviated the above changes induced by ZEN and the antagonistic effects of Gln were disturbed by PI3K inhibitor (LY294002). To conclude, this study revealed that Gln exhibited significant protective effects on ZEN-induced apoptosis, and this effect may be attributed to the PI3K/Akt signaling pathway.

Cyanidin-3-O-glucoside (C3G), an active ingredient in anthocyanins, mainly exists in dark cereals. C3G was investigated for its effect on human gastric cancer (GC) cells, together with its molecular mechanism. The CCK-8 assay results showed that C3G had significant antiproliferative effects on GC cells, but it had little effect on normal cells. Western blot and flow cytometry results showed that C3G regulated the reduction of mitochondrial membrane potential and arrested the cell cycle in the G2/M phase through the AKT signaling pathway, causing the cells to undergo apoptosis. Additionally, in MKN-45 cells, C3G markedly raised intracellular reactive oxygen species (ROS) levels. The wound healing assay and Transwell assay results showed that MKN-45 cell migration was significantly inhibited. Western blot results showed that the expression of E-cadherin protein was upregulated and the expressions of β-catenin, N-cadherin, and Vimentin were downregulated. Additionally, following N-acetylcysteine treatment, the expression levels of these proteins were reduced. In conclusion, C3G caused MKN-45 cells to undergo apoptosis; arrested the cell cycle in the G2/M phase; hindered cell migration; and activated the MAPK, STAT3, and NF-κB signaling pathways, by inducing an increase in ROS levels. Thus, C3G may be a promising new medication for the treatment of GC. [ABSTRACT FROM AUTHOR]

Stroke often results in neurological and neuropsychiatric sequela. Exosomes derived from brain endothelial cells (EC-Exo) protect neurons from hypoxic injury. However, the biological role of exosomes in apoptosis and synaptic plasticity remains unclear. This research aimed to assess whether cerebral microvascular endothelial cells inhibit apoptosis and promote synaptic remodeling through exosome-mediated cell–cell interaction after the ischemic attack. The effects of EC-Exo on primary neuronal apoptosis and synapses in oxyglucose deprivation reoxygenation (OGD/R) injury were first assessed in vitro. Animal experiments were performed using C57BL/6J mice, divided into three groups: a sham group, a model (middle cerebral artery occlusion/reperfusion, MCAO/R) group, and an EC-Exo group (tail vein injection of EC-Exo, once/2 days for 14 days) to evaluate the neuromotor and exploratory abilities of mice after MCAO/R. Apoptosis and synaptic protein expression levels were detected. The results demonstrated that EC-Exo inhibited neuronal apoptosis and increased synaptic length after OGD/R. In vivo, EC-Exo not only improved neural motor behavior and increased regional cerebral blood flow (rCBF) in MCAO/R-injured mice but also promoted the expression of synaptic regulatory proteins and inhibited apoptosis in the brain. These results suggest that EC-Exo may provide neuroprotection against stroke by promoting synaptic remodeling and inhibiting apoptosis from protecting neurons. [ABSTRACT FROM AUTHOR]