Yu Lei,Chengkun Wang,Quan Jiang,Xiaoyi Sun,Yongzhong Du,Yaofeng Zhu,Yingmei Lu
The toxicity of engineered nanoparticles remains a concern. The knowledge of biohazards associated with particular nanoparticles is crucial to make this cutting-edge technology more beneficial and safe. Here, we evaluated the toxicity of Ga 2 O 3 nanoparticles (NPs), which are frequently used to enhance the performance of metal catalysts in a variety of catalytic reactions. The potential inflammatory signaling associated with the toxicity of HA/β-Ga 2 O 3 :Cr 3+ NPs in primary cortical neurons was examined. We observed a dose-dependent decrease in cell viability and an increase in apoptosis in neurons following various concentrations (0, 1, 5, 25, 50, 100 µg/ml) of HA/β-Ga 2 O 3 :Cr 3+ NPs treatment. Consistently, constitutively active forms of calcineurin (48 kDa) were significantly elevated in cultured primary cortical neurons, which was consistent with calpain activation indicated by the breakdown products of spectrin. Moreover, HA/β-Ga 2 O 3 :Cr 3+ NPs result in the elevation of LC3-II formation, SQSTM/p62, and Cathepsin B, whereas phosphorylation of CaMKII (Thr286) and Synapsin I (Ser603) were downregulated in the same context. Taken together, these results demonstrate for the first time that calpain activation and a disturbance of autophagy signaling are evoked by exposure to HA/β-Ga 2 O 3 :Cr 3+ NPs, which may contribute to neuronal injury in vitro .
T-2 toxin, classified as a mycotoxin, harms immune and cognitive systems. Recently, an increasing number of studies have focused on the neurotoxic effects of T-2 toxin. However, there is still a need for a better understanding of the molecular mechanisms involved. In this study, we aimed to elucidate the protective effect of resveratrol (Res) supplementation against T-2 toxin-induced spatial learning and memory impairment and to investigate the communication mechanisms between the gut and the brain. Mice received a single intraperitoneal dose of T-2 toxin (4 mg/kg) followed by Res (100 mg/kg) administered via the same route. The Morris water maze and novel object recognition tests demonstrated that T-2 toxin had a profound negative impact on spatial learning and memory in mice. However, the administration of Res successfully mitigated the cognitive impairments caused by T-2 toxin and notably enhanced the levels of brain-derived neurotrophic factor (BDNF), synaptophysin I (SYN1), and postsynaptic density protein 95 (PSD-95). Moreover, Res demonstrated a protective effect against T-2 toxin-induced damage to hippocampal tissue. Simultaneously, it played a pivotal role in restoring gut microbiota equilibrium and maintaining the integrity of intestinal tight junctions, effectively curbing both localized and systemic inflammation triggered by T-2 toxin exposure. In conclusion, our findings suggest that resveratrol may alleviate T-2 toxin-induced spatial learning and memory deficits, possibly via gut-brain axis modulation.
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