Trans-cinnamaldehyde loaded chitosan based nanocapsules display antibacterial and antibiofilm effects against cavity-causing Streptococcus mutans.

Background: Dental caries is a multifactorial disease, and the bacteria such as Streptococcus mutans (S. mutans) is one of the risk factors. The poor effect of existing anti-bacterial is mainly related to drug resistance, the short time of drug action, and biofilm formation. Methods: To address this concern, we report here on the cinnamaldehyde (CA) loaded chitosan (CS) nanocapsules (CA@CS NC) sustained release CA for antibacterial treatment. The size, ζ-potential, and morphology were characterized. The antibacterial activities in vitro were studied by growth curve assay, pH drop assay, biofilm assay, and qRT-PCR In addition, cytotoxicity assay, organ index, body weight, and histopathology results were analyzed to evaluate the safety and biocompatibility in a rat model. Results: CA@CS NC can adsorb the bacterial membrane due to electronic interaction, releasing CA slowly for a long time. At the same time, it has reliable antibacterial activity against S. mutans and downregulated the expression levels of QS, virulence, biofilm, and adhesion genes. In addition, it greatly reduced the cytotoxicity of CA and significantly inhibited dental caries in rats without obvious toxicity. Conclusion: Our results showed that CA@CS NC had antibacterial and antibiofilm effects on S. mutans and inhibit dental caries. Besides, it showed stronger efficacy and less toxicity, and was able to adsorb bacteria releasing CA slowly, providing a new nanomaterial solution for the treatment of dental caries.

Upregulation of Sec22b plays a neuroprotective role in a rat model of traumatic brain injury via inducing protective autophagy.

Cortical neuronal cell death following traumatic brain injury (TBI) evoked by the cortical impact is a significant factor that contributes to neurological deficits. In the current study, we harvested the injured area and perilesional area of the injured brain induced by TBI. We explored the functions of Sec22b, an apoptosis-promoting kinase, and a pivotal bridge builder of apoptotic signaling in the etiopathogenesis of an experimental rat model of TBI. We found that Sec22b was expressed in neurons in the injured cortical area, and the expression level significantly decreased after TBI, especially at 24 h. Administration of Sec22b overexpressed plasmid significantly ameliorated TBI-induced apoptosis, neurological deficits, and blood-brain barrier permeability, accompanied by the activation of autophagy. However, the administration of Sec22b knockdown resulted in the opposite eff ;ects. Altogether, these findings indicated that Sec22b plays a neuroprotective role after TBI, suggesting that Sec22b may be a potential therapeutic target for TBI. We speculated that this neuroprotective effect might be achieved by upregulating autophagy levels and required further studies to explore.

Inhibition of Lats1/p-YAP1 pathway mitigates neuronal apoptosis and neurological deficits in a rat model of traumatic brain injury.

AIMS: To investigate the roles of Lats1/p-YAP1 pathway in TBI-induced neuronal apoptosis and neurological deficits in rats. RESULTS: We found that Lats1 and YAP1 were expressed in cerebral cortex neurons of Sprague-Dawley rats, and the phosphorylation levels of Lats1 and YAP1 in injured regions were significantly increased after TBI. Furthermore, inhibition of Lats1 not only decreased the level of p-YAP1, but also attenuated neuronal apoptosis and neurological impairment. CONCLUSIONS: Our work demonstrates that inhibition of Lats1/p-YAP1 pathway mitigates neuronal apoptosis and neurological deficits in a rat model of TBI.