LACC1 Promoted Nerve Injury in an Anesthesia-Induced Cognitive Disorder Model via RIP2 Expression through ROS-NOD2...

This study aimed to investigate the impact of laccase domain-containing 1 (LACC1) on the model of anesthesia-induced cognitive disorder and its underlying mechanisms.

We collected and analyzed data from 24 patients with postoperative cognitive dysfunction (POCD) through microarray analysis. In the animal model, mice were exposed to 1.3% isoflurane in a humidified atmosphere with 30% oxygen as the carrier gas. Additionally, PC12 cells were stimulated with 2% isoflurane.

In mice subjected to anesthesia, both mRNA and protein expression levels of LACC1 were up-regulated. Moreover, LACC1 expression was increased in the anesthesia-induced cognitive disorder model. In vitro, LACC1 promoted the production of reactive oxygen species (ROS). Furthermore, LACC1 was found to exacerbate cognitive impairment in mice under anesthesia. The induction of RIP2 expression mediated this effect via the ROS-NOD2 pathway. The regulation of ROS-NOD2 played a critical role in controlling the impacts of LACC1 in both in vivo and in vitro models.

Our findings demonstrate that LACC1 contributes to nerve injury in the anesthesia-induced cognitive disorder model by inhibiting the ROS-NOD2/RIP2 signaling pathway. This discovery offers a novel perspective for understanding anesthesia-induced cognitive disorders.