The Effects Of Porphyromonas Gingivalis On The Apoptosis Of Hippocampal Cells In Sprague-Dawley Rats And Its Underlying Mechanisms

Neuron loss caused by neuronal apoptosis is one of the main pathological changes of Alzheimer's disease (AD). As a common infectious disease, chronic periodontitis has been found to be closely related to the occurrence and development of AD. Porphyromonas gingivalis (P. gingivalis) is one of the main pathogenic bacteria of periodontitis. In this study, we used a P. gingivalis peripheral infection model to study the effects and mechanisms of P. gingivalis on the apoptosis of hippocampal cells in Sprague-Dawley rats. After intravenous injections of P. gingivalis for 4 and 12 weeks, hematoxylin & eosin staining showed that the morphology of the cells in the hippocampus of the experimental group was changed. Nissl staining showed that cells in the hippocampus of the experimental group were loosely arranged and that the number of Nissl bodies was reduced. The TUNEL method revealed different levels of cell apoptosis in the experimental group and an increased expression of the cleaved caspase-3 protein, which indicates the existence of apoptosis. To explore the possible mechanisms of the cell apoptosis, we measured the expression levels of the N-methyl-D-aspartate receptor subunit NR2B and the postsynaptic density protein PSD-95, and the results showed increased expressions of both proteins. Elevated intracellular calcium concentrations were also detected in the hippocampal cells. In conclusion, we speculated that the high expression of the NR2B and PSD95 proteins in the hippocampus caused by venous infection with P gingivalis induced excitatory amino acid toxicity, leading to an extracellular calcium influx in the hippocampus, and eventually inducing apoptosis.