Hypercholesterolemia aggravates sevoflurane-induced cognitive impairment in aged rats by inducing neurological inflammation and apoptosis

We aimed to explore the effects of hypercholesterolemia on sevoflurane-induced cognitive impairment in aged rats and the underlying mechanism(s). Aged rats were administrated with high-fat diet, sevoflurane, or both. Thereafter, the plasma levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) were evaluated. The Morris water maze task was performed to evaluate the spatial learning and memory ability of rats. Moreover, Nissl and Evans blue staining were conducted to test nerve damage and detect the blood-brain barrier permeability, respectively. The percentage of apoptotic cells was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The messenger RNA expression of inflammatory factors and protein expression of microglial activation markers and apoptosis-related proteins were tested by real-time polymerase chain reaction, enzyme-linked immunosorbent assay, or western blot analysis, respectively. High-fat diet induced high levels of TC, TG, and LDL but decreased levels of HDL. However, sevoflurane had no effects on these levels. In contrast, sevoflurane significantly induced the impairment of learning and memory, nerve damage, neuroinflammatory damage, and neuronal apoptosis. Hypercholesterolemia exacerbated the sevoflurane-induced impairment in aged rats. These results suggested that hypercholesterolemia aggravates sevoflurane-induced cognitive impairment in aged rats, possibly by inducing neurological inflammation and apoptosis.

Automated summary

This study aimed to investigate the effects of hypercholesterolemia on sevoflurane-induced cognitive impairment in aged rats. The results showed that hypercholesterolemia aggravated the cognitive impairment induced by sevoflurane, possibly by inducing neuroinflammation and apoptosis.