To investigate the effect of L-carnitine on hypoxic-ischemic brain damage in neonatal mice by regulating PI3K/AKT pathway.

Eighty mice with successful hypoxic-ischemic brain damage models were randomly divided into model group, L-carnitine low-dose group, L-carnitine medium-dose group and L-carnitine high-dose group, with 20 mice in each group, and 20 mice without modeling were used as sham operation group. The mice in the L-carnitine low-dose group, L-carnitine medium-dose group and L-carnitine high-dose group were intraperitoneally injected with L-carnitine at 100, 250 and 500 mg·kg^-1, respectively. The mice in the sham-operation group and the model group were intraperitoneally injected with the same amount of normal saline, the administration lasted for one week. The pathological changes of brain tissue were analyzed by hematoxylin-eosin staining. TCC staining was used to analyze the cerebral infarction area. The apoptosis of neurons in mouse brain tissue was analyzed by in situ terminal assay. The levels of inflammatory factors in brain tissue of mice were detected by enzyme-linked immunosorbent assay. The expression levels of PI3K/AKT pathway-related proteins were detected by Western blotting.

The brain tissue cells of the sham operation group were closely arranged and the structure was intact. In the model group, the brain tissue structure was disordered, a large number of cells were shed, the intercellular space was enlarged, and the morphology was swollen. The brain tissue loss of mice in different L-carnitine dose groups was gradually improved. The cerebral infarction rates in the sham-operated group, the model group, the low-dose L-carnitine group, the middle-dose L-carnitine group, and the high-dose L-carnitine group were (0.83±0.08)%, (59.32±3.12)%, (33.72±1.55)%, (25.58±1.21)%, and (9.81±1.07)%, respectively; the apoptosis rates of neurons were (1.85±0.18)%, (37.31±1.25)%, (21.67±1.02)%, (15.62±2.31)% and (6.63±0.88)%, respectively; the levels of interleukin-6 were (1.32±0.08), (13.21±1.16), (9.33±0.19), (6.03±0.18) and (3.73±0.15) pg·mL^-1, respectively; the levels of tumor necrosis factor α were (2.02±0.15), (15.07±1.26), (10.08±2.06), (7.13±1.16) and (4.06±0.08) pg·mL^-1, respectively; the relative expression levels of PI3K protein were 0.65±0.09, 0.10±0.01, 0.19±0.03, 0.35±0.03 and 0.55±0.06, respectively; the relative AKT protein expression levels were 0.69±0.05, 0.11±0.02, 0.21±0.02, 0.39±0.03 and 0.63±0.06, respectively. Compared with the model group, the above indicators in the L-carnitine low-dose group, the L-carnitine medium-dose group and the L-carnitine high-dose group had statistically significant differences (all P<0.05).

L-carnitine can alleviate hypoxic-ischemic brain damage in neonatal mice, and its mechanism may be related to the regulation of PI3K/AKT signaling pathway.