动物造模 z-bio 2022-03-01 315

　　Objective: To investigate the protective effect of Apelin-13 on focal cerebral ischemia-reperfusion injury (CIRI) in rats and its possible mechanism.

　　Methods: The SD rat focal CIRI model was established by the modified suture method, and divided into five groups: sham operation group, model group, low-dose Apelin-13 intervention group A, medium-dose group B, and high-dose C group. After injection into the lateral ventricle, neurological function scores, brain edema and cerebral infarction volumes were measured, and cell apoptosis was observed; brain tissue malondialdehyde (MDA), superoxide dismutase (SOD) activity and extracellular regulated protein kinase 1 were detected. /2 (ERK1/2).

　　Results: (1) Compared with the model group, group B and C had lower neurological function scores (P<0.05), water content and cerebral infarction volume (P<0.05); the model group showed edema, necrosis, more hyperchromatic, solid The number of TUNEL positive cells in groups B and C was lower than that in the model group (P<0.05); (2) The content of MDA in the brain tissue around ischemia in groups B and C decreased, and the activity of SOD increased (P<0.05); 2="" erk1="" p="">0.05 in each group; p-ERK1/2 protein expression in model group and intervention group was higher than that in sham operation group (P<0.05); intervention group was higher than model group (P<0.05) ).

　　Conclusion: Apelin-13 may protect against focal CIRI in rats by inhibiting oxidative stress; ERK1/2 signaling pathway may be involved in the protective mechanism of Apelin-13.