动物造模,局灶性脑缺血-再灌注损伤 z-bio 2022-03-25 521

　　Objective: To discuss the maintenance 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 improving the suture method, and divided into sham operation group, model group, low-dose Apelin-13 intervention group A, medium-dose group B, and high-dose C group, a total of 5 groups, and Apelin-13 was stopped. After injection into the lateral ventricle, the neurological function score, brain edema and cerebral infarction volume were measured, and cell apoptosis was observed; brain tissue malondialdehyde (MDA), superoxide dismutase (SOD) activity and extracellular opsonizing protein kinase 1 /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 infarcted tissue in 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 play a maintenance role in focal CIRI in rats by inhibiting oxidative stress response; ERK1/2 signaling pathway may be involved in the maintenance mechanism of Apelin-13.