大鼠局灶性脑缺血-再灌注损伤 z-bo 2020-11-11 328

　　Objective: To explore 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 modified suture method, divided into sham operation group, model group, low-dose Apelin-13 intervention group A, medium-dose group B, and high-dose group C. Apelin-13 was performed. Intracerebroventricular injection, neurological function score, cerebral edema, cerebral infarction volume measurement, cell apoptosis; detection of brain tissue malonaldehyde (MDA), superoxide dismutase (SOD) activity and extracellular regulatory protein kinase 1 /2 (ERK1/2).

　　Results: (1) Compared with the model group, the neurological function scores of groups B and C were lower (P<0.05), water content and cerebral infarction volume were reduced (P<0.05); edema and necrosis were seen in the infarct tissues of the model group, with more deep staining and solidification. Shrinkage nucleus cells; 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="" each="" group="" erk1="" p="">0.05); the expression of p-ERK1/2 protein in model group and intervention group was higher than that of sham operation group (P<0.05); intervention group was higher than model group (P<0.05) ).

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