动物造模,脑缺血再灌注损伤 z-bio 2022-07-08 247

　　Objective To investigate the effect of curcumin on cognitive function, neurological function and mechanism of cerebral ischemia-reperfusion injury in mice.

　　Methods The mouse model of cerebral ischemia-reperfusion injury was established by suture method. The low-molecular-weight heparin sodium group, the low-dose and high-dose curcumedione groups and the models were administered by intragastric administration of 1 mg/(kg.d), 20 mg/( kg.d), 60 mg/(kg.d), Morris water maze test, behavioral score, cerebral infarction rate, and brain tissue water content were observed in each group of mice, and serum 6-keto-PGF1α and 6-keto-PGF1α/ TXB2 ratio, brain tissue homogenate cAMP and p-CREB expression levels.

　　Results Compared with the sham operation group, the escape latency of mice in the model group was significantly prolonged, the number of platform crossings was significantly reduced (P<0.01), and the behavioral score, cerebral infarction rate, brain tissue water content, and serum TXB2 content were significantly increased (P<0.01). <0.01), serum 6-keto-PGF1α, 6-keto-PGF1α/TXB2 ratio, brain tissue homogenate cAMP, p-CREB were significantly decreased (P<0.01). The escape latency of the drug group was significantly shortened (P<0.05), the number of platform crossings was significantly increased (P<0.05), the behavioral score, cerebral infarction rate and brain tissue water content were significantly decreased (P<0.05). The content of TXB2 was significantly decreased (P<0.01), the ratio of serum 6-keto-PGF1α, 6-keto-PGF1α/TXB2, brain tissue homogenate cAMP, and p-CREB were significantly increased (P<0.05). dose-dependent.

　　Conclusion Curcumedione has a good protective effect on cognitive function and neurological function in mice with cerebral ischemia-reperfusion injury, and its mechanism may be related to improving microcirculation disturbance and activating cAMP/CREB/BDNF signaling pathway.