Cerebral ischemia/reperfusion (I/R) typically occurs after mechanical thrombectomy to treat ischemic stroke, generation of reactive oxygen species (ROS) after reperfusion may result in neuronal insult, ultimately leading to disability and death. Regulated in development and DNA damage responses 1 (REDD1) is a conserved stress response protein under various pathogenic conditions. Recent research confirms the controversial role of REDD1 in injury processes. Nevertheless, the role of REDD1 in cerebral I/R remains poorly defined. In the current study, increased expression of REDD1 was observed in neurons exposed to simulated I/R via oxygen glucose deprivation/reoxygenation (OGD/R) treatment. Knockdown of REDD1 enhanced OGD/R‐inhibited cell viability, but suppressed lactate dehydrogenase (LDH) release in neurons upon OGD/R. Simultaneously, suppression of REDD1 also antagonized OGD/R‐evoked cell apoptosis, Bax expression, and caspase‐3 activity. Intriguingly, REDD1 depression abrogated neuronal oxidative stress under OGD/R condition by suppressing ROS, MDA generation, and increasing antioxidant SOD levels. Further mechanism analysis corroborated the excessive activation of autophagy in neurons upon OGD/R with increased expression of autophagy‐related LC3 and Beclin‐1, but decreased autophagy substrate p62 expression. Notably, REDD1 inhibition reversed OGD/R‐triggered excessive neuronal autophagy. More importantly, depression of REDD1 also elevated the expression of p‐mTOR. Preconditioning with mTOR inhibitor rapamycin engendered not only a reduction in mTOR activation, but also a reactivation of autophagy in REDD1 knockdown‐neurons upon OGD/R. In addition, blocking the mTOR pathway muted the protective roles of REDD1 inhibition against OGD/R‐induced neuron injury and oxidative stress. Together these data suggested that REDD1 may regulate I/R‐induced oxidative stress injury in neurons by mediating mTOR‐autophagy signaling, supporting a promising therapeutic strategy against brain ischemic diseases.

Background: This study aimed to study the expression level of cofilin after electroacupuncture (EA) pretreatment, using ischemic brain injury model in mice. In addition, infarct volume and neurological functions were measured to understand whether electroacupuncture stimulation could restore the functions of the brain.Methods: Total of 36 mice was randomly divided into three groups: sham group, middle cerebral artery occlusion model (MACO), and middle cerebral artery occlusion model pretreated with EA (MACO + EA). Mice were stimulated at "Baihui (G20)" and "Dazhui (G14)" 24 hours before focal cerebral ischemia. Infarct volume and neuronal function of brain tissue were scored among different experimental groups. The expression level of cofilin and phosphocofilin of brain tissue were evaluated by using Western blot analysis. TUNEL assay was performed to determine the degree of cell apoptosis.Results: Compared with the sham group, the level of cofilin was dramatically reduced in the MACO group. EA pretreatment could reduce the protein level of cofilin, while EA therapy could also upregulate the protein level of phosphocofilin. Improved neuronal function, smaller infarct volume, and reduced neuronal apoptosis were observed among the mice underwent EA before middle artery occlusion. Conclusion:Our results from Western blot analysis and TUNEL assay might suggest that the upregulation of cofilin was concerned with the EA protects rats from ischemic brain injury. Cofilin might be a potential target for developing drugs against brain ischemia.

Background:</B> This study aims to investigate the therapeutic effect of electroacupuncture stimulation at acupoints of the heart meridian on vascular dementia (VD). <B>Methods:</B> A total of 120 VD patients were enrolled and randomly divided into two groups: observation group, the patients were treated with electroacupuncture stimulation; control group, the patients were treated with oral medicine. Cognitive function was assessed using the Mini-mental State Examination (MMSE), Activity of Daily Living (ADL) and functional activities questionnaire (FAQ). <B>Results:</B> The total effective rate was 75% in the observation group and 73.33% in the control group, and the difference between these two groups was not statistically significant (P>0.05). After treatment, the MMSE, ADL and FAQ scores in these two groups significantly improved, when compared to scores before treatment (P<0.01). After treatment, the differences in MMSE, ADL and FAQ scores between these two groups were not statistically significant (P>0.05). <B>Conclusion:</B> Electroacupuncture stimulation at acupoints of the heart meridian has a definite effect in improving the cognitive function of VD patients.