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Background and Purpose— This study aimed to explore safety of tirofiban in endovascular treatment of acute ischemic stroke. Methods— Two hundred eighteen ischemic stroke patients receiving endovascular thrombectomy were prospectively recruited, with 94 treated with intra-arterial tirofiban and 124 were not. The 2 groups were compared in terms of symptomatic intracranial hemorrhage (ICH) and fatal ICH rate by the χ 2 test and logistic regression. Results— Patients treated with tirofiban compared with those without tirofiban had significantly higher rate of symptomatic ICH (14.6% versus 5.7%; P =0.027) and fatal ICH (8.8% versus 1.6%; P =0.014). Tirofiban-treated patients had increased odds of symptomatic ICH by 2.9-fold (95% CI, 1.1–7.5), and odds of fatal ICH increased by 5.9-fold (95% CI, 1.2–28.4). Conclusions— Tirofiban treatment increases risk of major ICH after endovascular thrombectomy for acute ischemic stroke in this nonrandomized study.

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The treatment of neural deficiency after cerebral infarction is challenging, with limited therapeutic options. The transplantation of mesenchymal stem cells (MSCs) to the ischemic penumbra is a potential therapeutic approach. In the present study, a cerebral infarction model was generated by performing middle cerebral artery occlusion (MCAO) in SD rats. The expression of CXCR4 increased, and the number of MSCs migrating to the peri‐infarct area was higher in rats transplanted with preconditioned MSCs than in rats transplanted with untreated MSCs. The rate of apoptosis, as evaluated by TUNEL staining and immunoblotting assays, was reduced in rats receiving preconditioned MSCs. A significant amelioration of neural regeneration and improved neurological function were observed in rats injected with preconditioned MSCs compared with those injected with untreated MSCs. However, the application of an siRNA targeting CXCL12 significantly inhibited the protective role of preconditioned MSCs against apoptosis and promoted the migration of MSCs to the ischemic area, leading to impaired neuronal regeneration and limited recovery of neuronal function. Hypoxic preconditioning of MSCs prior to transplantation suppressed apoptosis and increased their migration abilities, leading to the promotion of neuronal regeneration and improvement in neural function after transplantation. This preconditioning strategy may be considered as a potential approach for the modification of MSCs prior to cell transplantation therapy in patients with cerebral infarction.Significance of the StudyWe found that hypoxic preconditioning of MSCs improved their ability to promote neuronal regeneration and the recovery of neuronal function. Moreover, we showed that CXCR4 inhibited apoptosis, improved cell homing, and promoted neuronal differentiation, without influencing angiogenesis. Our study provides a relatively safe preconditioning method for potential use for cell transplantation therapy in ischemic cerebral infarction. The results presented here will facilitate the development of novel strategies and techniques to improve the tolerance and migration ability of transplanted cells for the treatment of cerebral infarction sequelae.

Background: Epilepsy is a chronic neurological disorder affecting an estimated 50 mil-lion people worldwide. Emerging evidences have accumulated over the past decades supporting the role of inflammation in the pathogenesis of epilepsy. Curcumin is a nature-derived active molecule demonstrating anti-inflammation efficacy. However, its effects on epilepsy and corresponding mech-anisms remain elusive.Objective: To investigate the effects of curcumin on epilepsy and its underlying mechanism.Method: Forty Sprague Dawley rats were divided into four groups: (1) control group; (2) Kainic Acid (KA)-induced epilepsy group; (3) curcumin group; and (4) curcumin pretreatment before KA stimulation group. Morris water maze was utilized to assess the effect of curcumin on KA-induced epilepsy. The hippocampi were obtained from rats and subjected to western blot. Immunohistochem-istry was conducted to investigate the underlying mechanisms.Results: Rats received curcumin demonstrated improvement of recognition deficiency and epilepsy syndromes induced by KA. Western blot showed that KA stimulation increased the expression of IL-1β and NLRP3, which were reduced by curcumin treatment. Further investigations revealed that curcumin inhibited the activation of NLPR3/inflammasome in epilepsy and reduced neuronal loss in hippocampus.Conclusion: Curcumin inhibits KA-induced epileptic syndromes via suppression of NLRP3 in-flammasome activation; therefore, offers a potential therapy for epilepsy.

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