ABSTRACT
OBJECTIVE: To investigate the safety and efficacy of intravenous Tirofiban infusion after mechanical thrombectomy in patients with acute ischemic stroke. METHODS: A consecutive series of patients with acute ischemic stroke who underwent mechanical thrombectomy were included. The patients were categorized into two groups according to whether they received intravenous Tirofiban infusion after mechanical thrombectomy. Intracranial hemorrhage (ICH) and all-cause mortality were studied as safety outcomes; recanalization of target vessel evaluated by thrombolysis in cerebral infarct (TICI) scale, and neurological improvement evaluated by Institutes of Health Stroke Scale (NIHSS) and modified Rankin scale (mRS) were studied as efficacy outcomes. RESULTS: A total of 31 patients who underwent mechanical thrombectomy were enrolled, among which 8 (25.81%) received a standard dose of intravenous Tirofiban infusion after mechanical thrombectomy. There was no significant difference in baseline characteristics between the two groups (all P>0.05). None (0.00%) of the patients suffered ICH in the Tirofiban group, while 3 (13.04%) suffered ICH in the control group (P=0.550); similar all-cause mortality rates were found in both groups (25.00% versus 17.39%, P=0.634). In the Tirofiban group, all patients achieved successful recanalization defined by TICI groups (25.00% versus 17.39%, P=0.634). In the und in both groups (25.00% versus 17.39%, P=0.634). In th4). In thle, and neurological improvement evaluated so, 'et al' is notned by 3-month mRS≤2, which were not statistically significant when compared to the control group (all P>0.05). CONCLUSION: Intravenous Tirofiban infusion after mechanical thrombectomy is safe and effective in patients with acute ischemic stroke.
ABSTRACT
OBJECTIVE: To explore the role and of miR-132, HMGA2 and PI3K/AKT pathway in mice with Alzheimer's disease (AD). METHODS: The mice were divided into 7 groups: the normal group, the model group (AD model mice), the NC group (AD mice injected with negative control (NC) vector), the miR-132 mimic group (AD mice injected with miR-132 mimics), the miR-132 inhibitor group (AD mice injected with miR-132 inhibitor), the si-HMGA2 group (AD mice injected with HMGA2 silencing vector), and the miR-132 inhibitor + si-HMGA2 group (model mice treated with miR-132 inhibitor and si-HMGA2). Y-maze experiment and related molecular biology experiments were performed. RESULTS: The double-luciferase reporter assay verified that miR-132 could target and inhibit the expression of HMGA2A. Compared with the NC group, model mice had decreased learning and memory ability, reduced miR-132, p-PI3K/PI3K, p-AKT/AKT, AQP4 expression as well as GFAP GSH-Px, SOD, ATP, and T-AOC levels, but increased expression of HMGA2 and the levels of TNF-α, IL-6, NO, IL-1ß, MAO, and MDA (P<0.017). Up-regulation of miR-132 or silencing HMGA2 could partly reverse the changes, but inhibition of miR-132 would exaggerate the brain injury and these molecular changes (P<0.017). The combination uses of si-HMGA2 and miR-132 inhibitor could reverse the changes caused by miR-132 inhibitor (P<0.017). CONCLUSION: miR-132 could downregulate the expression of HMGA2 and promote the expression of the PI3K/AKT pathway, so as to achieve a protective effect on brain in AD mice.
