OBJECTIVE: The objective of this study was to examine whether the National Institute of Health Stroke Scale was associated with the short- and long-term prognosis of patients with acute ischemic stroke treated with intravenous thrombolysis. METHODS: A total of 247 patients with acute ischemic stroke admitted to the hospital from April 2019 to October 2020 were retrospectively selected as study subjects, and the immediate and long-term prognosis after thrombolysis was assessed using the modified Rankin Scale and divided into good prognosis group (119 cases) and poor prognosis group (128 cases) based on the effect of thrombolysis. Both groups were treated with alteplase, the National Institute of Health Stroke Scale of the two groups was compared, and the factors affecting the prognosis of acute ischemic stroke were analyzed. RESULTS: After intravenous thrombolysis, 24 h, and 7 days of treatment, the National Institute of Health Stroke Scale in the poor prognosis group was higher than those of patients in the good prognosis group, and the differences were statistically significant (p<0.05). The results of the multivariate analysis suggested that National Institute of Health Stroke Scale before treatment was an independent factor associated with the 3-month (OR: 1.068, 95%CI 1.015–1.123, p=0.011) and long-term poor prognosis (OR: 1.064, 95%CI 1.012–1.119, p=0.015) in patients with acute ischemic stroke receiving intravenous thrombolysis after adjustment of age, gender, body mass index, smoking, alcohol consumer, onset-to-door time, door-to-needle time, and imaging score. CONCLUSION: The National Institute of Health Stroke Scale could be a promising indicator for the prognosis, and active intervention is needed to improve the quality of life in patients with acute ischemic stroke. OBJECTIVE short longterm long term METHODS 201 202 subjects 119 (11 cases 128 (12 alteplase compared analyzed RESULTS 2 h p<0.05. p005 p p<0.05 . 0 05 (p<0.05) 3month month 3 OR (OR 1068 1 068 1.068 95CI CI 95 10151123 015 123 1.015–1.123 p=0.011 p0011 011 1064 064 1.064 10121119 012 1.012–1.119 p=0.015 p0015 age gender index smoking consumer onsettodoor onset door time doortoneedle needle score CONCLUSION 20 11 (1 12 p00 p<0.0 (p<0.05 106 06 1.06 9 1015112 01 1.015–1.12 p=0.01 p001 1012111 1.012–1.11 ( p0 p<0. (p<0.0 10 1.0 101511 1.015–1.1 p=0.0 101211 1.012–1.1 p<0 (p<0. 1. 10151 1.015–1. p=0. 10121 1.012–1. p< (p<0 1015 1.015–1 p=0 1012 1.012–1 (p< 101 1.015– p= 1.012– (p 1.015 1.012 1.01

ABSTRACT Purpose: Intravenous anesthetics have excellent analgesic activity without inducing the side effect in the respiratory system. The aim and objective of the current experimental study was to access the neuroprotective effect of sevoflurane against isoflurane induced cognitive dysfunction in rats. Methods: Isoflurane was used for induction the neurodysfunction in the rats, and rats received the oral administration of sevoflurane (2.5, 5 and 10 mg/kg). Morris water test was carried out for the estimation of cognitive function. Neurochemical parameters, antioxidant parameters and pro-inflammatory cytokines were also estimated. Results: Sevoflurane significantly (P < 0.001) altered the neurochemical parameters such as anti-choline acetyltransferase, acetylcholine esterase, acetylcholine, protein carbonyl, choline brain-derived neurotrophic factor, and amyloid β; antioxidant parameters such as glutathione, superoxide dismutase, and malondialdehyde; pro-inflammatory cytokines include interleukin (IL-2, IL-10, IL-4, IL-6, IL-10, IL-1β), and tumor necrosis factor-α. Sevoflurane significantly reduced the activity of caspase-3. Conclusions: Sevoflurane exhibited the neuroprotection against the cognitive dysfunction in rats via anti-inflammatory and antioxidant mechanism. Purpose system Methods 2.5, 25 2 (2.5 1 mg/kg. mgkg mg/kg . mg kg mg/kg) function proinflammatory pro inflammatory estimated Results P 0.001 0001 0 001 anticholine anti acetyltransferase esterase carbonyl brainderived brain derived factor β glutathione dismutase malondialdehyde IL2, IL2 IL 2, (IL-2 IL10, IL10 10, IL-10 IL4, IL4 4, 4 IL-4 IL6, IL6 6, 6 IL-6 IL1β, IL1β ILβ 1β , IL-1β) factorα. factorα α. α factor-α caspase3. caspase3 caspase 3. 3 caspase-3 Conclusions antiinflammatory mechanism 2.5 (2. 0.00 000 00 (IL- IL1 IL-1 IL- IL-1β caspase- 2. (2 0.0 (IL ( 0.