title: Astragaloside IV alleviates early brain injury following experimental subarachnoid hemorrhage in rats.
abstract: Astragaloside IV, one of the main effective components isolated from Astragalus membranaceus, has multiple neuroprotective properties, while the effects of astragaloside IV on the attenuation of subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) and its possible mechanisms are unknown. In the present study, we aimed to determine whether astragaloside IV could inhibit oxidative stress, reduce neuronal apoptosis, and improve neurological deficits after experimental SAH in rats. Rats (n=68) were randomly divided into the following groups: Sham group, SAH group, SAH+vehicle group, and SAH+astragaloside IV group. Astragaloside IV or an equal volume of vehicle was administered at 1 h and 6 h after SAH, all the rats were subsequently sacrificed at 24 h after SAH. Mortality, neurological scores, and brain edema were assessed, biochemical tests and histological studies were also performed at that point. SAH induced an increase in the malondialdehyde (MDA) level, neuronal apoptosis, cleaved caspase 3, brain edema and decreased activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Astragaloside IV treatment reversed these changes and improved neurobehavioral outcomes of SAH rats. Our findings suggested that astragaloside IV may alleviate EBI after SAH through antioxidative and anti-apoptotic effects.
authors.affiliation: 1. Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China;
authors.forename: Anwen
authors.initials: A
authors.lastname: Shao
authors.affiliation: 2. Department of Burns, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China;
authors.forename: Songxue
authors.initials: S
authors.lastname: Guo
authors.affiliation: 3. First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.
authors.forename: Sheng
authors.initials: S
authors.lastname: Tu
authors.affiliation: 1. Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China;
authors.forename: Al-baadani
authors.initials: AB
authors.lastname: Ammar
authors.affiliation: 1. Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China;
authors.forename: Junjia
authors.initials: J
authors.lastname: Tang
authors.affiliation: 1. Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China;
authors.forename: Yuan
authors.initials: Y
authors.lastname: Hong
authors.affiliation: 1. Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China;
authors.forename: Haijian
authors.initials: H
authors.lastname: Wu
authors.affiliation: 1. Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China;
authors.forename: Jianmin
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000188:drug therapy*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012503:Saponins / Q000627:therapeutic use*; D013345:Subarachnoid Hemorrhage / Q000188:drug therapy* / Q000401:mortality; D014315:Triterpenes / Q000627:therapeutic use*
chemical_list: D012503:Saponins; D014315:Triterpenes; C052064:astragaloside A
keywords: apoptosis; astragaloside IV; early brain injury; oxidative stress; subarachnoid hemorrhage.