Platycarya strobilacea leaf extract protects mice brain with focal cerebral ischemia by antioxidative property

Abstract

The leaf extract of Platycarya strobilacea (PSL) has long been recognized as possessing various health-promoting activities. However, information on its possible protective effects against ischemic stroke is currently lacking. Here, using a mouse model of focal cerebral ischemia (fCI), we studied the protective potential of an oral supplement of PSL. Mice were randomly divided into four groups: SO, a group subjected to a sham-operation; VEH, pretreated with distilled water and subjected to middle cerebral artery occlusion and reperfusion (MCAO/R); PSL-L and PSL-H, pretreated with low (20 mg/ kg) and high (100 mg/kg) doses of PSL, respectively, and subjected to the MCAO/R procedure. PSL was administered via an oral route daily for 8 days prior to surgery. We then measured the infarct volumes and sensorimotor deficits and studied the underlying antioxidant mechanisms by quantifying apoptosis, reactive oxygen species (ROS) generation, oxidative damages, and antioxidant enzymes in the ischemic cortex. The results showed a marked attenuation in infarct volume and sensorimotor deficits in both the PSL-L and PSL-H groups when compared with VEH. The terminal deoxynucleotidyl transferase dUTP nick end labeling and the immunohistochemical detection of the cleaved caspase-3 revealed that PSL could reduce cellular apoptosis in the ischemic lesion in a dose-dependent manner. The dihydroethidium-fluorescence, 4-hydroxynonenal, and 8-hydroxyl-2'-deoxyguanosine immunoreactivities in the ischemic lesion were markedly attenuated in the PSL-L group compared with the VEH group, indicating that PSL could attenuate ROS generation and the associated oxidative damage in the ischemic cortex. Finally, western blot results indicated that PSL can upregulate levels of heme oxygenase-1 (HO-1), an antioxidant enzyme, in the lesion area. Together, these results suggest that PSL can exert protective effects against fCI, and the mechanism may involve HO-1 upregulation.

Physcion Protects Rats Against Cerebral Ischemia-Reperfusion Injury via Inhibition of TLR4/NF-kB Signaling Pathway

“…ROS generation is implicated in the I/R injury, increased ROS could lead to neuronal cell death. 16 , 20 In addition, oxidative damage can consume intracellular antioxidants (GSH and SOD), and lead to the production of MDA. 21 , 22 Evidences have shown that cerebral I/R injury could increase ROS generation and induce oxidative stress by suppressing the activities of antioxidant biomarkers, 23 , 24 which were again confirmed in the current study.…”

“…SD rats (8 weeks old) were obtained from Shanghai SLAC Animal Center. Middle cerebral artery occlusion (MCAO) was performed in accordance with methods described by Lee et al 16 Briefly, rats were anaesthetized with ketamine (30 mg/kg) and xylazine cocktail (20 mg/kg). After that, a 7–0 surgical nylon monofilament with a rounded tip was inserted into the internal carotid artery (ICA), then occluding the middle cerebral artery (MCA).…”

“…TTC staining was performed as described previously. 16 The brain tissues (n = 6 per group) were cut into six slices with 1 mm thickness, and the sections were stained with 2% TTC (Sigma-Aldrich, St. Louis, MO, USA) for 20 min at 37°C. The ipsilateral infarct area was analyzed by ImageJ software.…”

Neuroprotective Effects of Water Extract from Brown Algae Petalonia binghamiae in an Experimental Model of Focal Cerebral Ischemia In Vitro and In Vivo

“…The procedure of MCAO/R was conducted under isoflurane anesthesia (2% induction, 1.5% maintenance), following a previous established protocol [35]. A midline neck incision was made, and the left common carotid artery (CCA) and the external carotid artery were tied off.…”

“…In accordance with our previous research [35], we employed neurological deficit scoring (NDS) as the initial assessment for sensorimotor deficits. Briefly, at 24 h after MCAO/R, we evaluated the sensorimotor functions of mice (n = 10 per group) using a scoring scale with four categories: 0 for no neurological deficit, 1 for failure to spread out the affected forepaw, 2 for unidirectional circling, 3 for falling to one side, and 4 for no voluntary movement.…”