Schisandrin B Inhibits NLRP3 Inflammasome Pathway and Attenuates Early Brain Injury in Rats of Subarachnoid Hemorrhage.
10.1007/s11655-021-3348-z
- Author:
Song CHEN
1
;
Yi-Hang DING
1
;
Song-Sheng SHI
1
;
Xian-Kun TU
2
Author Information
1. Department of Neurosurgery, Fujian Medical University Union Hospital, Neurosurgery Research Institute of Fujian Province, Fuzhou, 350001, China.
2. Department of Neurosurgery, Fujian Medical University Union Hospital, Neurosurgery Research Institute of Fujian Province, Fuzhou, 350001, China. unionnstu@hotmail.com.
- Publication Type:Journal Article
- Keywords:
Chinese medicine;
early brain injury;
inflammation;
neuronal apoptosis;
nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3;
schisandrin B;
subarachnoid hemorrhage
- MeSH:
Animals;
Apoptosis;
Brain/pathology*;
Brain Injuries/pathology*;
Caspase 3/metabolism*;
Cyclooctanes;
Evans Blue;
Inflammasomes/metabolism*;
Interleukin-18/metabolism*;
Lignans;
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism*;
Polycyclic Compounds;
Proto-Oncogene Proteins c-bcl-2/metabolism*;
Rats;
Rats, Sprague-Dawley;
Subarachnoid Hemorrhage/drug therapy*;
Water;
bcl-2-Associated X Protein/metabolism*
- From:
Chinese journal of integrative medicine
2022;28(7):594-602
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To determine whether Schisandrin B (Sch B) attenuates early brain injury (EBI) in rats with subarachnoid hemorrhage (SAH).
METHODS:Sprague-Dawley rats were divided into sham (sham operation), SAH, SAH+vehicle, and SAH+Sch B groups using a random number table. Rats underwent SAH by endovascular perforation and received Sch B (100 mg/kg) or normal saline after 2 and 12 h of SAH. SAH grading, neurological scores, brain water content, Evan's blue extravasation, and terminal transferase-mediated dUTP nick end-labeling (TUNEL) staining were carried out 24 h after SAH. Immunofluorescent staining was performed to detect the expressions of ionized calcium binding adapter molecule 1 (Iba-1) and myeloperoxidase (MPO) in the rat brain, while the expressions of B-cell lymphoma 2 (Bcl-2), Bax, Caspase-3, nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis-associated specklike protein containing the caspase-1 activator domain (ASC), Caspase-1, interleukin (IL)-1β, and IL-18 in the rat brains were detected by Western blot.
RESULTS:Compared with the SAH group, Sch B significantly improved the neurological function, reduced brain water content, Evan's blue content, and apoptotic cells number in the brain of rats (P<0.05 or P<0.01). Moreover, Sch B decreased SAH-induced expressions of Iba-1 and MPO (P<0.01). SAH caused the elevated expressions of Bax, Caspase-3, NLRP3, ASC, Caspase-1, IL-1β, and IL-18 in the rat brain (P<0.01), all of which were inhibited by Sch B (P<0.01). In addition, Sch B increased the Bcl-2 expression (P<0.01).
CONCLUSION:Sch B attenuated SAH-induced EBI, which might be associated with the inhibition of neuroinflammation, neuronal apoptosis, and the NLRP3 inflammatory signaling pathway.
