Gastrodin Alleviates Cerebral Ischaemia/Reperfusion Injury by Inhibiting Pyroptosis by Regulating the lncRNA NEAT1/miR-22-3p Axis

Cerebral ischaemia/reperfusion (I/R) injury-induced irreversible brain injury is a major cause of mortality and functional impairment in ageing people. Gastrodin (GAS), derived from the traditional Chinese herbal medicine Tianma, has been reported to inhibit the progression of stroke, but the mechan...

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Bibliographic Details
Published in:Neurochemical research 2021-07, Vol.46 (7), p.1747-1758
Main Authors: Zhang, Heng-Sheng, Ouyang, Bo, Ji, Xiong-Ying, Liu, Mei-Fang
Format: Article
Language:English
Subjects:
Aging
Animals
Benzyl Alcohols - therapeutic use
Biochemistry
Biomedical and Life Sciences
Biomedicine
Brain - pathology
Brain injury
Caspase-1
Cell Biology
Cell Hypoxia - physiology
Cell viability
Cerebral blood flow
Cerebral infarction
Deprivation
Enzyme-linked immunosorbent assay
Flow cytometry
Glucose - deficiency
Glucosides - therapeutic use
Head injuries
Herbal medicine
IL-1β
In vivo methods and tests
Infarction
Infarction, Middle Cerebral Artery - drug therapy
Infarction, Middle Cerebral Artery - metabolism
Infarction, Middle Cerebral Artery - pathology
Inflammation
Inflammation - drug therapy
Interleukin 18
Ischemia
L-Lactate dehydrogenase
Lactate dehydrogenase
Lactic acid
Male
MicroRNAs - metabolism
Modulation
Neurochemistry
Neurology
Neurons - drug effects
Neurons - metabolism
Neuroprotective Agents - therapeutic use
Neurosciences
Occlusion
Original Paper
Oxygen - metabolism
Pyroptosis
Pyroptosis - drug effects
Rats
Rats, Sprague-Dawley
Reperfusion
Reperfusion Injury - drug therapy
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
RNA, Long Noncoding - metabolism
Surgery
Triphenyltetrazolium chloride
Western blotting
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Summary:Cerebral ischaemia/reperfusion (I/R) injury-induced irreversible brain injury is a major cause of mortality and functional impairment in ageing people. Gastrodin (GAS), derived from the traditional Chinese herbal medicine Tianma, has been reported to inhibit the progression of stroke, but the mechanism whereby GAS modulates the progression of cerebral I/R remains unclear. The middle cerebral artery occlusion method was used as a model of I/R in vivo. Rats were pretreated with GAS by intraperitoneal injection 7 days before I/R surgery and were then treated with GAS for 7 days after I/R surgery. Additionally, an oxygen–glucose deprivation/reoxygenation model using neuronal cells was established in vitro to simulate I/R injury. 2,3,5-Triphenyltetrazolium chloride and Nissl staining were used to evaluate infarct size and neuronal damage, respectively. Lactate dehydrogenase release and cell counting kit-8 assays were used to assess neuronal cell viability. Enzyme-linked immunosorbent assay, qPCR, flow cytometry and western blotting were performed to analyse the expression levels of inflammatory factors (IL-1β, IL-18), lncRNA NEAT1, miR-22-3p, NLRP3 and cleaved caspase-1. Luciferase reporter experiments were performed to verify the association between lncRNA NEAT1 and miR-22-3p. The results indicated that GAS could significantly improve the neurological scores of rats and reduce the area of cerebral infarction. Meanwhile, GAS inhibited pyroptosis by downregulating NLRP3, inflammatory factors (IL-1β, IL-18) and cleaved caspase-1. In addition, GAS attenuated I/R-induced inflammation in neuronal cells through the modulation of the lncRNA NEAT1/miR-22-3p axis. GAS significantly attenuated cerebral I/R injury via modulation of the lncRNA NEAT1/miR-22-3p axis. Thus, GAS might serve as a new agent for the treatment of cerebral I/R injury.
ISSN:0364-3190
1573-6903
DOI:10.1007/s11064-021-03285-2