PUBLICATION
Rutin protects hemorrhagic stroke development via supressing oxidative stress and inflammatory events in a zebrafish model
- Authors
- Rana, A.K., Sharma, S., Saini, S.K., Singh, D.
- ID
- ZDB-PUB-220427-4
- Date
- 2022
- Source
- European Journal of Pharmacology 925: 174973 (Journal)
- Registered Authors
- Singh, Damanpreet
- Keywords
- Flavonoid, Glycogen synthase kinase-3 beta, Haemorrhagic stroke, Matrix metalloproteinases, Protein carbonylation, β-catenin
- MeSH Terms
-
- Animals
- Glycogen Synthase Kinase 3 beta/metabolism
- Hemorrhagic Stroke*
- NF-E2-Related Factor 2/metabolism
- Oxidative Stress
- Rutin/pharmacology
- Rutin/therapeutic use
- Stroke*/drug therapy
- Stroke*/prevention & control
- Zebrafish/metabolism
- PubMed
- 35469838 Full text @ Eur. J. Pharmacol.
Citation
Rana, A.K., Sharma, S., Saini, S.K., Singh, D. (2022) Rutin protects hemorrhagic stroke development via supressing oxidative stress and inflammatory events in a zebrafish model. European Journal of Pharmacology. 925:174973.
Abstract
Intracerebral haemorrhagic (ICH) stroke is a major cause of death and disability globally, with no proper treatment available so far. Rutin, a dietary flavonoid, has shown protection against cerebral ischemic stroke due to its antioxidant and anti-inflammatory attributes. However, the efficacy of rutin against ICH stroke remained unexplored. Therefore, in the current study, we investigated the effect of rutin in an ICH stroke zebrafish larva model. The larvae were exposed to atorvastatin (1.25 μM) in system water for induction of experimental ICH. Rutin treatment reduced the hematoma size, ROS production and decreased apoptosis in the zebrafish larvae brains. Reduction in the malondialdehyde and protein carbonyl level in the rutin-treated larvae also indicated quenching of the free radicals. The treatment increased the expression of tight junction protein claud5a and decreased the mRNA level of matrix metalloproteases (mmp2 and mmp9). Furthermore, rutin treatment also attenuated the genomic expression of oxidative markers (nrf2, hmox1a, sod1, and gpx) and inflammatory genes (il6, tnfa, il10, and irf2a) related to ICH. The Gsk-3β activity was also downregulated, and a normal pool of β-catenin and Nrf2 was maintained in the larvae treated with rutin. The current study suggested that rutin protects ICH stroke via suppressing oxidative stress and inflammatory events in a zebrafish model.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping