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Neuroprotective effect of fisetin against cerebral ischemia-reperfusion damage via suppression of oxidative stress and inflammatory parameters

Blood Daily News

2021 MAR 25 (NewsRx) -- By a News Reporter-Staff News Editor at Blood Daily News -- Fresh data on Central Nervous System Diseases and Conditions - Brain Ischemia are presented in a new report. According to news reporting from Shaanxi, People’s Republic of China, by NewsRx journalists, research stated, “It is well established that inflammatory reactions and oxidative stress play an imperial role in cerebral ischemia-reperfusion pathogenesis. Fisetin is a flavonoid and has an antioxidant and anti-inflammatory effect on various diseases.”

The news correspondents obtained a quote from the research from the Department of Neurosurgery, “In this study, we have been working to examine the neuroprotective effect of fisetin in brain injuries triggered by cerebral ischemic-reperfusion and explore the potential role of nuclear factor kappa B (NF-kappa B) signaling. In vitro, fisetin was examined against the cell viability, lactate dehydrogenase (LDH) leakage, cytokines, and apoptosis after ischemia/reperfusion (I/R) induced in the cells. In vivo, I/R injury was induced in the brain via transient middle cerebral artery occlusion (2 h) and reperfusion (20 h). The infarction area, brain water content, and neurofunctional parameters were also estimated. Inflammatory cytokines and brain injury markers were scrutinized at the end of the study. Fisetin treatment alleviated cell injury and suppressed the inflammatory cytokines (interleukin-1 (IL-1), tumor necrosis factor- alpha (TNF-alpha), inducible nitric oxide synthase (iNOS), interleukin-1 beta (IL-1 beta), cyclooxygenase-2 (COX-2), interleukin-16 (IL-6), and prostaglandin E-2 (PGE(2))) and antioxidant parameters in a dose-dependent manner. Fisetin significantly (P < 0.001) reduced the infarct volume, brain water content. Fisetin significantly (P < 0.001) suppressed the neurological parameters and inflammatory cytokines such as IL-1, TNF-alpha, iNOS, IL-1 beta, COX-2, IL-6, PGE(2), and oxidative markers in a dose-dependent manner. Fisetin significantly (P < 0.001) reduced the inflammatory mediators including NF-kappa B and intercellular adhesion molecule 1 (ICAM-1). Further studies also showed that fisetin significantly inhibited the NF-kappa B activity via inflammatory and antioxidant pathways.”

According to the news reporters, the research concluded: “By suppressing inflammatory cytokines, fisetin protected the brain tissue against I/R injury, and this effect could be due to reduced NF-kappa B activity.”

This research has been peer-reviewed.

For more information on this research see: Neuroprotective Effect of Fisetin Against the Cerebral Ischemia-reperfusion Damage Via Suppression of Oxidative Stress and Inflammatory Parameters. Inflammation, 2021. Inflammation can be contacted at: Springer|plenum Publishers, 233 Spring St, New York, NY 10013, USA. (Springer - www.springer.com; Inflammation - http://www.springerlink.com/content/0360-3997/)

Our news journalists report that additional information may be obtained by contacting Jian Cui, Xian 1 Hosp, Dept. of Neurosurgery, 30 South St, Powder Lane, Xian 710002, Shaanxi, People’s Republic of China.

The direct object identifier (DOI) for that additional information is: https://doi.org/10.1007/s10753-021-01434-x. This DOI is a link to an online electronic document that is either free or for purchase, and can be your direct source for a journal article and its citation.

(Our reports deliver fact-based news of research and discoveries from around the world.)