Neuroprotective effect of resveratrol against radiation after surgically induced brain injury by reducing oxidative stress, inflammation, and apoptosis through NRf2/HO-1/NF-κB signaling pathway

J Biochem Mol Toxicol. 2020 Dec;34(12):e22600. doi: 10.1002/jbt.22600. Epub 2020 Aug 20.

Abstract

The impact of resveratrol (RSV) on radiation (RAD)-induced brain injury in rats' brains was investigated. A total of 40 male Wistar Albino rats were randomly divided into four groups (control, RAD, RAD + RSV, and RSV groups, with 10 rats in each group). The results revealed a significant decrease in catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase activities, as well as glutathione (GSH) content. Further, a significant elevation in malondialdehyde, nitric oxide, interleukin-1-beta (IL-1β), IL-6, and transforming growth factor-β1 levels were observed. Furthermore, decreased B-cell lymphoma 2 (Bcl-2), increased Bcl-2-associated X, and tumor necrosis factor-α genes expression, decreased nuclear factor erythroid-related factor 2, heme oxygenase-1, and increased nuclear factor-κB protein levels were noticed. Also, an apoptosis marker, caspase-3-positive cells, was seen in the hippocampus. Those effects were observed in the RAD group of rats. The treatment of RSV displayed a significant amendment of the studied parameters in the brain tissues of the RAD group of animals. This effect is interrelated to the ability of RSV to scavenge the free radicals, enhance the activity of the antioxidant enzymes, increase GSH contents, and downregulate the inflammatory responses and apoptosis markers in the brain tissues of RAD animals. In conclusion, this study demonstrated that the potent antioxidant, anti-inflammatory, and antiapoptotic activities of RSV can improve the antioxidant status and suppress the inflammatory responses and apoptosis in the brain tissues of RAD animals.

Keywords: Bcl-2; NF-κB; Nrf2; caspase-3; neurosurgery; radiation; resveratrol.

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Brain Injuries / etiology*
  • Brain Injuries / metabolism
  • Heme Oxygenase (Decyclizing) / metabolism
  • Male
  • NF-E2-Related Factor 2 / metabolism
  • NF-kappa B / metabolism
  • Neuroprotective Agents / pharmacology*
  • Oxidative Stress / drug effects*
  • Rats
  • Rats, Wistar
  • Resveratrol / pharmacology*
  • Signal Transduction / drug effects*

Substances

  • NF-E2-Related Factor 2
  • NF-kappa B
  • Neuroprotective Agents
  • Nfe2l2 protein, rat
  • Heme Oxygenase (Decyclizing)
  • Hmox1 protein, rat
  • Resveratrol