The effects of oxyresveratrol abrogates inflammation and oxidative stress in rat model of spinal cord injury.

Abstract

Oxyresveratrol and its glycoside are important natural active materials. As an effective tyrosine kinase inhibitor, oxyresveratrol may prevent herpes virus infection, inflammation and oxidative stress, as well as protect nerves. In addition, it is known to inhibit cell apoptosis following cerebral ischemia. In recent years, oxyresveratrol and its glycoside have been widely investigated, and their useful biological activities have been explored, indicating that they may be worthy of further comprehensive research. The aim of the present study was to evaluate the photoprotective effects of oxyresveratrol and its ability to abrogate inflammation and oxidative stress in a rat model of spinal cord injury (SCI). The authors identified that oxyresveratrol significantly reversed the SCI‑induced inhibition of Basso, Beattie, and Bresnahan scores, inhibited the SCI‑mediated increase in spinal cord water content, significantly suppressed SCI‑induced nuclear factor‑κB/p65, tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6 activities and reversed the malondialdehyde, superoxide dismutase, glutathione (GSH) and GSH peroxidase activities in SCI rats. SCI‑induced granulocyte‑macrophage colony‑stimulating factor (GM‑CSF), inducible nitric oxide synthase (iNOS) and cyclo‑oxygenase‑2 (COX‑2) protein expression was significantly suppressed by oxyresveratrol, and SCI‑mediated inhibition of nuclear factor (erythroid‑derived 2)‑like 2 (Nrf2) protein expression was significantly increased by oxyresveratrol. In conclusion, these results suggest that the effects of oxyresveratrol restores SCI, and abrogates inflammation and oxidative stress in rat model of SCI via the GM‑CSF, iNOS, COX‑2 and Nrf2 signaling pathway.

• Authors: Hongmei Du, Lili Ma, Guangdong Chen, Shan Li
• Journal: Molecular medicine reports (Mol Med Rep) Vol. 17 Issue 3 Pg. 4067-4073 (03 2018) ISSN: 1791-3004 [Electronic] Greece
• PMID: 29257323 (Publication Type: Journal Article)

Chemical References

• Antioxidants
• IL1B protein, rat
• Interleukin-1beta
• Interleukin-6
• Neuroprotective Agents
• Plant Extracts
• Rela protein, rat
• Stilbenes
• Transcription Factor RelA
• Tumor Necrosis Factor-alpha
• puag-haad
• Malondialdehyde
• Granulocyte-Macrophage Colony-Stimulating Factor
• Glutathione Peroxidase
• Nitric Oxide Synthase Type II
• Nos2 protein, rat
• Superoxide Dismutase

Topics

• Animals
• Antioxidants (pharmacology)
• Disease Models, Animal
• Drug Administration Schedule
• Female
• Gene Expression Regulation
• Glutathione Peroxidase (genetics, metabolism)
• Granulocyte-Macrophage Colony-Stimulating Factor (genetics, metabolism)
• Inflammation
• Injections, Intraperitoneal
• Interleukin-1beta (antagonists & inhibitors, genetics, metabolism)
• Interleukin-6 (antagonists & inhibitors, genetics, metabolism)
• Locomotion (drug effects)
• Malondialdehyde (metabolism)
• Neuroprotective Agents (pharmacology)
• Nitric Oxide Synthase Type II (genetics, metabolism)
• Oxidative Stress
• Plant Extracts (pharmacology)
• Rats
• Rats, Sprague-Dawley
• Spinal Cord (drug effects, metabolism, pathology)
• Spinal Cord Injuries (drug therapy, genetics, metabolism, pathology)
• Stilbenes (pharmacology)
• Superoxide Dismutase (genetics, metabolism)
• Transcription Factor RelA (antagonists & inhibitors, genetics, metabolism)
• Tumor Necrosis Factor-alpha (antagonists & inhibitors, genetics, metabolism)