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Background <p>During acute ischemic stroke, a cascade of pathophysiological reactions leads to brain cell injury, primarily via disruptions in energy metabolism and increased oxidative stress. In this study, we scrutinized the neuroprotective effects of bryodulcosigenin (BRY) against acute cerebral ischemia/reperfusion (CIR) injury in rats.</p> Material and methods <p>To induce middle cerebral artery occlusion (MCAO) in rats, a nylon monofilament suture with a silicon-coated tip was inserted into the internal carotid artery. The cerebral infarct volume, brain water content, neurological deficits, brain edema, Evan Blue extravasation and blood brain barrier (BBB) leakage were estimated. The antioxidant, cytokines, inflammatory and matrix metalloproteinases (MMP) parameters were evaluated. mRNA expression and histopathological study were performed.</p> Results <p>Bryodulcosigenin significantly suppressed the neurological deficits, cerebral infarct volume, brain edema, brain water content, BBB leakage and Evan Blue extravasation. It also suppressed brain injury markers like K<sup>+</sup>-Cl<sup>−</sup> cotransporter 1 (KCC1), S100 calcium-binding protein B (S-100β), neuron specific enolase (NSE), occludin and clusterin. Moreover, bryodulcosigenin altered antioxidant levels via enhancing the level of glutathione peroxidase (GPx), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), while reducing malonaldehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OhdG). It altered the pro-inflammatory cytokines like tumor necrosis factor-α (TNF-α), interleukin (IL)-1, IL-1β, IL-4, IL-6, IL-10, as well as inflammatory mediators such as inducible nitric oxide (iNOS), cyclooxygenase-2 (COX-2), vascular endothelium growth factor (VEGF), prostaglandin (PGE<sub>2</sub>), nuclear factor kappa B (NF-κB) and MMP (MMP-2, MMP-3 and MMP-9) level in the serum and brain tissue. Additionally, bryodulcosigenin modulated the mRNA expression of Toll-Like Receptor 4 (TLR4), syndecan-1, cerebrospinal fluid (CSF), aquaporin-1 (AQP1), organic cation transporter 3 (OCT3), reduced expression 1 (REX1) and improved the histopathological condition.</p> Conclusion <p>Bryodulcosigenin exerted anti-inflammatory and neuroprotective effects against CIR injury via alteration of TLR4/NF-κB signaling pathways.</p>

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Anti-inflammatory and neuroprotective effect of bryodulcosigenin against cerebral ischemia/reperfusion injury via modulation of inflammatory signaling pathways

  • 期刊论文

  • 发表日期：

    2025年11月21日

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  • Xiaoran Zhang,
  • Bohu Liu,
  • Dongchuan Shao,
  • Zhe Li,
  • Xiwen Lin,
  • Zhiwei Cao,
  • Wenbiao Huang,
  • Ankit Kumar,
  • Tianhong Wang,
  • Nan Zhao

摘要

Background

During acute ischemic stroke, a cascade of pathophysiological reactions leads to brain cell injury, primarily via disruptions in energy metabolism and increased oxidative stress. In this study, we scrutinized the neuroprotective effects of bryodulcosigenin (BRY) against acute cerebral ischemia/reperfusion (CIR) injury in rats.

Material and methods

To induce middle cerebral artery occlusion (MCAO) in rats, a nylon monofilament suture with a silicon-coated tip was inserted into the internal carotid artery. The cerebral infarct volume, brain water content, neurological deficits, brain edema, Evan Blue extravasation and blood brain barrier (BBB) leakage were estimated. The antioxidant, cytokines, inflammatory and matrix metalloproteinases (MMP) parameters were evaluated. mRNA expression and histopathological study were performed.

Results

Bryodulcosigenin significantly suppressed the neurological deficits, cerebral infarct volume, brain edema, brain water content, BBB leakage and Evan Blue extravasation. It also suppressed brain injury markers like K+-Cl− cotransporter 1 (KCC1), S100 calcium-binding protein B (S-100β), neuron specific enolase (NSE), occludin and clusterin. Moreover, bryodulcosigenin altered antioxidant levels via enhancing the level of glutathione peroxidase (GPx), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), while reducing malonaldehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OhdG). It altered the pro-inflammatory cytokines like tumor necrosis factor-α (TNF-α), interleukin (IL)-1, IL-1β, IL-4, IL-6, IL-10, as well as inflammatory mediators such as inducible nitric oxide (iNOS), cyclooxygenase-2 (COX-2), vascular endothelium growth factor (VEGF), prostaglandin (PGE2), nuclear factor kappa B (NF-κB) and MMP (MMP-2, MMP-3 and MMP-9) level in the serum and brain tissue. Additionally, bryodulcosigenin modulated the mRNA expression of Toll-Like Receptor 4 (TLR4), syndecan-1, cerebrospinal fluid (CSF), aquaporin-1 (AQP1), organic cation transporter 3 (OCT3), reduced expression 1 (REX1) and improved the histopathological condition.

Conclusion

Bryodulcosigenin exerted anti-inflammatory and neuroprotective effects against CIR injury via alteration of TLR4/NF-κB signaling pathways.