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Benzydamine attenuates microglia-mediated neuroinflammation and ischemic brain injury by targeting cathepsin s

Yuxin Zhang1, Lixuan Yang2, Yonghui Gan1

  • 1Department of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210008, China; Department of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210008, China.

International Immunopharmacology
|December 19, 2024
PubMed

Insights

Benzydamine (BA) reduces neuroinflammation and brain injury after ischemic stroke by inhibiting microglia activation. This non-steroidal anti-inflammatory drug targets cathepsin S, offering a new neuroprotective strategy.

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Microglia are key immune cells in the central nervous system, driving neuroinflammation in ischemic stroke.
  • Targeting neuroinflammation is a critical strategy for improving stroke outcomes.
  • Benzydamine (BA), an NSAID, shows anti-inflammatory potential but its role in stroke-related microglial activation is unknown.

Purpose of the Study:

  • To investigate the effect of Benzydamine (BA) on microglial activation and neuroinflammation in ischemic stroke.
  • To determine if BA can mitigate brain injury in experimental stroke models.
  • To elucidate the molecular mechanism underlying BA's action in neuroinflammation.

Main Methods:

  • Primary microglia were stimulated with lipopolysaccharide (LPS) to assess inflammatory responses.
  • Benzydamine (BA) treatment effects on inflammatory markers (e.g., IL-1β mRNA) were quantified.
  • Experimental stroke mice were used to evaluate BA's efficacy in mitigating brain injury and neuroinflammation.
  • The interaction of BA with cathepsin S (CTSS) was investigated.

Main Results:

  • BA significantly suppressed LPS-induced pro-inflammatory responses in primary microglia, reducing IL-1β mRNA levels by up to 59.1% at 10 μM.
  • BA treatment attenuated ischemic brain injury and neuroinflammation in experimental stroke mice.
  • BA was found to directly inhibit cathepsin S (CTSS) activity, reducing pro-inflammatory factor release and microglial activation.

Conclusions:

  • Benzydamine (BA) effectively suppresses microglial activation and neuroinflammation post-ischemic stroke.
  • BA acts as a cathepsin S (CTSS) inhibitor, offering a novel mechanism for neuroprotection.
  • BA presents a promising therapeutic candidate for managing ischemic stroke and associated neuroinflammation.
Keywords:
BenzydamineIschemic strokeMicrogliaNeuroinflammationcathepsin S(CTSS)

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