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Siji Antiviral Mixture Protects against CA16 Induced Brain Injury through Inhibiting PERK/STAT3/NF-κB Pathway

Huimin Xiao1, Rong Zhao2, Yue He1

  • 1Department of Chinese Materia Medica and Natural Medicines, Air Force Medical University, No. 169, West Changle Road, Xi'an 710032, China.

Biomed Research International
|September 7, 2018
PubMed

Insights

Siji Antiviral Mixture (SAM) effectively treats Coxsackievirus 16 (CA16) infections, reducing hand, foot, and mouth disease symptoms and preventing brain injury in mice by inhibiting key inflammatory pathways.

Area of Science:

  • Virology
  • Neuroscience
  • Pharmacology

Background:

  • Coxsackievirus 16 (CA16) is a significant pathogen causing hand, foot, and mouth disease (HFMD) in infants and young children.
  • CA16 infection can lead to severe neurological complications, highlighting the need for effective treatments.

Purpose of the Study:

  • To investigate the antiviral and neuroprotective effects of Siji Antiviral Mixture (SAM) against CA16 infection.
  • To elucidate the molecular mechanisms underlying SAM's protective actions.

Main Methods:

  • In vivo studies using neonatal mice and in vitro studies using SH-SY5Y cells infected with CA16.
  • ELISA and Western blotting were employed to assess cytokine levels and protein expression.
  • Gene silencing (siRNA transfection) and High-Performance Liquid Chromatography (HPLC) were utilized to explore mechanisms and characterize SAM.

Main Results:

  • SAM treatment reduced clinical scores and delayed disease progression in CA16-infected mice.
  • SAM significantly decreased markers of cell damage (LDH, CK-MB), apoptosis (caspase 3, Bax), ER stress, and inflammation.
  • CA16-induced ER stress and inflammation were found to be mediated through the PERK/STAT3/NF-κB signaling pathway.

Conclusions:

  • Siji Antiviral Mixture (SAM) demonstrates significant potential in combating CA16 infection and mitigating associated brain injuries.
  • The protective effects of SAM are attributed to its ability to inhibit the PERK/STAT3/NF-κB signaling pathway, thereby reducing ER stress and inflammation.

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