Mechanism of salvianolic acid B neuroprotection against ischemia/reperfusion induced cerebral injury

Brain Res. 2018 Jan 15:1679:125-133. doi: 10.1016/j.brainres.2017.11.027. Epub 2017 Nov 24.

Abstract

The purpose of this study was to evaluate the cerebral protection of salvianolic acid B (Sal B) against cerebral I/R injury and investigate the underlying mechanism. As shown by 2,3,5-Triphenyltetrazolium chloride (TTC) staining and magnetic resonance imaging (MRI) analyses, Sal B significantly reduced cerebral infarct size, and accompanied with improved neurobehavioral functions as indicated by the modified Bederson score and Longa five-point scale. Sal B decreased the production of reactive oxygen species (p < .05, n = 10). The data of Western blotting and reverse transcription quantitative real time polymerase chain reaction (qRT-PCR) analyses showed that the expression of GFAP, Iba1, IL-1β, IL-6, TNF-α and Cleaved-caspase 3 was significantly reduced by Sal B in I/R injured brain tissues as compared to corresponding controls (p < .05, n = 10). Over activation of astrocytes and microglia were inhibited by Sal B as shown by immunostaining of GFAP and Iba 1. These data suggest that Sal B has neural protective effects against I/R-induced cerebral injury and could be an effective candidate for further development of clinical therapy.

Keywords: Danshen; Inflammation; Oxidative stress; Salvianolic acid B; Stroke.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzofurans / therapeutic use*
  • Brain Injuries / drug therapy*
  • Brain Injuries / etiology*
  • Calcium-Binding Proteins / genetics
  • Calcium-Binding Proteins / metabolism
  • Caspase 3 / genetics
  • Caspase 3 / metabolism
  • Cerebral Infarction / etiology
  • Cerebral Infarction / prevention & control
  • Cytokines / genetics
  • Cytokines / metabolism
  • Disease Models, Animal
  • Gene Expression Regulation / drug effects
  • Glial Fibrillary Acidic Protein / genetics
  • Glial Fibrillary Acidic Protein / metabolism
  • Infarction, Middle Cerebral Artery / complications*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Microfilament Proteins / genetics
  • Microfilament Proteins / metabolism
  • Neuroprotective Agents / therapeutic use*
  • Reperfusion / adverse effects*

Substances

  • Aif1 protein, mouse
  • Benzofurans
  • Calcium-Binding Proteins
  • Cytokines
  • Glial Fibrillary Acidic Protein
  • Microfilament Proteins
  • Neuroprotective Agents
  • salvianolic acid B
  • Caspase 3