Frontiers in Pharmacology (Apr 2021)

Galectin-3 Mediated Inflammatory Response Contributes to Neurological Recovery by QiShenYiQi in Subacute Stroke Model

  • Yule Wang,
  • Yule Wang,
  • Yule Wang,
  • Shuang He,
  • Shuang He,
  • Xinyan Liu,
  • Xinyan Liu,
  • Zhixiong Li,
  • Zhixiong Li,
  • Lin Zhu,
  • Lin Zhu,
  • Guangxu Xiao,
  • Guangxu Xiao,
  • Xiaoli Du,
  • Xiaoli Du,
  • Xiaoli Du,
  • Hongxia Du,
  • Hongxia Du,
  • Wen Zhang,
  • Wen Zhang,
  • Yiqian Zhang,
  • John Orgah,
  • John Orgah,
  • Yuxin Feng,
  • Yuxin Feng,
  • Boli Zhang,
  • Yan Zhu,
  • Yan Zhu

DOI
https://doi.org/10.3389/fphar.2021.588587
Journal volume & issue
Vol. 12

Abstract

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Effective therapies for stroke are still limited due to its complex pathological manifestations. QiShenYiQi (QSYQ), a component-based Chinese medicine capable of reducing organ injury caused by ischemia/reperfusion, may offer an alternative option for stroke treatment and post-stroke recovery. Recently, we reported a beneficial effect of QSYQ for acute stroke via modulation of the neuroinflammatory response. However, if QSYQ plays a role in subacute stroke remains unknown. The pharmacological action of QSYQ was investigated in experimental stroke rats which underwent 90 min ischemia and 8 days reperfusion in this study. Neurological and locomotive deficits, cerebral infarction, brain edema, and BBB integrity were assessed. TMT-based quantitative proteomics were performed to identify differentially expressed proteins following QSYQ treatment. Immunohistochemistry, western blot analysis, RT-qPCR, and ELISA were used to validate the proteomics data and to reveal the action mechanisms. Therapeutically, treatment with QSYQ (600 mg/kg) for 7 days significantly improved neurological recovery, attenuated infarct volume and brain edema, and alleviated BBB breakdown in the stroke rats. Bioinformatics analysis indicated that protein galectin-3 and its mediated inflammatory response was closely related to the beneficial effect of QSYQ. Specially, QSYQ (600 mg/kg) markedly downregulated the mRNA and protein expression levels of galectin-3, TNF-α, and IL-6 in CI/RI brain as well as serum levels of TNF-α and IL-6. Overall, our findings showed that the effective action of QSYQ against the subacute phase of CI/RI occurs partly via regulating galectin-3 mediated inflammatory reaction.

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