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Journal of Chinese Pharmaceutical Sciences ›› 2026, Vol. 35 ›› Issue (1): 38-53.DOI: 10.5246/jcps.2026.01.003

• Original articles • Previous Articles     Next Articles

Baicalein attenuates neuroinflammation in thrombotic stroke by downregulating the TLR4/MyD88/NF-κB signaling pathway

Yufu Shang, Dongni Liu, Wenfang Zhang, Wandi Feng, Danhong Feng, Shuang Xu, Wenle Zhao, Guanhua Du, Yuehua Wang*()   

  1. Beijing Key Laboratory of Innovative Drug Discovery and Polymorphic Druggability Research for Cerebrovascular Diseases, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China
  • Received:2025-09-04 Revised:2025-10-20 Accepted:2025-11-05 Online:2026-01-31 Published:2026-01-31
  • Contact: Yuehua Wang
  • Supported by:
    The Natural Science Foundation of Beijing Municipality (Grant No. 7232299) and the CAMS Innovation Fund for Medical Sciences (CIFMS, 2021-I2M-1-069).

Abstract:

Baicalein (BAI) has been reported to offer neuroprotection against cerebral ischemia. However, its effects on thrombotic cerebral stroke have yet to be fully elucidated. In the present study, we aimed to explore both the efficacy and underlying mechanisms of BAI in a mouse model of photothrombotic-induced thrombotic cerebral stroke. BAI demonstrated significant protective effects against neuronal injury and reduced the infarct area in mice subjected to thrombotic cerebral stroke. Furthermore, BAI lowered the levels of pro-inflammatory cytokines and chemokines within cortical tissues, suppressed glial cell activation, inhibited neuronal apoptosis, and attenuated apoptotic processes throughout the progression of thrombotic stroke. Importantly, additional investigations revealed that BAI downregulated the TLR4/MyD88/NF-κB signaling pathway. In conclusion, BAI exerted neuroprotective effects during the subacute phase of thrombotic cerebral stroke, likely through its anti-neuroinflammatory action mediated by inhibition of the TLR4/MyD88/NF-κB pathway. These findings offered new insights into the molecular mechanisms by which BAI might contribute to the treatment of thrombotic cerebral stroke.

Key words: Baicalein, Ischemic stroke, Neuroinflammation

Supporting: