Tongqiao Huoxue decoction alleviates neurological impairment following ischemic stroke via the PTGS2/NF-kappa B axis

• Published in: Brain research 2023-04, Vol.1805, p.148247-148247, Article 148247
• Main Authors: Zhou, Zheyi, Dun, Linglu, Yang, Qian, Tao, Jingrui, Yu, Peishan, Xu, Hong, Zhao, Na, Zheng, Na, An, Hongwei, Yi, Ping
• Format: Article
• Language: English
• Subjects: Animals; Brain Ischemia - genetics; Cyclooxygenase 2 - metabolism; Ischemic Stroke; Mice; Mice, Inbred C57BL; Network pharmacology; Neurological impairment; NF-kappa B - metabolism; NF-kappa B signaling pathway; Prostaglandin-endoperoxide synthase 2; Signal Transduction - genetics; Stroke - genetics; Tongqiao Huoxue decoction
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2023.148247

•TQHXD protects against neurological impairment induced by IS.•TQHXD protects IS-induced neurological damage by downregulating PTGS2.•TQHXD downregulates NF-kappa B and PTGS2 expression in OGD/R-exposed cells.•TQHXD inhibits OGD/R-caused neuronal cell apoptosis and alleviates inflammation.•The study offers a theoretical basis for identification of molecular targets for IS. Traditional Chinese medicine has emerged as promising targets for ischemic stroke (IS) therapy, yet the mechanism remains elusive. The current study was performed with an aim to investigate the action and mechanism of Tongqiao Huoxue decoction (TQHXD) affecting the neurological impairment secondary to IS based on network pharmacology. Based on network pharmacology and bioinformatics analysis, target genes and pathways involved in the treatment of TQHXD against IS were predicted. Serum containing TQHXD was prepared through blood collection from C57BL/6 mice after intragastric administration of TQHXD. The main results exhibited that Prostaglandin-endoperoxide synthase 2 (PTGS2) exhibited an abundance in IS and enrichment in the NF-kappa B signaling pathway, holding the potential as targets related to TQHXD treatment for IS. TQHXD was found to rescue cell viability, inhibit apoptosis, and alleviate inflammation under oxygen and glucose deprivation and reoxygenation (OGD/R) exposure. Furthermore, our in vivo experiment validated the protective function of TQHXD in ischemic brain damage stimulated by middle cerebral artery occlusion (MCAO). This protective action of TQHXD could be attenuated by overexpressing nuclear factor (NF)-kappa B, which was dependent on PTGS2. Collectively, TQHXD was demonstrated to ameliorate IS-induced neurological impairment by blocking the NF-kappa B signaling pathway and down-regulating PTGS2.