Flavonoids From Qi-Regulating and Blood-Stasis-Resolving Traditional Chinese Medicines Against Qi Stagnation and Blood Stasis: A Pharmacological Review

Qi stagnation and blood stasis (QSBS) is a core pathogenesis in traditional Chinese medicine (TCM), with clinical correlates to multifactorial modern diseases involving inflammation, microvascular occlusion, oxidative injury, and neuroendocrine-immune dysregulation. This review comprehensively summarizes the flavonoid constituents from Qi- and Blood-regulating TCM herbs and examines the pharmacological mechanisms that may contribute to their efficacy against QSBS. A comprehensive literature search was conducted using PubMed, Web of Science, and China National Knowledge Infrastructure (CNKI) databases, focusing on studies of the chemical constituents and pharmacology of flavonoids related to “activating blood, resolving stasis, regulating Qi, and dissipating masses.” Flavonoids, representative bioactive constituents of Qi- and Blood-regulating TCMs (e.g., Salvia miltiorrhiza and Ligusticum chuanxiong ), have shown potential for QSBS intervention due to their polypharmacological profiles. Key flavonoids such as hydroxysafflor yellow A, quercetin, luteolin, hesperidin, and naringenin have been reported to act through multiple signaling pathways (NF-κB, Nrf2, and MAPK), covering antioxidative stress, anti-inflammation, microcirculation restoration, and platelet inhibition. However, most mechanistic evidence is derived from isolated compounds and preclinical models, and human pharmacokinetic data remain limited. Flavonoids represent one important class of bioactive constituents that may contribute to QSBS intervention. Their coordinated regulation of multiple cascades is consistent with the TCM doctrine of “Qi-blood co-regulation.” This review provides a theoretical basis for the development of flavonoid-based therapeutics and their potential clinical application. Because direct evidence linking flavonoids to measurable neuroendocrine and neuroimmune endpoints in QSBS remains scarce, the neuro-vascular-immune interpretation of “Qi” is presented here as a hypothesis-generating framework rather than an established mechanism.