Kaiyi Lai, Jiayu Zhang, Wenbo Gao, Yu Jiang, Ying Liu
LQ exerts diverse pharmacological effects through coordinated regulation of multiple signaling pathways. Its anti-inflammatory is primarily associated with suppression of NF-κB signaling and NLRP3 inflammasome, coupled with upregulation of the Nrf2-dependent antioxidant pathway. Anticancer effects involve suppression of tumor growth, metastasis, and survival through modulation of ER, ERK, PI3K/AKT/mTOR, HSP90, and glutamate receptor signaling pathways. Hepatoprotection is facilitated through PI3K/AKT-driven metabolic regulation and inhibition of TGF-β1/Smadmediated fibrotic processes. Neuroprotective effects are linked to ERβ activation, stimulation of the BDNF/ERK/CREB axis, and downregulation of PI3K/AKT/mTOR signaling. Cardioprotection involves attenuation of fibrosis, oxidative stress, and calcium overload. In the skeletal system, LQ promotes osteogenesis while inhibiting osteoclast activity. Additional protective effects have been documented in renal, testicular, cutaneous, and embryonic tissues through diverse signaling pathways.
INTRODUCTION: Liquiritigenin (LQ), a bioactive flavonoid derived from licorice, exhibits a wide range of pharmacological activities. This review comprehensively summarizes the therapeutic potential of LQ and elucidates the molecular mechanisms underlying its principal effects, including hepatoprotective, anticancer, anti-inflammatory, cardioprotective, neuroprotective, and boneprotective activities.
METHODS: A literature search was conducted using PubMed, ResearchGate, and Web of Science. Studies investigating the therapeutic efficacy of LQ and related signaling pathways were selected for critical analysis.
RESULTS: LQ exerts diverse pharmacological effects through coordinated regulation of multiple signaling pathways. Its anti-inflammatory is primarily associated with suppression of NF-κB signaling and NLRP3 inflammasome, coupled with upregulation of the Nrf2-dependent antioxidant pathway. Anticancer effects involve suppression of tumor growth, metastasis, and survival through modulation of ER, ERK, PI3K/AKT/mTOR, HSP90, and glutamate receptor signaling pathways. Hepatoprotection is facilitated through PI3K/AKT-driven metabolic regulation and inhibition of TGF-β1/Smadmediated fibrotic processes. Neuroprotective effects are linked to ERβ activation, stimulation of the BDNF/ERK/CREB axis, and downregulation of PI3K/AKT/mTOR signaling. Cardioprotection involves attenuation of fibrosis, oxidative stress, and calcium overload. In the skeletal system, LQ promotes osteogenesis while inhibiting osteoclast activity. Additional protective effects have been documented in renal, testicular, cutaneous, and embryonic tissues through diverse signaling pathways.
DISCUSSION AND CONCLUSION: This review consolidates evidence for the multifaceted pharmacological activities of LQ and provides a mechanistic synthesis of its actions. These findings offer a valuable framework for future preclinical and translational investigations while highlighting important opportunities and challenges for further development.