GPCR-mediated natural products and compounds: Potential therapeutic targets for the treatment of neurological diseases

• Published in: Pharmacological research 2024-10, Vol.208, p.107395, Article 107395
• Main Authors: Wang, Xing Xia, Ji, Xiang, Lin, Jing, Wong, Io Nam, Lo, Hang Hong, Wang, Jian, Qu, Liqun, Wong, Vincent Kam Wai, Chung, Sookja Kim, Law, Betty Yuen Kwan
• Format: Article
• Language: English
• Subjects: Animals; Biological Products - pharmacology; Biological Products - therapeutic use; Central nervous system; Drugs, Chinese Herbal - pharmacology; Drugs, Chinese Herbal - therapeutic use; G protein-coupled receptors; Humans; Natural products; Nervous System Diseases - drug therapy; Nervous System Diseases - metabolism; Neurological disorders; Receptors, G-Protein-Coupled - metabolism; Signal Transduction - drug effects
• ISSN: 1043-6618; 1096-1186; 1096-1186
• DOI: 10.1016/j.phrs.2024.107395

G protein-coupled receptors (GPCRs), widely expressed in the human central nervous system (CNS), perform numerous physiological functions and play a significant role in the pathogenesis of diseases. Consequently, identifying key therapeutic GPCRs targets for CNS-related diseases is garnering immense interest in research labs and pharmaceutical companies. However, using GPCRs drugs for treating neurodegenerative diseases has limitations, including side effects and uncertain effective time frame. Recognizing the rich history of herbal treatments for neurological disorders like stroke, Alzheimer's disease (AD), and Parkinson's disease (PD), modern pharmacological research is now focusing on the understanding of the efficacy of traditional Chinese medicinal herbs and compounds in modulating GPCRs and treatment of neurodegenerative conditions. This paper will offer a comprehensive, critical review of how certain natural products and compounds target GPCRs to treat neurological diseases. Conducting an in-depth study of herbal remedies and their efficacies against CNS-related disorders through GPCRs targeting will augment our strategies for treating neurological disorders. This will not only broaden our understanding of effective therapeutic methodologies but also identify the root causes of altered GPCRs signaling in the context of pathophysiological mechanisms in neurological diseases. Moreover, it would be informative for the creation of safer and more effective GPCR-mediated drugs, thereby establishing a foundation for future treatment of various neurological diseases. [Display omitted]