RESUMEN
The incidence of depression has been steadily rising in recent years, making it one of the most prevalent mental illnesses. As the pursuit of novel antidepressant drugs captivates the pharmaceutical field, the therapeutic efficacy of Traditional Chinese Medicine (TCM) has been widely explored. Chaihu (Bupleurum) has been traditionally used for liver conditions such as hepatitis, liver inflammation, liver fibrosis, and liver cancer. It is believed to have hepatoprotective effects, promoting liver cell regeneration and protecting against liver damage. In addition, Bupleurum has also been used as a Jie Yu (depression-relieving) medicine in China, Japan, Republic of Korea, and other Asian countries for centuries. This review article aims to summarize the research conducted on the antidepressant properties and mechanisms of Bupleurum, as well as discuss the potential of TCM formulas containing Bupleurum. This review highlights various antidepressant ingredients isolated from Bupleurum, including saikosaponin A, saikosaponin D, rutin, puerarin, and quercetin, each with distinct mechanisms of action. Additionally, Chinese herb prescriptions and extracts containing Bupleurum, such as Chaihu Shugansan, Xiaoyaosan, and Sinisan, are also included due to their demonstrated antidepressant effects. This review reveals that these Bupleurum compounds exhibit antidepressant effects through the regulation of neurotransmitter mechanisms (such as 5-HT and DA), the NMDA (N-methyl-D-aspartate) system, brain-derived neurotrophic factor (BDNF), and other intracellular signaling pathways. Collectively, this comprehensive review provides insights into the multiple applications of Bupleurum in the treatment of depression and highlights its potential as an alternative or complementary approach to traditional therapies. However, it is essential to consider the potential adverse effects and clinical restrictions of Bupleurum despite its promising potential. Further research is needed to elucidate its specific mechanisms of action and evaluate its effectiveness in human subjects.
RESUMEN
BACKGROUND: Parkinson's disease (PD) is one of the most common neurodegenerative diseases in the world. Mitophagy has been implicated in PD etiology for decades and its pharmacological activation is recognized as a promising treatment strategy for PD. For mitophagy initiation, low mitochondrial membrane potential (ΔΨm) is essential. We identified a natural compound morin that could induce mitophagy without affecting ΔΨm. Morin is a flavonoid that can be isolated from fruits like mulberry. PURPOSE: To reveal the effect of morin on the PD mice model and their potential underlying molecular mechanism. METHODS: Mitophagy process induced by morin in N2a cells meditation were measured using flow cytometry and immunofluorescence. JC-1 fluorescence dye used to detect the mitochondrial membrane potential (ΔΨm). The TFEB nuclear translocation were examined by immunofluorescence staining and western blot assay. The PD mice model was induced by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) intraperitoneal administration. RESULTS: We found that morin also promoted nuclear translocation of the mitophagy regulator TFEB and activated the AMPK-ULK1 pathway. In MPTP-induced PD in vivo models, morin protected DA neurons from MPTP neurotoxicity and ameliorated behavioral deficit. CONCLUSION: Although morin was previously reported to be neuroprotective in PD, the detailed molecular mechanisms remain to be elucidated. For the first time, we report morin served as a novel and safe mitophagy enhancer underlying AMPK-ULK1 pathway and exhibited anti-Parkinsonian effects indicating its potential as a clinical drug for PD treatment.