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Moracin O, CAS number 123702-97-6, is a natural 2-aryl benzofuran compound isolated from mulberry (Morus alba Linn.). In recent years, as the importance of natural products in drug development has become increasingly prominent, Sanxin O has gradually become a hot topic in pharmacology research due to its remarkable biological activity, especially its potential applications in neuroprotection, anti-inflammation, and anti-tumor fields. Sansinin O not only strongly inhibits hypoxia-inducing factor-1α (HIF-1α), but also effectively reduces the production of reactive oxygen species (ROS) induced by oxygen glucose deprivation (OGD), demonstrating good antioxidant and cell-protective functions. This paper aims to systematically review the chemical structure and physicochemical properties of Sanxin O (Oxin O), plant origin and extraction methods, pharmacological activity, mechanism of action, druggability evaluation, and its clinical application prospects, aiming to provide a theoretical foundation and reference for related research and development.
Sancinin O belongs to the 2-aryl benzofuran class of natural products, with a molecular formula of C_20H_18O_5 and a molecular weight of 326.35. Its core structure consists of a benzofuran backbone and aryl side chains, featuring multiple hydroxyl and ether bonds, giving it excellent polarity and hydrogen bond formation capabilities. The LogP value of Sanxin O is 2.8, indicating moderate lipid solubility, with some water and lipid solubility, which is beneficial for distribution in vivo and cell membrane penetration. Its topological pole surface area (TPSA) is 86.18 Ų, and it has 5 hydrogen bond acceptors, suggesting that it may form a stable hydrogen bond network when binding to biological targets.
From a pharmacochemical perspective, Sanxin O is structurally stable and does not exhibit adverse properties such as hepatotoxicity, cardiotoxicity, or hERG channel inhibition, indicating good safety potential. However, its blood-brain barrier penetration capacity is relatively low, which may limit direct action in the central nervous system, but its activity in neuroprotection suggests it may act through indirect mechanisms or metabolites.
Cincintin O is mainly isolated from mulberry trees (Morus alba Linn.). As a traditional Chinese medicinal material and economic crop, mulberry trees are widely distributed across many regions of Asia. The roots, leaves, fruits, and bark of mulberry trees are rich in polyphenols and benzofuran compounds, with Sanxin O being one of the important active ingredients.
Common methods for extracting Sanxin O include solvent extraction, chromatographic separation, and purification. Generally, ethanol or methanol is used as extraction solvents, and crude extracts are obtained by reflux extraction or ultrasound-assisted extraction. Subsequently, silica gel column chromatography and reversed-phase high-performance liquid chromatography (RP-HPLC) were used for separation and purification. In recent years, the application of supercritical CO_2 extraction and membrane separation technologies has also provided new approaches for efficient extraction of Sanxin O. Higher purity sansinol O can be identified and quality controlled through nuclear magnetic resonance (NMR), mass spectrometry (MS), and infrared spectroscopy (IR).
Sancinol O exhibits significant inhibitory effects across various tumor cell lines. Its antitumor mechanism involves multiple signaling pathways and key targets, including MCL1, BCL2, STAT3, MMP2, TOP1, HIF1A, TOP2A, MAPK1, ESR1, and CYP19A1. By inhibiting anti-apoptotic proteins MCL1 and BCL2, Sancinin O promotes tumor cell apoptosis; At the same time, it inhibits cell proliferation and metastasis by blocking the STAT3 signaling pathway. Additionally, inhibition of matrix metalloproteinase MMP2 by Sanxinsu O helps reduce tumor cell invasion and metastasis.
In ischemic stroke models, sanxinsu O exerts significant neuroprotective effects by inhibiting hypoxia-induced factor-1α (HIF1A) and reducing OGD-induced reactive oxygen species (ROS) production. Its antioxidant effect effectively reduces oxidative stress in ischemia-reperfusion injury and lowers the rate of neuronal apoptosis. Additionally, Sancinin O can regulate the nuclear factor κB (NFKB1) signaling pathway, inhibit the expression of the pro-inflammatory cytokine IL-1β, reduce inflammatory responses, and thus protect brain tissue function.
Sancinol O demonstrates good anti-inflammatory activity in chronic inflammatory diseases. Its main targets include nuclear factor κB (NFKB1), tumor necrosis factor α (TNF), interleukin-6 (IL6), cyclooxygenase-2 (PTGS2), and reactive oxygen species (ROS). By inhibiting the expression and activity of these key inflammatory mediators, Sansinol O effectively reduces inflammatory responses and protects tissues from inflammatory damage.
For Alzheimer's and Parkinson's diseases, Sancinsu O has shown certain therapeutic potential. It slows the progression of neurodegenerative lesions by regulating the activities of β-amyloid precursor protein (APP), Tau protein (MAPT), α-synuclein (SNCA), and acetylcholinesterase (ACHE). At the same time, Sanxin O inhibits the reactive oxygen species and nuclear factor κB signaling pathways, helping to alleviate neuroinflammation and protect neuronal function.
The pharmacological activity of Sanxin O is closely related to its multi-target and multi-pathway regulation. Its main mechanisms of action include:
Inhibits hypoxia-inducing factor-1α (HIF-1α)
Sancinol O acts directly or indirectly on HIF-1α, inhibiting its expression and activity under hypoxic conditions, blocking adaptive responses in tumors and ischemic brain injury, and reducing cell viability and inflammatory responses.
Antioxidant effects
Sancinol O significantly reduces the production of OGD-induced reactive oxygen species (ROS), alleviating oxidative stress damage. Its antioxidant mechanism may involve activating endogenous antioxidant enzyme systems and directly scavenging free radicals.
Regulates inflammatory signaling pathways
By inhibiting the expression of nuclear factor κB (NFKB1) and downstream pro-inflammatory factors (TNF, IL-1β, IL-6, PTGS2), Sanxin O effectively suppresses the inflammatory cascade and alleviates tissue inflammatory damage.
Regulates apoptosis and proliferation
Sanxin O promotes tumor cell apoptosis and inhibits cell proliferation and migration by regulating the BCL2 family proteins (MCL1, BCL2), STAT3, and MAPK1 signaling pathways.
Regulation of neuroprotection-related targets
Sanxin O regulates key proteins such as APP, MAP, SNCA, and ACHE in neurodegenerative diseases, slowing pathological protein deposition and neurological dysfunction.
The molecular weight of Sancinol O is 326.35, which fits the drug affinity range of the Lipinski rule. Its LogP value is 2.8, indicating that moderate lipid solubility favors cell membrane penetration. TPSA is 86.18 Ų, with 5 hydrogen bond receptors, indicating appropriate polarity that helps form stable binding to target proteins.
In terms of safety, Sancinsu O showed no hepatotoxicity, cardiotoxicity, or hERG channel inhibition, indicating promising safety potential. However, its low blood-brain barrier penetration limits its potential to act directly on the central nervous system, which may be overcome through drug structural modification or delivery system optimization.
Currently, pharmacokinetic data on Sanxin O are limited. Preliminary studies show that its oral bioavailability is average, metabolism in vivo is mainly carried out through hepatic enzyme systems, and the activity and safety of these metabolites require further research. Future research should focus on its in vivo distribution, metabolic pathways, and excretion mechanisms to guide clinical application and formulation development.
As a multi-target, multifunctional natural product, Sanxin O demonstrates broad pharmacological activity and good safety, showing great clinical application potential. Its role in anti-tumor treatment, ischemic stroke, neurodegenerative diseases, and chronic inflammatory diseases provides important evidence for the development of novel therapeutic drugs.
In the future, the clinical translation of Sanxin Su O needs to address the following key issues:
Enhances the permeability of the blood-brain barrier
Through structural modification, nanocarriers, or targeted delivery technologies, it enhances its effective concentration in the central nervous system, improving neuroprotective and neurodegenerative disease treatment outcomes.
Systematic pharmacokinetics and toxicology studies
Clarify its absorption, distribution, metabolism, and excretion characteristics in the body, and assess the safety and efficacy of long-term medication.
Preclinical and clinical trial design
By combining disease models to verify its efficacy and safety, Sanxin O is being promoted toward clinical application.
Multi-target combination therapy strategies
Leveraging the multi-target regulatory advantages of Sanxin O, combined therapy regimens are developed to improve treatment efficacy and reduce the risk of drug resistance.
In summary, Sancinol O, as a natural product with neuroprotective, anti-inflammatory, and antitumor activities, has the potential to become a candidate molecule for novel drugs. With further research, its application prospects in various diseases are promising.
Sancinsu O, a 2-aryl benzofuran isolated from mulberry trees, has become an important research subject in the field of natural product pharmacology due to its diverse pharmacological activities and good safety. Its inhibitory effects on HIF-1α, antioxidant and anti-inflammatory properties, provide new approaches for the treatment of anti-tumors, ischemic stroke, and neurodegenerative diseases. Although its current blood-brain barrier penetration capacity is limited, optimization of drug design and delivery technology is expected to break through this bottleneck and achieve clinical application. In the future, systematic research on Sanxin Su O will further reveal its mechanism of action, promoting its transition from the laboratory to clinical practice, and contributing new natural drug resources for the treatment of related diseases.
Shenshuai
Wenjing
Hedandan
