Food Frontiers
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2026
·Vol. 7
·期 3
·e70290
·
IF 6.3
Mengyao Fang,Kang Yang,Yiyan Cui,Ting Rong,Dun Deng,Pan Yang,Zhimei Tian,Min Song,Xianyong Ma,Miao Yu
Magnolol is a natural bioactive phenolic compound with potent antioxidant properties and plays an important role in modulating intestinal healthy. However, the underlying mechanisms of magnolol in alleviating intestinal oxidative stress damage and improving the intestinal barrier integrity remain unknown. Thus, this study aimed to evaluate the effects of magnolol on intestinal antioxidant capacity and barrier function in weaned piglets and 2,2′-azobis (2-methylpropionamidine) dihydrochloride (AAPH) challenged IPEC-J2 cell models. The results showed that magnolol supplementation significantly increased ( p < 0.05) serum T-AOC, jejunal mucosa T-SOD and GSH-PX, and ileal mucosa T-SOD activities in weaned piglets. Magnolol also upregulated ( p < 0.05) the mRNA expression of antioxidant enzymes ( SOD1 , CAT , GCLM , and GR ) in the small intestine, while decreased ( p < 0.05) the MDA level in both serum and jejunum. Meanwhile, magnolol improved intestinal barrier function, as evidenced by reduced ( p < 0.05) serum diamine oxidase activity, D-lactate acid, and endotoxin levels, while increased ( p < 0.05) villus height and jejunal and ileal protein expression of tight junction proteins (ZO-1, occludin, and claudin-1). It further downregulated ( p < 0.05) the proapoptosis protein (caspase-9, caspase-3, and Bax) and upregulated antiapoptosis protein Bcl2. In vitro studies further revealed that magnolol pretreatment effectively alleviated ( p < 0.05) AAPH-induced oxidative stress, barrier dysfunction, and apoptosis by activating the key proteins expression in Nrf2 signaling pathway in IPEC-J2 cells. These findings indicated that magnolol enhances intestinal antioxidant capacity and exerts antiapoptotic effects, while preserving epithelial barrier integrity, potentially via activation of the Nrf2 signaling pathway.
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BioNanoScience
·
2026
·Vol. 16
·期 5
·320
·
IF 4
Ma Yingying,Xue Linying,Wang Yancai
Alzheimer’s disease (AD), a progressive neurodegenerative disorder, is the leading clinical cause of dementia. Magnolol has promising therapeutic potential for AD. However, its poor aqueous solubility and the challenge of achieving brain-targeted delivery have severely hindered its clinical usage. This study designed a thermosensitive in situ hydrogel nasal spray for co-delivery of magnolol nanosuspensions and berberine, targeting AD treatment via nose-to-brain delivery. The magnolol nanosuspensions were prepared via a wet-milling approach to improve the drug’s solubility. A thermosensitive hydrogel based on poly(N-isopropylacrylamide) (PNIPAM) was synthesized and formulated as an in situ nasal spray to enable brain-targeted co-delivery of the two drugs. In vitro PC12 cells AD models and in vivo mice was used to evaluation the thermosensitive multifunctional in-situ hybrid gel effectiveness and distribution. Morphological characterization confirmed successful preparation of magnolol nanosuspensions with a mean particle size of 220 ± 10 nm, which exhibited a high dissolution rate of 82.36 ± 1.62% within 300 min. The nanosuspensions were embedded in the hydrogel, which has a lower critical solution temperature (LCST) of approximately 32 °C - allowing rapid phase transition in the nasal cavity (local temperature ~ 35 °C). On PC12 cells and mice AD models, the thermosensitive hydrogel co-delivery system increased cell survival by 27.13% and significantly enhanced drug accumulation in the brain. This multifunctional drug delivery system provides an efficient strategy for the brain-targeted delivery of magnolol nanosuspensions and berberine, offering a promising approach for AD treatment.
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EUROPEAN JOURNAL OF PHARMACOLOGY
·
2024
·
IF 4.2
Yi Chu,Sisi Gui,Yazhen Zheng,Jingwu Zhao,Yaxiang Zhao,Yingying Li,Xiaodong Chen
Non-alcoholic fatty liver disease (NAFLD) is closely associated with the body's energy metabolism. A potential strategy to regulate energy metabolism, combat obesity, and reduce NAFLD is by enhancing adipocyte thermogenesis and increasing energy expenditure. In this study, our objective was to examine the effects of phenolic extracts derived from Magnolia officinalis on the regulation of NAFLD. Specifically, we investigated the impact of Magnolol or Honokiol treatment on high-fat diet (HFD)-induced obese C57BL6/J male mice. Firstly, we monitored energy metabolism, dissected tissues, and analyzed tissue sections. Additionally, we conducted experiments on HepG2 and primary adipocytes to gain insights into the roles of Magnolol or Honokiol. To further understand the effects of these compounds on related signaling pathways and marker genes, we performed molecular docking, dual-luciferase assays, and interfered with target genes. Our findings revealed that Magnolol or Honokiol activate the peroxisome proliferator activated receptor alpha (PPARα) signaling pathway, leading to the alleviation of NAFLD. This activation promotes fatty acid oxidation, reduces lipogenesis, and enhances the expression and secretion of FGF21. Notably, Fibroblast growth factor 21 (FGF21), secreted by the liver, plays a crucial role in improving communication between the liver and adipocytes while also promoting the browning of adipose tissue. Additionally, Magnolol or Honokiol activate the peroxisome proliferator activated receptor gamma (PPARγ) signaling pathway, resulting in increased uncoupling protein 1 (UCP1) expression, heightened heat production in adipose tissue, and anti-obesity. Therefore, Magnolol or Honokiol alleviate NAFLD, promote adipose tissue browning and resist obesity through dual activation of PPARα/γ.
研究领域:
药理学
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代谢
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分子生物学
·
营养学
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BIOORGANIC CHEMISTRY
·
2024
·
IF 4.5
Yi Chen,Shasha Song,Yongfang Wang,Lili Wu,Jianbing Wu,Zhengmeng Jiang,Xinyu Li
Psoriasis (PSO) is a common inflammatory skin disease caused by multiple factors. Magnolia officinalis is an important medicinal plant in China, with various values such as ecology, medicine, food, and daily chemicals. However, its diverse application potential has not been fully explored. Magnolol (MGO) is the main active compound of Magnolia officinalis with significant anti-inflammatory effect. To investigate the application potential of MGO in inflammatory skin disease, the effects and underlying mechanisms of topical MGO treating psoriasis were explored in this study. Network pharmacology and molecular docking firstly predicted that topical MGO may treat psoriasis by regulating pyroptosis pathway and acting on caspase-1 (CASP1). In vitro experiments then demonstrated that MGO could inhibit the level of inflammatory cytokines and the key protein expression of NOD-like receptor protein 3 (NLRP3)/Caspase-1 pathway in lipopolysaccharide (LPS)-stimulated phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 cells. Meanwhile, MGO could inhibit CuSO 4 -induced neutrophils migration in Tg (mpx:EGFP) zebrafish by suppressing inflammation and pyroptosis. This study further indicated that topical application of MGO ameliorated imiquimod (IMQ)-induced psoriasis-like dermatitis by reducing the release of inflammatory factors and decreasing the key protein expression of pyroptosis-related NLRP3/Caspase-1 pathway. Metabolomics analysis revealed that topical application of MGO could significantly regulate tryptophan metabolism and affect the level of tryptophan in skin lesions. Tryptophan could also regulate inflammation-related genes and inhibit pyroptosis-related NLRP3/Caspase-1 pathway in LPS-stimulated PMA-differentiated THP-1 cells. In conclusion, this study suggested that topical MGO may ameliorate psoriasis-like dermatitis by inhibiting NLRP3/Caspase-1 pathway and regulating tryptophan metabolism.
研究领域:
药理学
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皮肤科
·
分子生物学
·
代谢组学
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POLYMER DEGRADATION AND STABILITY
·
2021
·
IF 5.03
Chao Ma,Lijun Qian,Juan Li
Functional group of a flame retardant may change performance and reaction mechanism of polymers to some extent. In this paper, magnolol-based cyclic phosphonates with double bond (DPDO) and epoxy group (EDPDO) were synthesized, and used in epoxy resin (EP). The EP/DPDO have better flame retardancy than that of EP/EDPDO in the UL-94 and LOI tests, while the pHRR of the latter decreases more that of the former in cone calorimetry test. Moreover, EP/EDPDO has higher glass transition temperature. Both DPDO and EDPDO do not deteriorate the mechanical properties and transparence of EP greatly. It is shown that the mechanism of the two is different. The DPDO is free in the resin, while the EDPDO is fixed in the framework of EP, therefore DPDO works in the gas and condensed phase, and EDPDO remains in the condensed phase. This work provides a simple solution to regulate the structure and performance of EP materials.
研究领域:
材料科学
·
化学工程
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PHYTOTHERAPY RESEARCH
·
2023
·
IF 7.2
Lin Niu,Yu-jie Lu,Xing-wang Zu,Wen Yang,Fu-kui Shen,Yan-yan Xu,Min Jiang,Yang Xie,Su-yun Li,Jie Gao,Gang Bai
Transient receptor potential vanilloid 4 (TRPV4) plays a role in regulating pulmonary fibrosis (PF). While several TRPV4 antagonists including magnolol (MAG), have been discovered, the mechanism of action is not fully understood. This study aimed to investigate the effect of MAG on alleviating fibrosis in chronic obstructive pulmonary disease (COPD) based on TRPV4, and to further analyze its mechanism of action on TRPV4. COPD was induced using cigarette smoke and LPS. The therapeutic effect of MAG on COPD-induced fibrosis was evaluated. TRPV4 was identified as the main target protein of MAG using target protein capture with MAG probe and drug affinity response target stability assay. The binding sites of MAG at TRPV4 were analyzed using molecular docking and small molecule interaction with TRPV4-ankyrin repeat domain (ARD). The effects of MAG on TRPV4 membrane distribution and channel activity were analyzed by co-immunoprecipitation, fluorescence co-localization, and living cell assay of calcium levels. By targeting TRPV4-ARD, MAG disrupted the binding between phosphatidylinositol 3 kinase γ and TRPV4, leading to hampered membrane distribution on fibroblasts. Additionally, MAG competitively impaired ATP binding to TRPV4-ARD, inhibiting TRPV4 channel opening activity. MAG effectively blocked the fibrotic process caused by mechanical or inflammatory signals, thus alleviating PF in COPD. Targeting TRPV4-ARD presents a novel treatment strategy for PF in COPD.
研究领域:
药理学
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肺科学
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分子生物学
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细胞生物学
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Scientific Reports
·
2026
·Vol. 16
·期 1
·29920
·
IF 4.9
Ahmadi Alireza,Ruhnke Niklas,Albesais Lamia S.,Quickert Stefanie,Reuken Philipp A.,Werz Oliver,Lorkowski Stefan,Schubert Ulrich S.,Schubert Stephanie,Stallmach Andreas,Gardey Elena
In cirrhosis, pathological translocation of gut bacteria disrupts immune balance and promotes spontaneous bacterial peritonitis. Peritoneal macrophages (PMs) play an important role in resolving peritoneal inflammation and controlling bacterial infections. However, their regulatory function can be impaired under cirrhotic conditions. Considering the anti-inflammatory and antioxidant properties of the natural compound magnolol, we hypothesized that it may exert these effects on human PMs. Moreover, encapsulation of magnolol into poly(lactic- co -glycolic acid) nanoparticles (PLGA-NPs) was expected to enhance its therapeutic potential. Herein, PMs were isolated from ascites of decompensated cirrhotic patients, stimulated with lipopolysaccharide (LPS), and exposed to magnolol-PLGA-NPs. Treated cells were analyzed using flow cytometry, fluorescence microscopy, ELISA, western blotting, and the CellROX Deep Red assay to check cellular uptake, inflammatory responses and oxidative stress. The results of the study indicated that encapsulation of magnolol into PLGA NPs improved its biocompatibility. Moreover, a robust uptake of labeled magnolol-PLGA-NPs by PMs was indicated. Upon LPS stimulation, treatment with magnolol-PLGA-NPs demonstrated both anti-inflammatory and antioxidant effects. They significantly suppressed TNF-α and IL-6 release, while preserving IL-10 levels, which may contribute to maintaining a balanced immune response. Treatment with magnolol-PLGA-NPs was also associated with reduced ERK1/2 and p38 phosphorylation, suggesting that modulation of MAPK signaling may contribute to the observed anti-inflammatory effects. Additionally, they significantly reduced oxidative stress in stimulated cells. Altogether, these results indicate that magnolol-encapsulated PLGA NPs exhibit anti-inflammatory and antioxidant effects in stimulated human PMs.
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Acta Pharmaceutica Sinica B
·
2026
·
IF 14.6
Yane Li,Li Yao,Jiaxuan Hou,Xingyun Yuan,Yuanyuan Zhu,Zhichao Deng,Chenxi Xu,Jinxing Chen,Bingyi Chen,Jiayan Li,Yifan Me,Shuang Liu,Shaoying Lu,Mingzhen Zhang,Hui Cai
Cerebral ischemia–reperfusion (I/R) injury is exacerbated by the infiltration of splenic monocytes/macrophages (Mo/M φ ) via the spleen–brain axis, where splenic-derived Mo/M φ migrate to cerebral lesions through C–C chemokine ligand 2/receptor 2 (CCL2/CCR2) chemotaxis, thereby amplifying oxidative stress and the neuroinflammatory cascade. Building on this endogenous pathway, we devised a delivery strategy that utilizes splenic Mo/M φ as “living vehicles” for targeted drug delivery. To this end, we developed a spleen-targeted magnolol liposome (Mag-PEG 5K ) through optimized PEGylation, ensuring its spleen-specific accumulation and uptake by splenic Mo/M φ . After cerebral I/R injury, these nanoparticle-laden cells migrate to the ischemic brain via the CCR2/CCL2 axis to remodel the immunomodulatory microenvironment. This targeted system orchestrates dual therapeutic mechanisms within the lesion: mitochondria-directed reactive oxygen species (ROS) scavenging mitigates oxidative stress and peroxisome proliferator-activated receptor gamma (PPAR γ ) activation reprograms macrophage polarization, suppressing pro-inflammatory M1 differentiation and curtailing tumor necrosis factor-alpha (TNF- α ) and interleukin-1beta (IL-1 β ) secretion. The attenuated cytokine release suppresses neuronal inflammatory cascades, thereby reducing apoptosis. In vivo , Mag-PEG 5K showed superior efficacy to free magnolol, effectively reducing infarct volume and improving long-term neurological outcomes. Supported by favorable biosafety, this work proposes spleen-targeted nanotherapy as an innovative strategy for reprogramming peripheral immunity via the spleen–brain axis, highlighting the translational potential of Mag-PEG 5K for addressing neuroinflammation and oxidative damage in ischemic stroke.
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FREE RADICAL BIOLOGY AND MEDICINE
·
2026
·
IF 8
Zhe Li,Bingbing Liu,Lianghong Zhou,Na Chen,Yi Wang,Su Yang,Xinyi Fan,Yuan Wang,Xiaodong Chen
Sarcopenic obesity (SO), characterized by concurrent muscle loss and excessive adiposity, lacks effective interventions. This study investigated the enhanced effects of the selenomethionine (Se-Met) and magnolol (Mag) combination against SO using an integrated computational-experimental approach. Network pharmacology and molecular docking predicted peroxisome proliferator-activated receptor γ (PPARγ) and the nuclear factor erythroid 2-related factor 2 - glutathione peroxidase 4 (Nrf2 - GPX4) axis as core targets, which was corroborated by single-cell transcriptomic data analysis showing their co-expression in muscle progenitor cells. In high-fat diet (HFD)-fed mice, the combined Se-Met and Mag treatment ameliorated metabolic dysregulation, reduced intramuscular lipid deposition, and improved muscle function more effectively than monotherapies. In C2C12 myotubes, the combination co-activated PPARγ to enhance lipid clearance and potentiated the Nrf2-GPX4 antioxidant axis. Notably, it modulated ferroptosis-related signaling by downregulating acyl-CoA synthetase long-chain family member 4 (ACSL4) and upregulating ferritin heavy chain 1 (FTH1) and heme oxygenase-1 (HO-1), an effect abolished by Nrf2 inhibition. Pharmacological inhibition of either PPARγ or Nrf2 reversed the protective benefits. Our findings reveal that Se-Met and Mag in combination target PPARγ and Nrf2-GPX4 pathways while regulating ferroptosis-related signaling to alleviate ferroptosis-associated markers, with phenotypic characteristics consistent with ferroptosis inhibition, thereby offering a novel nutraceutical strategy for SO.
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Chemical Science
·
2025
·
IF 7.4
Huifa Meng,Kaijin Chen,Chuying Li,Longfei Zhang,Yanwei He,Zining Zhao,Peixin Wu,Hai Zhu,Zhenguo Chi,Jiarui Xu,Siwei Liu,Yi Zhang
Traditional photosensitive polyimide (PSPI) materials require a high curing temperature and exhibit low transparency, limiting their applications in thermally sensitive optical devices. To overcome this challenge, soluble photosensitive polyimide resins were synthesized based on the structural design of bio-based magnolol monomer. It is noteworthy that the PI photoresist, developed by using the as-prepared polyimides and non-toxic solvents (2-acetoxy-1-methoxypropane, PGEMA) and other additives, demonstrated an impressive low-temperature curing performance (180 °C). Furthermore, the solvent residue presents in the cured film using PGEMA as solvent was markedly decrease when compared to that of the cured film using N-methyl pyrrolidone (NMP). In addition, the C-PI-3 films cured by photoinitiated thiol-ene radical reactions exhibited high transparency with an average visible light transmittance of 87.8 %, as well as excellent thermal stability, dielectric and breakdown properties, and photo-patternable capabilities. This partially bio-based and innocuous solvent-based PSPI with low-temperature curable and high transparency properties could be a pioneering example to resolve the challenges of energy efficiency and environmental sustainability, and are expected to be used in the field of color filters.
研究领域:
材料科学
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化学工程
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PubMed
高影响因子
World Journal of Clinical Cases
·
2021
·
IF 1.337
Shi-Hao Mao,Dan-Dan Feng,Xi Wang,Yi-Hui Zhi,Shu Lei,Xi Xing,Rong-Lin Jiang,Jian-Nong Wu
BACKGROUND Sepsis is a major medical challenge. Magnolol is an active constituent of Houpu that improves tissue function and exerts strong anti-endotoxin and anti-inflammatory effects, but the mechanism by which it reduces intestinal inflammation in sepsis is yet unclear. AIM To assess the protective effect of magnolol on intestinal mucosal epithelial cells in sepsis and elucidate the underlying mechanisms. METHODS Enzyme-linked immunosorbent assay was used to measure tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and regulated on activation, normal T-cell expressed and secreted (RANTES) levels in serum and ileal tissue in animal studies. The histopathological changes of the ileal mucosa in different groups were observed under a microscope. Cell Counting Kit-8 and cell permeability assays were used to determine the concentration of drug-containing serum that did not affect the activity of Caco2 cells but inhibited lipopolysaccharide (LPS)-induced decrease in permeability. Immunofluorescence and Western blot assays were used to detect the levels of RANTES, inhibitor of nuclear factor kappa-B kinase β (IKKβ), phosphorylated IKKβ (p-IKKβ), inhibitor of nuclear factor kappa-B kinase α (IκBα), p65, and p-p65 proteins in different groups in vitro . RESULTS In rats treated with LPS by intravenous tail injection in the presence or absence of magnolol, magnolol inhibited the expression of proinflammatory cytokines, IL-1β, IL-6, and TNF-α in a dose-dependent manner. In addition, magnolol suppressed the production of RANTES in LPS-stimulated sepsis rats. Moreover, in vitro studies suggested that magnolol inhibited the increase of p65 nucleation, thereby markedly downregulating the production of the phosphorylated form of IKKβ in LPS-treated Caco2 cells. Specifically, magnolol inhibited the translocation of the transcription factor nuclear factor-kappa B (NF-κB) from the cytosol into the nucleus and down-regulated the expression level of the chemokine RANTES in LPS-stimulated Caco2 cells. CONCLUSION Magnolol down-regulates RANTES levels by inhibiting the LPS/NF-κB signaling pathways, thereby suppressing IL-1β, IL-6, and TNF-α expression to alleviate the mucosal barrier dysfunction in sepsis.
研究领域:
药理学
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免疫学
·
病理学
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TALANTA
·
2013
·
IF 3.498
Xinjian Song,Bing Wang,Yina Huang,Liqing Li,Ting Li,Chunya Li,Shenghui Zhang
A polymeric film modified glassy carbon electrode was electrochemically fabricated with potential step technique using 1-butyl-3-[3-(N-pyrrole)propyl] imidazolium tetrafluoroborate ionic liquid as a monomer . Followed by being treated with sodium dodecyl sulfonate solution, a hydrophobic film bearing poly{1-butyl-3-[3-(N-pyrrolyl)propyl]imidazolium dodecyl sulfonate} moiety was modified onto electrode surface. The substitution was confirmed by X-ray photoelectron spectroscopy. The morphology of the polymeric film electrode surface was characterized with scanning electron microscopy. Electrochemical behaviors of magnolol at the hydrophobic polymeric film electrode were systematically investigated with voltammetry . Compared with the unmodified glassy carbon electrode, the oxidation peak shift slightly towards positive potential and the oxidation peak current significantly increased. Under optimal conditions, the oxidation peak current was linearly related to the magnolol concentration in the range of 1.0×10 –8 to 1.0×10 –6 mol L –1 and 1.0×10 –6 to 5.0×10 –5 mol L –1 . The detection limit was estimated to be 4.55×10 –9 mol L –1 (S/N=3). The polymerized ionic liquid film electrode was successfully used to analysis magnolol in M. officinalis . The result was consistent with that obtained by high performance liquid chromatography.
研究领域:
分析化学
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电化学
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