|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Magnolol additive as a replacer of antibiotic enhances the growth performance of Linwu ducks显示文摘Magnolol rich in Magnolia officinalis is a bioactive polyphenolic compound. The aim of this study was to examine the effects of magnolol additive(MA) on growth performance, expression levels of antioxidantrelated genes, and intestinal mucosal morphology of Linwu ducks aged from 49 to 70 days, comparing with that of an antibiotic additive(colistin sulfate [CS]). A total of 275,49-day-old ducks were assigned to5 groups with 5 cages of 11 ducks each and fed diets supplemented with 0,100, 200 and 300 mg of MA/kg and 300 mg of CS/kg for 3 weeks, respectively. The results showed that the average daily body weight gain(ADG) was increased significantly in MA-fed groups(200 and 300 mg/kg), compared with the basal diet(BD) group(P < 0.05). The mRNA levels of superoxide dismutase-1(SOD1), manganese superoxide dismutase-2(MnSOD2) and catalase(CAT) were also increased significantly in MA groups(P < 0.05). In addition, hematoxylin and eosin staining revealed that Linwu ducks fed the diets with MA had more intact intestinal mucosa than those fed the BD and CS diets. In addition, ileal villus height, ileal villus height/crypt depth ratio(V/C) and duodenal V/C were also improved significantly(P < 0.05). Taken together, these data demonstrated that MA is an effective feed additive to enhance the growth performance of the Linwu ducks by improving the antioxidant and intestinal mucosal status, suggesting that MA will be a potential additive to replace antibiotic(CS). | Qian Lin Jianfei Zhao Kun Xie Yushi Wang Guili Hu Guitao Jiang Qiuzhong Dai Zhiyong Fan Jianhua He Xi He De-Xing Hou | 2017 | Animal Nutrition2017，，2： | 14 |
| 2 | Supplemental magnolol or honokiol attenuates adverse effects in broilers infected with Salmonella pullorum by modulating mucosal gene expression and the gut microbiota显示文摘Background:Salmonella pullorum is one of the most harmful pathogens to avian species.Magnolol and honokiol,natural compounds extracted from Magnolia officinalis,exerts anti-inflammatory,anti-oxidant and antibacterial activities.This study was conducted to evaluate the effects of dietary supplemental magnolol and honokiol in broilers infected with S.pullorum.A total of 360 one-day-old broilers were selected and randomly divided into four groups with six replicates:the negative control group(CTL),S.pullorum-infected group(SP),and the S.pulloruminfected group supplemented with 300 mg/kg honokiol(SPH)or magnolol(SPM).Results:The results showed that challenging with S.pullorum impaired growth performance in broilers,as indicated by the observed decreases in body weight(P<0.05)and average daily gains(P<0.05),along with increased spleen(P<0.01)and bursa of Fabricus weights(P<0.05),serum globulin contents,and the decreased intestine villus height and villus/crypt ratios(P<0.05).Notably,supplemental magnolol and honokiol attenuated these adverse changes,and the effects of magnolol were better than those of honokiol.Therefore,we performed RNA-Seq in ileum tissues and 16S rRNA gene sequencing of ileum bacteria.Our analysis revealed that magnolol increased the α-diversity(observed species,Chao1,ACE,and PD whole tree)and β-diversity of the ileum bacteria(P<0.05).In addition,magnolol supplementation increased the abundance of Lactobacillus(P<0.01)and decreased unidentified Cyanobacteria(P<0.05)both at d 14 and d 21.Further study confirmed that differentially expressed genes induced by magnolol and honokiol supplementation enriched in cytokine-cytokine receptor interactions,in the intestinal immune network for IgA production,and in the cell adhesion molecule pathways.Conclusions:Supplemental magnolol and honokiol alleviated S.pullorum-induced impairments in growth performance,and the effect of magnolol was better than that of honokiol,which could be partially due to magnolol’s ability to improve the intestinal microbial and mucosal barrier. | Fang Chen Hao Zhang Encun Du Qiwen Fan Na Zhao Feng Jin Wei Zhang Wanzheng Guo Shaowen Huang Jintao Wei | 2022 | Journal of Animal Science and Biotechnology2022，13，1： | 9 |
| 3 | Magnolol protects against acute gastrointestinal injury in sepsis by down-regulating regulated on activation,normal T-cell expressed and secreted显示文摘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 kinaseβ(IKKβ),phosphorylated IKKβ(p-IKKβ),inhibitor of nuclear factor kappa-B kinaseα(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-αin 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 IKKβin 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-αexpression to alleviate the mucosal barrier dysfunction in sepsis. | Shi-Hao Mao Dan-Dan Feng Xi Wang Yi-Hui Zhi Shu Lei Xi Xing Rong-Lin Jiang Jian-Nong Wu | 2021 | World Journal of Clinical Cases2021，9，34： | 5 |
| 4 | Magnolol attenuates right ventricular hypertrophy and fibrosis in hypoxia-induced pulmonary arterial hypertensive rats through inhibition of the JAK2/STAT3 signaling pathway显示文摘OBJECTIVE Right ventricular(RV)remodeling is one of the essential pathological features in pulmonary arterial hypertension(PAH).RV hypertrophy or fibrosis are the leading causes of RV remodeling.Magnolol is a compound isolated from Magnolia officinalis.It possesses multiple pharmacological activities,such as anti-oxidation and anti-inflammation.This study aims to evaluate the effects and underlying mechanisms of magnolol on RV remodeling in hypoxia-induced PAH.METHODS①Male SD rats(220 g)were randomly divided into 5 groups(n=10):the normoxia group,the hypoxia group,the hypoxia plus Magnolol(10 and 20 mg·kg^(-1)·d-1)group,and the vehicle group.Rats in the normoxia group were kept in a normoxia environment for 4 weeks,while rats in the hypoxia group were kept in a hypoxic chamber(10%O2).The rats in the hypoxia plus magnolol groups were administered with magnolol at 10 or 20 mg·kg^(-1)(ip)once a day for 4 weeks.At the end of 4 weeks,the heart function was assessed by Doppler echocardiography,and then the rats were anesthetized with sodium pentobarbital(30 mg·kg^(-1),ip).The RVSP was measured by the right heart catheterization method.The heart tissues were collected and dissected to calculate the index of RV remodeling(RV/LV+IVS,RV/tibial length,or RV/body weight).Part of the RV samples was fixed with 4%paraformaldehyde for morphological analysis,while other samples were frozen at-80℃for molecular studies(measurements of ANP,BNP,α-SMA,and collagenⅠ/ⅢmRNA expression as well as p-JAK2/JAK2 and p-STAT3/STAT3 protein levels).②To evaluate the effect of magnolol on hypoxia-induced myocardial hypertrophy and fibrosis,H9c2 or cardiac fibroblasts were divided into 7 groups:the control group,cells were cultured under normal conditions;the hypoxia group,cells were cultured under hypoxic condition(3%O2);the hypoxia plus magnolol 10 mg·kg^(-1) group,magnolol10μmol·L^(-1) was added to the culture medium before the hypoxia treatment;the hypoxia plus magnolol 30 mg·kg^(-1) group,magnolol 20μmol·L^(-1) was added to the culture medium before the hypoxia treatment;the hypoxia plus TG-101348 group,TG-101348(a specific inhibitor of JAK2)1μmol·L^(-1) was added to the culture medium before the hypoxia treatment;the hypoxia plus JSI-124 group,JSI-124(a specific inhibitor of JAK2)1μmol·L^(-1) was added to the culture medium before the hypoxia treatment;and the hypoxia plus vehicle group,an equal volume of vehicle(DMSO)was added to the culture medium before the hypoxia treatment.At the end of the experiments,the cells were collected for morphological and molecular analysis.RESULTS In vivo,male Sprang-Daley rats were exposed to 10%O2 for 4 weeks to establish an RV remodeling model,which showed hypertrophic and fibrotic features(increases of RV remodeling index,cellular size,hypertrophic and fibrotic marker expression),accompanied by an elevation in phosphorylation levels of JAK2 and STAT3;these changes were attenuated by treating rats with magnolol.In vitro,the cultured H9c2 cells or cardiac fibroblasts were exposed to 3%O2 for 48 h to induce hypertrophy or fibrosis,which showed hypertrophic(increases in cellular size as well as the expression of ANP and BNP)or fibrotic features(increases in the expression of collagenⅠ,collagenⅢandα-SMA).Administration of magnolol and TG-101348 or JSI-124 (JAK2 selective inhibitors) could prevent the process of myocardial hypertrophy and fibrosis, accompanied by the decrease in the phosphorylation level of JAK2 and STAT3. CONCLUSION Magnolol can attenuate RV hypertrophy and fibrosis in hypoxia-induced PAH rats through a mechanism involving inhibition of the JAK2/STAT3 signaling pathway. | FU Min-yi LUO Fang-mei WANG E-li JIANG Yue-ping LIU Shao LUO Xiu-ju PENG Jun LIU Bin | 2021 | 中国药理学与毒理学杂志2021，35，10： | 4 |
| 5 | Achieving higher performances without an external curing agent in natural magnolol-based epoxy resin显示文摘Bio-based epoxy thermoset prepared from renewable biomass raw materials can alleviate fossil energy crisis and reduce environmental pollution,which satisfies the needs of sustainable social development.In this study,a bio-based epoxy thermoset precursor(MGOL-EP) was synthesized from a naturally occurring magnolol through a facile and efficient one-step process.And the fully bio-based epoxy thermoset(MGOL-EP-SC) was obtained by self-curing without adding any other hardener.MGOL-EP-SC revealed an extremely high glass-transition temperature(T_(g)) of 265℃ and char yield of 53.2%(in N;),which were at the highest level among the fully bio-based epoxy thermosets reported so far.In addition,when the MGOL-EP was cured with 4,4’-methylenedianiline(DDM),T_(g)of the MGOL-EP/DDM was decreased by 61℃ and the other comprehensive performance had also been decreased,which was due to a reduction in biphenyl structure content and cross-linking density by adding the external curing agents.Moreover,the MGOL-EP-SC presented certain killing rate(48.4%) to Staphylococcus aureus.These findings provide a new design strategy for engineering high-performance and functional epoxy thermoset with high biomass content. | Qi Cao Zhihuan Weng Yu Qi Jiahui Li Wentao Liu Chengde Liu Shouhai Zhang Zhiyong Wei Yousi Chen Xigao Jian | 2022 | Chinese Chemical Letters2022，33，4： | 2 |
| 6 | Synergistic effects of autophagy/mitophagy inhibitors and magnolol promote apoptosis and antitumor efficacy显示文摘Mitochondria as a signaling platform play crucial roles in deciding cell fate.Many classic anticancer agents are known to trigger cell death through induction of mitochondrial damage.Mitophagy,one selective autophagy,is the key mitochondrial quality control that effectively removes damaged mitochondria.However,the precise roles of mitophagy in tumorigenesis and anticancer agent treatment remain largely unclear.Here,we examined the functional implication of mitophagy in the anticancer properties of magnolol,a natural product isolated from herbal Magnolia officinalis.First,we found that magnolol induces mitochondrial depolarization,causes excessive mitochondrial fragmentation,and increases mitochondrial reactive oxygen species(mtROS).Second,magnolol induces PTEN-induced putative kinase protein 1(PINK1)-Parkin-mediated mitophagy through regulating two positive feedforward amplification loops.Third,magnolol triggers cancer cell death and inhibits neuroblastoma tumor growth via the intrinsic apoptosis pathway.Moreover,magnolol prolongs the survival time of tumor-bearing mice.Finally,inhibition of mitophagy by PINK1/Parkin knockdown or using inhibitors targeting different autophagy/mitophagy stages significantly promotes magnolol-induced cell death and enhances magnolol's anticancer efficacy,both in vitro and in vivo.Altogether,our study demonstrates that magnolol can induce autophagy/mitophagy and apoptosis,whereas blockage of autophagy/mitophagy remarkably enhances the anticancer efficacy of magnolol,suggesting that targeting mitophagy may be a promising strategy to overcome chemoresistance and improve anticancer therapy. | Yancheng Tang Liming Wang Tao Yi Jun Xu Jigang Wang Jiang-Jiang Qin Qilei Chen Ka-Man Yip Yihang Pan Peng Hong Yingying Lu Han-Ming Shen Hu-Biao Chen | 2021 | Acta Pharmaceutica Sinica B2021，11，12： | 2 |
| 7 | Deep sequencing of Magnoliae officinalis reveals upstream genes related to the lignan biosynthetic pathway显示文摘Magnoliae officinalis is the plant source of houpo, a widely used traditional Chinese medicine to treat symptoms of gastrointestinal diseases. Its main active components, magnolol(MG) and honokiol(HK), have excellent pharmacological actions, but little research has focused on the functional genes involved in the MG and HK metabolic pathways. In this study, using RNA-seq and gene expression profile, we present the first transcriptome characterization of M. officinalis leaves, twigs and stems.Based on similarity search against nonredundant protein databases, 30,660 contigs had at least a significant alignment to existing public database. Pathway analysis showed that 8707 contigs were assigned to 317 KEGG pathways. A second skeleton pathway with 14 putative homologous genes was also identified as involved in lignan biosynthesis. Expression profiles of these 14 genes showed that leaves and twigs seem to have higher transcript levels for lignan components than in stem tissue; this result was then verified by q RT-PCR. Our work will immensely facilitate metabolic research on lignan biosynthesis in M.officinalis. | Xiaodong Shi Langsheng Yang Jihai Gao Yuzhen Sheng Xiaoqing Li Yunjie Gu Guoqing Zhuang Fang Chen | 2017 | Journal of Forestry Research2017，28，4： | 0 |
| 8 | Synthesis of Bio-based Epoxy Containing Phosphine Oxide as a Reactive Additive Toward Highly Toughened and Fire-retarded Epoxy Resins显示文摘The integration of high mechanical toughness,impact strength as well as excellent flame-retardant properties toward epoxy resins(EPs)have always been a dilemma.The inadequate overall performance of EPs severely restricts their sustainable utilization in engineering aspects over long-term.Herein,a new bio-based agent(diglycidyl ether of magnolol phosphine oxide,referred as DGEMP)derived from magnolol(classified as lignan),extracted from natural plants Magnolia officinalis,was successfully synthesized and further employed as a flameretardant reactive additive to diglycidyl ether of bisphenol A(DGEBA).As demonstration,the composite resin,DGEBA/15DGEMP(15 wt%DGEMP),achieved an Underwriters Laboratories-94 V-0 rating with a high limiting oxygen index(LOI)value(41.5%).In cone calorimeter tests,it showed that heat release and smoke production were effectively inhibited during combustion,wherein the peak heat release rate(PHRR)value of DGEBA/15DGEMP was reduced by 50%compared to neat DGEBA.Additionally,it exhibited a superior tensile strength(82.8 MPa),toughness(5.11MJ/m^(3))and impact strength(36.5 k J/m^(2)),much higher than that of neat DGEBA(49.7 MPa,2.05 MJ/m^(3)and 20.9 k J/m^(2)).Thus,it is highly anticipated that DGEMP imparts significantly improved mechanical and fire-retarded properties to conventional EPs,which holds a great potential to address the pressing challenges in EP thermosets industry. | Chunxiang Wei Tianyu Gao Yu Xu Wenjie Yang Guangjian Dai Ruiting Li SanE Zhu Richard K.K.Yuen Wei Yang Hongdian Lu | 2023 | Chinese Journal of Polymer Science2023，41，11： | 0 |
| 9 | Exploring the mechanisms of magnolol in the treatment of periodontitis by integrating network pharmacology and molecular docking显示文摘Background:Magnolol,a bioactive extract of the Chinese herb Magnolia officinalis has a protective effect against periodontitis.This study is aimed to explore the mechanisms involved in the functioning of magnolol against periodontitis and provide a basis for further research.Methods:Network pharmacology analysis was performed based on the identification of related targets from public databases.The Protein-protein interaction(PPI)network was constructed to visualize the significance between the targets of magnolol and periodontitis.Subsequently,Gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)analysis were performed to predict the functions and the signal regulatory pathways involved in the action of magnolol against periodontitis.The“functiontarget-pathway”networks were constructed to analyze the core targets and pathways of magnolol against periodontitis.Molecular docking was used to verify the interaction of magnolol and core targets.Results:A total of 58 active targets of magnolol and 644 periodontitis-related targets were collected from public databases.A total of 25 targets of magnolol against periodontitis were identified based on the Venn diagram.GO analysis showed that magnolol has a role in the response to oxidative stress,nicotine,and lipopolysaccharide.KEGG enrichment analysis indicated that the mechanism of magnolol against periodontitis was mainly related to the tumor necrosis factor(TNF),phosphoinositide 3-kinase(PI3K/Akt),and mitogen-activated protein kinase(MAPK)signaling pathways.Combined with PPI network and molecular docking results,the core targets of magnolol against periodontitis included AKT1,MAPK8,MAPK14,TNF,and TP53.Conclusion:To summarize,the anti-periodontitis mechanisms of magnolol are potentially through regulating the TNF,PI3K/Akt,and MAPK signaling pathways. | DER-JEU CHEN CHENG-HUNG LAI | 2023 | BIOCELL2023，47，6： | 0 |
| 10 | A novel transgenic zebrafish sensor for screening of potential therapeutic drug for Parkinson disease显示文摘The sensitive tyrosine hydroxylase-green fluorescent protein (TH-GFP) transgenic zebrafish was originally developed and applied as a biosensor to assessments of the effects of addict drugs in our previous study. In this study, we found that the transgenic zebrafish unexpectedly be employed as an in fifo model to evaluate the neuro- protective effects of drug candidate for neurodegenerative disorder. Magnolol as predicted target owning to it rescued the deficit of motor behavior and restored TH loss in TH-GFP transgenic zebrafish after 250 μM 6-OHDA toxin in- sult. Subsequently, we challenge SH-SY5Y cells with 6-OHDA as an in vitro model to confirm the neuroprotective effects of magnolol and discover the underlying mechanisms. Our results demonstrate magnolol prevented 6-OHDA- induced reduction of cell viability in SH-SY5Y cells; it also significantly attenuated 6-OHDA induced apoptosis characterized by DNA fragmentation and caspase-3 activation. Furthermore, Western blot analysis showed magnolol inhibited 6-OHDA induced activation of p38, JNK and ERK mitogen-activated protein kinases (MAPK) signaling in SH-SY5Y cells. These results indicate magnolol may be useful as a potential therapeutic agent for the treatment of dopaminergic neuronal diseases. Importantly, we outspread transgenic zebrafish as a novel high-throughput live biosensor for screening drugs of Parkinson disease (PD). | | 2015 | 中国药理学通报2015，31，B11： | 0 |
| 11 | Magnolol and 5-fluorouracil synergy inhibition of metastasis of cervical cancer cells by targeting PI3K/AKT/mTOR and EMT pathways显示文摘Objective: This study is designed to investigate the mode of action of the synergistic effect of 5-fluorouracil(5-FU) and magnolol against cervical cancer.Methods: Network pharmacological approach was applied to predict the molecular mechanism of 5-FU combined with magnolol against cervical cancer. CCK-8 assay, colony formation assay, immunofluorescence staining, adhesion assay, wound healing mobility assay, cell migration and invasion assay and Western blot analysis were conducted to validate the results of in silico study.Results: Phosphatidylinositol 3 kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR) signaling pathway was identified as the key pathway in silico study. The experimental results showed that 5-FU combined with magnolol strongly inhibited cervical cancer cell proliferation, induced the morphological change of HeLa cells by down-regulating the expression of a-actinin, tensin-2 and vinculin. Moreover, magnolol enhanced inhibitory effect of 5-FU on the cell adhesion, migration and invasion. The phosphorylation of AKT and PI3K and the expression of mTOR were strongly inhibited by the combination of 5-FU and magnolol. Moreover, the expression of E-cadherin and β-catenin was upregulated and the expression of Snail, Slug and vimentin was down-regulated by the 5-FU together with magnolol.Conclusion: Taken together, this study suggests that 5-FU combined with magnolol exerts a synergistic anti-cervical cancer effect by regulating the PI3K/AKT/mTOR and epithelial-mesenchymal transition(EMT) signaling pathways. | Yuanyuan Chen Shanshan Chen Kaiting Chen Lanfang Ji Shuna Cui | 2024 | Chinese Herbal Medicines2024，16，1： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员