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  • 1
    Online Resource
    Online Resource
    Demethoxycurcumin Promotes Macrophage Cell Population and Phagocytosis in WEHI-3 Cell-generated Leukemia BALB/c Mice In Vivo
    Anticancer Research USA Inc. ; 2021
    In:  In Vivo Vol. 35, No. 6 ( 2021), p. 3253-3260
    Details
    In: In Vivo, Anticancer Research USA Inc., Vol. 35, No. 6 ( 2021), p. 3253-3260
    Type of Medium: Online Resource
    ISSN: 0258-851X , 1791-7549
    URL: Article
    DOI: 10.21873/invivo.12620
    Language: English
    Publisher: Anticancer Research USA Inc.
    Publication Date: 2021
    detail.hit.zdb_id: 807031-3
    detail.hit.zdb_id: 2492569-X
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Gypenosides inhibits migration and invasion of human oral cancer SAS cells through the inhibition of matrix metalloproteinase-2 -9 and urokinase-plasminogen by ERK1/2 and NF-kappa B signaling pathways
    SAGE Publications ; 2011
    In:  Human & Experimental Toxicology Vol. 30, No. 5 ( 2011-05), p. 406-415
    Details
    In: Human & Experimental Toxicology, SAGE Publications, Vol. 30, No. 5 ( 2011-05), p. 406-415
    Abstract: Gypenosides (Gyp), found in Gynostemma pentaphyllum Makino, has been used as a folk medicine in the Chinese population for centuries and is known to have diverse pharmacologic effects, including anti-proliferative and anti-cancer actions. However, the effects of Gyp on prevention from invasion and migration of oral cancer cells are still unsatisfactory. The purpose of this study was to investigate effects of Gyp treatment on migration and invasion of SAS human oral cancer cells. SAS cells were cultured in the presence of 90 and 180 μg/mL Gyp for 24 and 48 hours. Gyp induced cytotoxic effects and inhibited SAS cells migration and invasion in dose- and time-dependent response. Wound-healing assay and boyden chamber assay were carried out to investigate Gyp-inhibited migration and invasion of SAS cells. Gyp decreased the abundance of several proteins, including nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), extracellular signal-regulated kinase 1/2 (ERK1/ 2), matrix metalloproteinase-9, -2 (MMP-9, -2), sevenless homolog (SOS), Ras, urokinase-type plasminogen activator (uPA), focal adhesion kinase (FAK) and RAC-alpha serine/threonine-protein kinase (Akt), in a time-dependent manner. In addition, Gyp decreased mRNA levels of MMP-2, MMP-7, MMP-9 but did not affect FAK and Rho A mRNA levels in SAS cells. These results provide evidences for the role of Gyp as a potent anti-metastatic agent, which can markedly inhibit the metastatic and invasive capacity of oral cancer cells. The inhibition of NF-κB and MMP-2, -7 and -9 signaling may be one of the mechanisms that is present in Gyp-inhibited cancer cell invasion and migration.
    Type of Medium: Online Resource
    ISSN: 0960-3271 , 1477-0903
    URL: Article
    DOI: 10.1177/0960327110372405
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2011
    detail.hit.zdb_id: 1483723-7
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  • 3
    Online Resource
    Online Resource
    Roles of syndecan-4 and relative kinases in dorsal root ganglion neuron adhesion and mechanotransduction
    Elsevier BV ; 2015
    In:  Neuroscience Letters Vol. 592 ( 2015-04), p. 88-93
    Details
    In: Neuroscience Letters, Elsevier BV, Vol. 592 ( 2015-04), p. 88-93
    Type of Medium: Online Resource
    ISSN: 0304-3940
    URL: Article
    DOI: 10.1016/j.neulet.2015.02.058
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2015
    detail.hit.zdb_id: 1498535-4
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Probing the Effects and Mechanisms of Electroacupuncture at Ipsilateral or Contralateral ST36–ST37 Acupoints on CFA-induced Inflammatory Pain
    Springer Science and Business Media LLC ; 2016
    In:  Scientific Reports Vol. 6, No. 1 ( 2016-02-24)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 6, No. 1 ( 2016-02-24)
    Abstract: Transient receptor potential vanilloid 1 (TRPV1) and associated signaling pathways have been reported to be increased in inflammatory pain signaling. There are accumulating evidences surrounding the therapeutic effect of electroacupuncture (EA). EA can reliably attenuate the increase of TRPV1 in mouse inflammatory pain models with unclear signaling mechanisms. Moreover, the difference in the clinical therapeutic effects between using the contralateral and ipsilateral acupoints has been rarely studied. We found that inflammatory pain, which was induced by injecting the complete Freund’s adjuvant (CFA), (2.14 ± 0.1, p   〈  0.05, n = 8) can be alleviated after EA treatment at either ipsilateral (3.91 ± 0.21, p   〈  0.05, n = 8) or contralateral acupoints (3.79 ± 0.25, p   〈  0.05, n = 8). EA may also reduce nociceptive Nav sodium currents in dorsal root ganglion (DRG) neurons. The expression of TRPV1 and associated signaling pathways notably increased after the CFA injection; this expression can be further attenuated significantly in EA treatment. TRPV1 and associated signaling pathways can be prevented in TRPV1 knockout mice, suggesting that TRPV1 knockout mice are resistant to inflammatory pain. Through this study, we have increased the understanding of the mechanism that both ipsilateral and contralateral EA might alter TRPV1 and associated signaling pathways to reduce inflammatory pain.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/srep22123
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 2615211-3
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  • 5
    Online Resource
    Online Resource
    Effects of Electroacupuncture in a Mouse Model of Fibromyalgia: Role of N-Methyl-D-Aspartate Receptors and Related Mechanisms
    SAGE Publications ; 2017
    In:  Acupuncture in Medicine Vol. 35, No. 1 ( 2017-02), p. 59-68
    Details
    In: Acupuncture in Medicine, SAGE Publications, Vol. 35, No. 1 ( 2017-02), p. 59-68
    Abstract: N-methyl-D-aspartate receptor (NMDAR) activation and downstream transduction pathways are crucial for pain signalling. Fibromyalgia (FM) is a common pain syndrome of unclear aetiology that is often drug-refractory but may benefit from treatment with electroacupuncture (EA). We examined the contributions of NMDAR signalling to FM pain and EA responses in a mouse model. Methods A model of FM was established by acid saline injection in 32 mice and subgroups (n=8 each) were treated with EA (2 Hz, 15 min daily for 4 days) or minimal acupuncture (MA). Expression of NMDAR subunits, calmodulin-dependent protein kinase II (CaMKII), cyclic AMP response element binding protein (pCREB) and their corresponding phospho-activated forms were measured by Western blotting and immunohistochemistry. Results Acid saline injection induced significant mechanical hyperalgesia (paw withdrawal threshold 2.18±0.27 g, p 〈 0.05 vs controls), which was reversed by EA (4.23±0.33 g, p 〈 0.05 vs FM group) but not by MA (2.37±0.14 g, p 〈 0.05 vs EA group). Expression levels of phosphorylated N-methyl-D-aspartate receptor (pNR)1 and pNR2B were significantly increased in the dorsal root ganglion of FM model mice (132.21±14.4% and 116.69±3.22% of control values), whereas NR1 and NR2B levels were unchanged (97.31±3.79% and 97.07%±2.27%, respectively). Expression levels of pCaMKIIα and pCREB were also higher in the FM group, and these changes were reversed by EA but not by MA. Similar changes in expression were observed in spinal cord neurons. Conclusions Reduced NMDAR−CaMKIIα−pCREB signalling is implicated in the positive effects of EA in FM. NMDAR signalling components may represent promising therapeutic targets for FM treatment.
    Type of Medium: Online Resource
    ISSN: 0964-5284 , 1759-9873
    URL: Article
    DOI: 10.1136/acupmed-2015-010986
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2017
    detail.hit.zdb_id: 2126127-1
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  • 6
    Online Resource
    Online Resource
    Effects of diallyl trisulfide on induction of apoptotic death in murine leukemia WEHI‐3 cells in vitro and alterations of the immune responses in normal and leukemic mice in vivo
    Wiley ; 2015
    In:  Environmental Toxicology Vol. 30, No. 11 ( 2015-11), p. 1343-1353
    Details
    In: Environmental Toxicology, Wiley, Vol. 30, No. 11 ( 2015-11), p. 1343-1353
    Abstract: Diallyl trisulfide (DATS), a chemopreventive dietary constituent and extracted from garlic, has been shown to against cultured many types of human cancer cell liens but the fate of apoptosis in murine leukemia cells in vitro and immune responses in leukemic mice remain elusive. Herein, we clarified the actions of DATS on growth inhibition of murine leukemia WEHI‐3 cells in vitro and used WEHI‐3 cells to generate leukemic mice in vivo , following to investigate the effects of DATS in animal model. In in vitro study, DATS induced apoptosis of WEHI‐3 cells through the G0/G1 phase arrest and induction of caspase‐3 activation. In in vivo study DATS decreased the weight of spleen of leukemia mice but did not affect the spleen weight of normal mice. DATS promoted the immune responses such as promotions of the macrophage phagocytosis and NK cell activities in WEHI‐3 leukemic and normal mice. However, DATS only promotes NK cell activities in normal mice. DATS increases the surface markers of CD11b and Mac‐3 in leukemia mice but only promoted CD3 in normal mice. In conclusion, the present study indicates that DATS induces cell death through induction of apoptosis in mice leukemia WHEI‐3 cells. DATS also promotes immune responses in leukemia and normal mice in vivo . © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 1343–1353, 2015.
    Type of Medium: Online Resource
    ISSN: 1520-4081 , 1522-7278
    URL: Issue
    URL: Article
    DOI: 10.1002/tox.v30.11
    DOI: 10.1002/tox.22005
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2027534-1
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  • 7
    Online Resource
    Online Resource
    Alpha‐phellandrene‐induced apoptosis in mice leukemia WEHI ‐3 cells in vitro
    Wiley ; 2016
    In:  Environmental Toxicology Vol. 31, No. 11 ( 2016-11), p. 1640-1651
    Details
    In: Environmental Toxicology, Wiley, Vol. 31, No. 11 ( 2016-11), p. 1640-1651
    Abstract: Although reports have shown that α‐phellandrene (α‐PA) is one of the monoterpenes and is often used in the food and perfume industry, our previous studies have indicated that α‐PA promoted immune responses in normal mice in vivo . However, there is no available information to show that α‐PA induced cell apoptosis in cancer cells, thus, we investigated the effects of α‐PA on the cell morphology, viability, cell cycle distribution, and apoptosis in mice leukemia WEHI‐3 cells in vitro . Results indicated that α‐PA induced cell morphological changes and decreased viability, induced G0/G1 arrest and sub‐G1 phase (apoptosis) in WEHI‐3 cells. α‐PA increased the productions of reactive oxygen species (ROS) and Ca 2+ and decreased the levels of mitochondrial membrane potential (Δ Ψ m ) in dose‐ and time‐dependent manners in WEHI‐3 cells that were analyzed by flow cytometer. Results from confocal laser microscopic system examinations show that α‐PA promoted the release of cytochrome c, AIF, and Endo G from mitochondria in WEHI‐3 cells. These results are the first findings to provide new information for understanding the mechanisms by which α‐PA induces cell cycle arrest and apoptosis in WEHI‐3 cells in vitro . © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1640–1651, 2016.
    Type of Medium: Online Resource
    ISSN: 1520-4081 , 1522-7278
    URL: Issue
    URL: Article
    DOI: 10.1002/tox.v31.11
    DOI: 10.1002/tox.22168
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2027534-1
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  • 8
    Online Resource
    Online Resource
    Gypenosides Suppress Growth of Human Oral Cancer SAS Cells In Vitro and in a Murine Xenograft Model : The Role of Apoptosis Mediated by Caspase-Dependent and Caspase-Independent Pathways
    SAGE Publications ; 2012
    In:  Integrative Cancer Therapies Vol. 11, No. 2 ( 2012-06), p. 129-140
    Details
    In: Integrative Cancer Therapies, SAGE Publications, Vol. 11, No. 2 ( 2012-06), p. 129-140
    Abstract: Purpose. Gypenosides (Gyp) are the major components of Gynostemma pentaphyllum Makino. The authors investigated the effects of Gyp on cell morphology, viability, cell cycle distribution, and induction of apoptosis in human oral cancer SAS cells and the determination of murine SAS xenograft model in vivo. Experimental design. Flow cytometry was used to quantify the percentage of viable cells; cell cycle distribution; sub-G1 phase (apoptosis); caspase-3, -8, and -9 activity; reactive oxygen species (ROS) production, intracellular Ca 2+ determination; and the level of mitochondrial membrane potential (ΔΨ m ). Western blotting was used to examine levels of apoptosis-associated proteins, and confocal laser microscopy was used to examine the translocation of proteins in cells. Results. Gyp induced morphological changes, decreased the percentage of viable cells, caused G0/G1 phase arrest, and triggered apoptotic cell death in SAS cells. Cell cycle arrest induced by Gyp was associated with apoptosis. The production of ROS, increased intracellular Ca 2+ levels, and the depolarization of ΔΨ m were observed. Gyp increased levels of the proapoptotic protein Bax but inhibited the levels of the antiapoptotic proteins Bcl-2 and Bcl-xl. Gyp also stimulated the release of cytochrome c and Endo G. Translocation of GADD153 to the nucleus was stimulated by Gyp. Gyp in vivo attenuated the size and volume of solid tumors in a murine xenograft model of oral cancer. Conclusions. Gyp-induced cell death occurs through caspase-dependent and caspase-independent apoptotic signaling pathways, and the compound reduced tumor size in a xenograft nu/nu mouse model of oral cancer.
    Type of Medium: Online Resource
    ISSN: 1534-7354 , 1552-695X
    URL: Article
    DOI: 10.1177/1534735411403306
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2012
    detail.hit.zdb_id: 2101248-9
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  • 9
    Online Resource
    Online Resource
    Targeting TRPV1 for Body Weight Control using TRPV1−/− Mice and Electroacupuncture
    Springer Science and Business Media LLC ; 2015
    In:  Scientific Reports Vol. 5, No. 1 ( 2015-12-01)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 5, No. 1 ( 2015-12-01)
    Abstract: Obesity is a global social medical problem resulting in morbidity as high as 20–30%. Here we investigated whether the manipulation of TRPV1 can control mice body weight through electroacupuncture (EA). The results demonstrated that body weight increased with time in the control group (108.19 ± 1.31%, n = 7). The increase of mice body weight was significantly less in the EA group (104.41 ± 0.76%, p  〈  0.05, compared with the control group, n = 7) but not in the sham EA group (109.1 ± 0.63%, p  〈  0.05, compared with EA group, n = 7). EA did not decrease the gain of body weight in TRPV1 knock mice (107.94 ± 0.41% and 107.79 ± 1.04% for TRPV1 −/− and TRPV1 −/− with EA, respectively, p  〉  0.05). The visceral white adipose tissue (WAT) weight was lower in the EA group at 4 weeks after manipulation. Moreover, the protein levels of TRPV1, pPKA, pPKC and pERK were increased in the dorsal root ganglion (DRG) and spinal cord (SC) after EA treatment but not in the sham EA and TRPV1 −/− mice. This study suggests that targeting TRPV1 is beneficial in controlling body weight and TRPV1-associated mechanisms in mice.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/srep17366
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2015
    detail.hit.zdb_id: 2615211-3
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  • 10
    Online Resource
    Online Resource
    Electroacupuncture Restores Spatial Learning and Downregulates Phosphorylated N-Methyl-D-Aspartate Receptors in a Mouse Model of Parkinson's Disease
    SAGE Publications ; 2017
    In:  Acupuncture in Medicine Vol. 35, No. 2 ( 2017-04), p. 133-141
    Details
    In: Acupuncture in Medicine, SAGE Publications, Vol. 35, No. 2 ( 2017-04), p. 133-141
    Abstract: Parkinson's disease (PD) is a degenerative disorder of the central nervous system. PD can be classified as idiopathic, acquired or hereditary and may be caused by various factors such as oxidative stress, loss of mitochondrial function, neuronal excitotoxicity or calcium imbalance. Methods We hypothesised that electroacupuncture (EA) at KI3 would reduce neuronal excitotoxicity by regulating N-methyl-D-aspartate (NMDA) receptor function and may represent a novel therapeutic approach for PD. Results Our results showed that deficits in spatial learning (reflected by the escape latency time in the Morris water maze task) and long-term potentiation (LTP) caused by systemic 6-hydroxydopamine (6-OHDA) administration (that damages dopaminergic neurons) could be rescued by EA on day 3. In PD mice, phosphorylated NMDA receptor subunits NR1 and NR2B were elevated (134.03±10.17% and 123.46±3.47% of baseline levels, respectively) but total NR1 and NR2B was unaffected (101.37±3.87% and 102.61±4.22% of baseline, respectively). Elevated levels of pNR1 and pNR2B, and phosphorylated forms of protein kinase A, protein kinase C, α Ca 2+ /calmodulin-dependent protein kinase extracellular signal-regulated kinases (pERK), and cAMP response element-binding protein were also reduced following EA. Conclusions These novel findings suggest that EA can rescue learning and LTP deficits in a rodent model of PD. The results point to a possible role for EA-based approaches in the clinical treatment of learning deficits associated with PD.
    Type of Medium: Online Resource
    ISSN: 0964-5284 , 1759-9873
    URL: Article
    DOI: 10.1136/acupmed-2015-011041
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2017
    detail.hit.zdb_id: 2126127-1
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