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Li Gao - One of the best experts on this subject based on the ideXlab platform.

  • Pentazocine protects sn4741 cells against mpp induced cell damage via up regulation of the canonical wnt β catenin signaling pathway
    Frontiers in Aging Neuroscience, 2017
    Co-Authors: Jiancai Wang, Gang Zhu, Dayun Feng, Wei Guo, Keyong Tian, Guodong Gao, Li Gao
    Abstract:

    The Wnt/β-catenin signaling pathway has been linked to many neurodegenerative diseases including Parkinson’s disease (PD). A glycoprotein named Dickkopf-1(Dkk1) can combine with the receptor complex on cell membrane to inhibit Wnt/β-catenin signaling. Opioids, a series of compounds including morphine, fentanyl and Pentazocine, have been reported to contribute to the up-regulation of Wnt/β-catenin signaling. Naloxone is an antagonist that has been used as an antidote to opioids through mu-opioid receptor. MPP+, which serves as a selective toxin for dopaminergic neurons, has been used to create experimental models of PD. In our study, we examined the protective effects of Pentazocine against MPP+-induced cell death in the nigral dopaminergic cell line, SN4741 and tried to elucidate the molecular mechanisms underlying such protective effects. The data showed that pretreatment with Pentazocine significantly rescued the SN4741 cell against MPP+. Moreover, the MPP+-exposed SN4741 cells exhibited a down-regulation of β-catenin, which could be restored by treatment with Pentazocine. However, Dkk1 but not naloxonewas associated with the abrogation of protective effect of Pentazocine. These results suggest that Pentazocine alleviates MPP+-induced SN4741 cells apoptosis via the up-regulation of canonical Wnt/β-catenin signaling.

  • Pentazocine Protects SN4741 Cells Against MPP+-Induced Cell Damage via Up-Regulation of the Canonical Wnt/β-Catenin Signaling Pathway
    Frontiers Media S.A., 2017
    Co-Authors: Jiancai Wang, Gang Zhu, Dayun Feng, Wei Guo, Keyong Tian, Guodong Gao, Li Gao
    Abstract:

    The Wnt/β-catenin signaling pathway has been linked to many neurodegenerative diseases including Parkinson’s disease (PD). A glycoprotein named Dickkopf-1 (Dkk1) can combine with the receptor complex on cell membrane to inhibit Wnt/β-catenin signaling. Opioids, a series of compounds including morphine, fentanyl and Pentazocine, have been reported to contribute to the up-regulation of Wnt/β-catenin signaling. Naloxone is an antagonist that has been used as an antidote to opioids through mu-opioid receptor. 1-methyl-4-phenylpyridinium (MPP+), which serves as a selective toxin for dopaminergic neurons, has been used to create experimental models of PD. In our study, we examined the protective effects of Pentazocine against MPP+-induced cell death in the nigral dopaminergic cell line, SN4741 and tried to elucidate the molecular mechanisms underlying such protective effects. The data showed that pretreatment with Pentazocine significantly rescued the SN4741 cell against MPP+. Moreover, the MPP+-exposed SN4741 cells exhibited a down-regulation of β-catenin, which could be restored by treatment with Pentazocine. However, Dkk1 but not naloxonewas associated with the abrogation of protective effect of Pentazocine. These results suggest that Pentazocine alleviates MPP+-induced SN4741 cells apoptosis via the up-regulation of canonical Wnt/β-catenin signaling

Wayne D Bowen - One of the best experts on this subject based on the ideXlab platform.

  • dissociation of the motor effects of Pentazocine from binding to σ1 sites
    European Journal of Pharmacology, 1996
    Co-Authors: Wayne D Bowen, Rae R Matsumoto, Michael J Walker, Saundra L Patrick, Alexander C Zambon, Daniel D Truong, Brian R De Costa, Kenner C Rice
    Abstract:

    Abstract Radioligand binding and behavioral studies were conducted to determine whether a relationship existed between the motor effects produced by (+)-Pentazocine and its binding to σ sites. Scatchard analyses revealed decreased [ 3 H](+)-Pentazocine binding in middle aged rats (5–6 months old) compared to young adult rats (2–3 months old). However, there was no difference between the extent of circling behavior or dystonia produced by microinjection of (+)-Pentazocine into the substantia nigra or red nucleus in the older animals compared to the young adult rats. There was also a significant decrease in [ 3 H](+)-Pentazocine binding in rats chronically treated with haloperidol. Again, however, despite the reduction in [ 3 H](+)-Pentazocine binding, there was no difference between the extent of dystonia produced by unilateral intrarubral microinjection of (+)-Pentazocine into animals chronically treated with haloperidol vs. saline. The postural changes produced by (+)-Pentazocine could not be attenuated with coadministration of the putative σ receptor antagonist BD1047 ( N -[2-(3,4-dichlorophenyl)ethyl]- N -methyl-2-(dimethylamino)ethylamine), or the opiate receptor antagonist naloxone. However, the (+)-opiate, (+)-nordihydrocodeinone, partially attenuated the postural effects of (+)-Pentazocine, despite its very low affinity for σ 1 , σ 2 , or opiate receptors. Taken together with previous studies, the results suggest that [ 3 H](+)-Pentazocine is a potent and selective probe for σ 1 binding sites, but the in vivo effects of (+)-Pentazocine cannot be fully attributed to actions through these sites. Some of the in vivo effects of (+)-Pentazocine appear to involve other binding sites that are not detected under the conditions normally used in in vitro assays.

  • sigma 1 and sigma 2 receptors are expressed in a wide variety of human and rodent tumor cell lines
    Cancer Research, 1995
    Co-Authors: Bertold J Vilner, Christy S John, Wayne D Bowen
    Abstract:

    Abstract Thirteen tumor-derived cell lines of human and nonhuman origin and from various tissues were examined for the presence and density of sigma-1 and sigma-2 receptors. Sigma-1 receptors of a crude membrane fraction were labeled using [3H](+)-Pentazocine, and sigma-2 receptors were labeled with [3H]1,3-di-o-tolylguanidine ([3H]DTG); in the presence or absence of dextrallorphan. [3H](+)-Pentazocine-binding sites were heterogeneous. In rodent cell lines (e.g., C6 glioma, N1E-115 neuroblastoma, and NG108-15 neuroblastoma × glioma hybrid), human T47D breast ductal carcinoma, human NCI-H727 lung carcinoid, and human A375 melanoma, [3H](+)-Pentazocine bound to high- and low-affinity sites with Kd1 = 0.67–7.0 nm, Bmax1 = 25.5–108 fmol/mg protein, Kd2 = 127–600 nm, and Bmax2 = 942–5431 fmol/mg protein. However, [3H](+)-Pentazocine bound to a single site in other cell lines. In human U-138MG glioblastoma, SK-N-SH neuroblastoma, and LNCaP.FGC prostate, Kd = 28–61 nm and Bmax = 975–1196 fmol/mg protein, whereas in ThP-1 leukemia Kd = 146 nm and Bmax = 1411 fmol/mg protein. The sigma-1-like nature of [3H](+)-Pentazocine-binding sites was confirmed by competition studies which revealed high affinity for haloperidol and enantioselectivity for (+)-Pentazocine over (-)-Pentazocine. Interestingly, human MCF-7 breast adenocarcinoma showed little or no specific binding of [3H](+)-Pentazocine, suggesting the absence of sigma-1 receptors in this cell line. All cell lines examined expressed a high density of sigma-2 receptors with Kd values for [3H]DTG ranging from 20 to 101 nm and Bmax values of 491 to 7324 fmol/mg protein. Competition studies indicated possible heterogeneity of sigma-2 receptors. While sites labeled by [3H]DTG in all cell lines tested exhibited affinity for haloperidol and preference for (-)-Pentazocine over the (+)-enantiomer, human cell lines generally showed 4- to 7-fold lower affinity for haloperidol and approximately 10-fold lower affinity for (-)-Pentazocine compared with the rodent cell lines. The high density of sigma-1 and sigma 2-binding sites in these cell lines suggests important cellular functions in cancer, as well as potential diagnostic utility for tumor-imaging agents which target sigma sites. These cell lines may be useful as model systems in which to study the functions of sigma sites in normal tissues, as well as their possible role in tumor biology.

  • autoradiographic distribution of 3h Pentazocine and 3h 1 3 di o tolylguanidine dtg binding sites in guinea pig brain a comparative study
    Brain Research, 1992
    Co-Authors: Michael J Walker, Wayne D Bowen, Saundra L Patrick, Susanne R Goldstein, Archie H Roberts, Andrea G Hohmann, B R Decosta
    Abstract:

    Binding studies suggested the selectivity of (+)-Pentazocine for sigma receptors, and subsequent synthesis and testing of [3H](+)-Pentazocine confirmed its high potency and selectivity for sigma sites. Newer data have demonstrated the selectivity of (+)-Pentazocine for a subtype of the sigma receptor called sigma-1. Based on these findings, the distribution of [3H](+)-Pentazocine binding sites in the guinea pig brain was examined using in vitro autoradiography. [3H](+)-Pentazocine binding was high in the cingulate cortex, dorsal diagonal band, periaqueductal gray, cerebellum and cranial nerve nuclei. It was relatively low in the nucleus accumbens, neocortical areas and caudate nucleus. A significant correlation was found between the binding of [3H](+)-Pentazocine and [3H]1,3-di-o-tolylguanidine, a selective sigma ligand across brain regions. However, certain nuclei exhibited markedly different ratios of binding of the two ligands. Since DTG is not selective for the sigma subtypes, while (+)-Pentazocine is selective for the sigma-1 type, the data are suggestive of relative differences in the distributions of sigma-1 and sigma-2 sites.

Jiancai Wang - One of the best experts on this subject based on the ideXlab platform.

  • Pentazocine protects sn4741 cells against mpp induced cell damage via up regulation of the canonical wnt β catenin signaling pathway
    Frontiers in Aging Neuroscience, 2017
    Co-Authors: Jiancai Wang, Gang Zhu, Dayun Feng, Wei Guo, Keyong Tian, Guodong Gao, Li Gao
    Abstract:

    The Wnt/β-catenin signaling pathway has been linked to many neurodegenerative diseases including Parkinson’s disease (PD). A glycoprotein named Dickkopf-1(Dkk1) can combine with the receptor complex on cell membrane to inhibit Wnt/β-catenin signaling. Opioids, a series of compounds including morphine, fentanyl and Pentazocine, have been reported to contribute to the up-regulation of Wnt/β-catenin signaling. Naloxone is an antagonist that has been used as an antidote to opioids through mu-opioid receptor. MPP+, which serves as a selective toxin for dopaminergic neurons, has been used to create experimental models of PD. In our study, we examined the protective effects of Pentazocine against MPP+-induced cell death in the nigral dopaminergic cell line, SN4741 and tried to elucidate the molecular mechanisms underlying such protective effects. The data showed that pretreatment with Pentazocine significantly rescued the SN4741 cell against MPP+. Moreover, the MPP+-exposed SN4741 cells exhibited a down-regulation of β-catenin, which could be restored by treatment with Pentazocine. However, Dkk1 but not naloxonewas associated with the abrogation of protective effect of Pentazocine. These results suggest that Pentazocine alleviates MPP+-induced SN4741 cells apoptosis via the up-regulation of canonical Wnt/β-catenin signaling.

  • Pentazocine Protects SN4741 Cells Against MPP+-Induced Cell Damage via Up-Regulation of the Canonical Wnt/β-Catenin Signaling Pathway
    Frontiers Media S.A., 2017
    Co-Authors: Jiancai Wang, Gang Zhu, Dayun Feng, Wei Guo, Keyong Tian, Guodong Gao, Li Gao
    Abstract:

    The Wnt/β-catenin signaling pathway has been linked to many neurodegenerative diseases including Parkinson’s disease (PD). A glycoprotein named Dickkopf-1 (Dkk1) can combine with the receptor complex on cell membrane to inhibit Wnt/β-catenin signaling. Opioids, a series of compounds including morphine, fentanyl and Pentazocine, have been reported to contribute to the up-regulation of Wnt/β-catenin signaling. Naloxone is an antagonist that has been used as an antidote to opioids through mu-opioid receptor. 1-methyl-4-phenylpyridinium (MPP+), which serves as a selective toxin for dopaminergic neurons, has been used to create experimental models of PD. In our study, we examined the protective effects of Pentazocine against MPP+-induced cell death in the nigral dopaminergic cell line, SN4741 and tried to elucidate the molecular mechanisms underlying such protective effects. The data showed that pretreatment with Pentazocine significantly rescued the SN4741 cell against MPP+. Moreover, the MPP+-exposed SN4741 cells exhibited a down-regulation of β-catenin, which could be restored by treatment with Pentazocine. However, Dkk1 but not naloxonewas associated with the abrogation of protective effect of Pentazocine. These results suggest that Pentazocine alleviates MPP+-induced SN4741 cells apoptosis via the up-regulation of canonical Wnt/β-catenin signaling

Hiroshi Seno - One of the best experts on this subject based on the ideXlab platform.

  • rapid analysis of Pentazocine in human plasma by liquid chromatography mass spectrometry with sonic spray ionization
    Analytica Chimica Acta, 2003
    Co-Authors: Tetsuya Arinobu, Takeshi Kumazawa, Akira Ishii, Osamu Suzuki, Hideki Hattori, Xiaopen Lee, Sadao Kojima, Hiroshi Seno
    Abstract:

    Abstract A rapid determination method for Pentazocine in human plasma without complicated pretreatments has been constructed by liquid chromatography/mass spectrometry (LC/MS) with sonic spray ionization (SSI) using an Oasis HLB cartridge column. The reliability on our method was investigated for human plasma samples spiked with Pentazocine and dextromethorphan as internal standard. The regression equation for Pentazocine showed good linearity in the ranges of 30–1,250 and 1,250–10,000 ng ml−1; the detection limit was 19.5 ng ml−1 in human plasma. The sensitivity, accuracy and precision were satisfactory to quantify the wide range of therapeutic to toxic levels. Our method established enabled the determination of a single sample of Pentazocine in human plasma only within 4 min, and allowed analysis of more than 100 samples per day. The present method seems applicable for actual cases encountered in the forensic and clinical practices.

  • determination of Pentazocine in human whole blood and urine by gas chromatography surface ionization organic mass spectrometry
    Journal of Mass Spectrometry, 2000
    Co-Authors: Hiroshi Seno, Takeshi Kumazawa, Akira Ishii, Hajime Matsushima, Kanako Watanabesuzuki, Osamu Suzuki
    Abstract:

    Pentazocine has been found to be measurable with much higher sensitivity by gas chromatography (GC)/surface ionization (SI) organic mass spectrometry (OMS) than by the conventional GC/electron ionization (EI) mass spectrometry. The compound was extracted from human whole blood and urine with Sep-Pak C18 cartridges before analysis by GC/SIOMS; recoveries were > 96.6% for both samples. The calibration curves were linear in the range 6.25–100 ng ml−1 and the detection limits were 500 pg ml−1 of a sample by selected ion monitoring (SIM) with GC/SIOMS. The intra- and inter-day relative standard deviations for the determination of Pentazocine in whole blood and urine were not greater than 9.6%. The sensitivity for Pentazocine obtained by SI-SIM was about 60 times higher than that obtained by EI-SIM. To validate the present GC/SIOMS method for Pentazocine, whole blood and urine samples collected from two volunteers 1–6 h after intramuscular injection of 15 mg of Pentazocine were analyzed. The concentrations were 13.5–59.3 ng ml−1 for whole blood and 0.39–4.00 µg ml−1 for urine. Copyright © 2000 John Wiley & Sons, Ltd.

Dayun Feng - One of the best experts on this subject based on the ideXlab platform.

  • Pentazocine protects sn4741 cells against mpp induced cell damage via up regulation of the canonical wnt β catenin signaling pathway
    Frontiers in Aging Neuroscience, 2017
    Co-Authors: Jiancai Wang, Gang Zhu, Dayun Feng, Wei Guo, Keyong Tian, Guodong Gao, Li Gao
    Abstract:

    The Wnt/β-catenin signaling pathway has been linked to many neurodegenerative diseases including Parkinson’s disease (PD). A glycoprotein named Dickkopf-1(Dkk1) can combine with the receptor complex on cell membrane to inhibit Wnt/β-catenin signaling. Opioids, a series of compounds including morphine, fentanyl and Pentazocine, have been reported to contribute to the up-regulation of Wnt/β-catenin signaling. Naloxone is an antagonist that has been used as an antidote to opioids through mu-opioid receptor. MPP+, which serves as a selective toxin for dopaminergic neurons, has been used to create experimental models of PD. In our study, we examined the protective effects of Pentazocine against MPP+-induced cell death in the nigral dopaminergic cell line, SN4741 and tried to elucidate the molecular mechanisms underlying such protective effects. The data showed that pretreatment with Pentazocine significantly rescued the SN4741 cell against MPP+. Moreover, the MPP+-exposed SN4741 cells exhibited a down-regulation of β-catenin, which could be restored by treatment with Pentazocine. However, Dkk1 but not naloxonewas associated with the abrogation of protective effect of Pentazocine. These results suggest that Pentazocine alleviates MPP+-induced SN4741 cells apoptosis via the up-regulation of canonical Wnt/β-catenin signaling.

  • Pentazocine Protects SN4741 Cells Against MPP+-Induced Cell Damage via Up-Regulation of the Canonical Wnt/β-Catenin Signaling Pathway
    Frontiers Media S.A., 2017
    Co-Authors: Jiancai Wang, Gang Zhu, Dayun Feng, Wei Guo, Keyong Tian, Guodong Gao, Li Gao
    Abstract:

    The Wnt/β-catenin signaling pathway has been linked to many neurodegenerative diseases including Parkinson’s disease (PD). A glycoprotein named Dickkopf-1 (Dkk1) can combine with the receptor complex on cell membrane to inhibit Wnt/β-catenin signaling. Opioids, a series of compounds including morphine, fentanyl and Pentazocine, have been reported to contribute to the up-regulation of Wnt/β-catenin signaling. Naloxone is an antagonist that has been used as an antidote to opioids through mu-opioid receptor. 1-methyl-4-phenylpyridinium (MPP+), which serves as a selective toxin for dopaminergic neurons, has been used to create experimental models of PD. In our study, we examined the protective effects of Pentazocine against MPP+-induced cell death in the nigral dopaminergic cell line, SN4741 and tried to elucidate the molecular mechanisms underlying such protective effects. The data showed that pretreatment with Pentazocine significantly rescued the SN4741 cell against MPP+. Moreover, the MPP+-exposed SN4741 cells exhibited a down-regulation of β-catenin, which could be restored by treatment with Pentazocine. However, Dkk1 but not naloxonewas associated with the abrogation of protective effect of Pentazocine. These results suggest that Pentazocine alleviates MPP+-induced SN4741 cells apoptosis via the up-regulation of canonical Wnt/β-catenin signaling