estrogen receptor β erβ antagonist  (Santa Cruz Biotechnology)

Journal: Endocrinology

Article Title: BPA Differentially Regulates NPY Expression in Hypothalamic Neurons Through a Mechanism Involving Oxidative Stress.

doi: 10.1210/endocr/bqaa170

Figure Lengend Snippet: Figure 9. Summary. BPA induces oxidative stress and increases pAMPK levels in both mHypoA-59 and mHypoE-46 cells. Activation of pAMPK is re- quired for the BPA-mediated increase in Npy, but not the decrease. Whereas antioxidants NBA, TUDCA, SP600125, NDGA, NAC, and vitamin B6 prevent BPA-mediated upregulation of Npy expression in the mHypoA-59 cells, only NBA, TUDCA, and SP600125 block the BPA-mediated downregulation of Npy in the mHypoE-46 cells. Thus, oxidative stress is implicated in the BPA-mediated dysregulation of Npy, despite the involvement of different downstream events. These differential mechanisms may include activation of GPR30 or ERβ in the mHypoE-46 cells as the respective antagonists, G15 and PHTPP, reverse the BPA-mediated decrease in Npy. NBA also blocks the BPA-mediated changes in Esr1 and Esr2 mRNA levels in the re- spective cell lines, and vitamin B6 mitigates the BPA-induced decrease in Esr2 in the mHypoA-59 cells.

Article Snippet: The G-protein coupled estrogen receptor (GPER1 or GPR30) antagonist G15 (cat. #3678), the estrogen receptor β (ERβ) antagonist PHTPP (cat. #2662), and the aryl hydrocarbon receptor antagonist CH223191 (cat. #3858) were purchased from Tocris BioScience (Cedarlane, Burlington, ON, Canada).

Techniques: Activation Assay, Expressing, Blocking Assay

Journal: Frontiers in Microbiology

Article Title: HIV-1 Tat and cocaine mediated synaptopathy in cortical and midbrain neurons is prevented by the isoflavone Equol

doi: 10.3389/fmicb.2015.00894

Figure Lengend Snippet: R-Equol (RE) and S-Equol (SE) prevented synaptic loss induced by HIV-1 Tat (50 nM) via an estrogen receptor mediated mechanism. (A) Conversion of the soy isoflavone daidzein to SE. The dotted circle identifies a chiral center on carbon 3 wherein a conformational change produces RE. However, only SE may be produced by mammalian gut bacteria. (B) A moderate concentration of RE (50 nM), but not a low concentration (33 nM), prevented significant F-actin puncta loss induced by HIV-1 Tat (50 nM; p ≤ 0.01). (C) Both the low (33 nM) and moderate (50 nM) concentrations of SE prevented HIV-1 Tat induced F-actin puncta loss ( p ≤ 0.05 and p ≤ 0.001, respectively). (D) 1 h pre-treatment with TMX (100 nM) blocked the protective effects of RE and SE (50 nM) against HIV-1 Tat (50 nM) in midbrain neurons. Mean ± SEM, ∗ p ≤ 0.05 compared to HIV-1 Tat treatment.

Article Snippet: In order to determine which estrogenic receptors were necessary for SE and RE neuroprotection, cells were treated with TMX for 1 h prior to treatment with either SE (50 nM), RE (50 nM), 4-[2-Phenyl-5,7- bis (trifluoromethyl)pyrazolo[1,5- a ]pyrmidin-3-yl)phenol (PHTPP) estrogen receptor beta (ERβ) antagonist, final concentration 100 nM (Tocris Bioscience, Ellisville, MD, USA); 1,3- Bis (4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1 H -pyrazole dihydrochloride (MPP) estrogen receptor alpha antagonist; final concentration 100 nM (Tocris Bioscience, Ellisville, MD, USA), or (3a S ∗ ,4R ∗ ,9b R ∗ )-4-(6-Bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-3 H -cyclopenta[ c ]quinoline (G15) membrane estrogen receptor antagonist, final concentration 100 nM (Tocris Bioscience, Ellisville, MD, USA).

Techniques: Produced, Bacteria, Concentration Assay

Journal: Frontiers in Microbiology

Article Title: HIV-1 Tat and cocaine mediated synaptopathy in cortical and midbrain neurons is prevented by the isoflavone Equol

doi: 10.3389/fmicb.2015.00894

Figure Lengend Snippet: HIV-1 Tat (10 nM) + cocaine (1.6 μM) treatment produced significant synaptic loss in midbrain and cortical neurons, which was prevented by pre-treatment with either RE or SE. (A) Treatment with either SE, RE, HIV-1 Tat, or cocaine does not significantly alter the density of dendritic F-actin puncta compared to controls in midbrain neurons. Treatment with HIV-1 Tat + cocaine produced significant loss of F-actin puncta ( p ≤ 0.05). (B) Treatment with either SE, RE, HIV-1 Tat, or cocaine does not significantly alter the density of dendritic F-actin puncta compared to controls in cortical neurons. Treatment with HIV-1 Tat + cocaine produced significant loss of F-actin puncta ( p ≤ 0.05). (C) Pre-treatment with either RE or SE (50 nM) prevented dendritic F-actin puncta loss caused by HIV-1 Tat + cocaine treatments in midbrain neurons. Dendrites from pre-treated neurons are not significantly different from vehicle-treated controls (mean values, dotted line). (D) Pre-treatment with either RE or SE (50 nM) prevents HIV-1Tat + cocaine induced loss of dendritic F-actin puncta ( p ≤ 0.001) in cortical neurons. Dendrites from pre-treated neurons are not significantly different from vehicle-treated controls (mean values, dotted line). (E) Pre-treatment of midbrain neurons with TMX (100 nM) for 1 h prior to either RE or SE prevented the protective effects of RE and SE, suggesting an estrogen receptor mediated mechanism. Vehicle-treated control mean values are represented by dotted line. (F) Pre-treatment of cortical neurons with TMX (100 nM) for 1 h prior to either RE or SE prevented the protective effects of RE and SE, suggesting an estrogen receptor mediated mechanism. Control mean value represented by dotted line. Mean ± SEM, ∗ p ≤ 0.05 compared either to vehicle-treated controls (A,B) or HIV-1 Tat + cocaine (C,D) .

Article Snippet: In order to determine which estrogenic receptors were necessary for SE and RE neuroprotection, cells were treated with TMX for 1 h prior to treatment with either SE (50 nM), RE (50 nM), 4-[2-Phenyl-5,7- bis (trifluoromethyl)pyrazolo[1,5- a ]pyrmidin-3-yl)phenol (PHTPP) estrogen receptor beta (ERβ) antagonist, final concentration 100 nM (Tocris Bioscience, Ellisville, MD, USA); 1,3- Bis (4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1 H -pyrazole dihydrochloride (MPP) estrogen receptor alpha antagonist; final concentration 100 nM (Tocris Bioscience, Ellisville, MD, USA), or (3a S ∗ ,4R ∗ ,9b R ∗ )-4-(6-Bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-3 H -cyclopenta[ c ]quinoline (G15) membrane estrogen receptor antagonist, final concentration 100 nM (Tocris Bioscience, Ellisville, MD, USA).

Techniques: Produced, Control