trpv1 antagonist capsazepine  (Tocris)

Journal: ImmunoTargets and Therapy

Article Title: UVB Upregulates Inflammatory Cytokines in Rosacea Cell Model by Promoting the Expression of TRPVs and TLR2

doi: 10.2147/ITT.S571037

Figure Lengend Snippet: The influence of UVB on the mRNA and protein expressions of TRPV1, TRPV2, TRPV3, TRPV4 and TLR2 in the rosacea keratinocyte model. ( A ) The expression levels of TRPV1, TRPV2, TRPV3, TRPV4 and TLR2 mRNA in HaCaT cells and HaCaT cells treated by 8 μM LL-37 after 25 mJ/cm² UVB exposure were detected by qRT-PCR. ( B and C ) The protein expression levels of TRPV1, TRPV2, TRPV3, TRPV4 and TLR2 in HaCaT cells and HaCaT cells stimulated by 8 μM LL-37 after 25 mJ/cm² UVB irradiation were measured by Western blot. (n = 3, compared with the control group, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001; compared with the LL-37 + UVB group, ## P < 0.01, #### P < 0.0001.).

Article Snippet: The TRPV1 receptor antagonist capsazepine (10 μM, Selleck, China), TRPV4 receptor antagonist RN-1734 (20 μM, Selleck, China) and TLR2 receptor antagonist TLR2-IN-C29 (50 μM, Selleck, China) were used to treat HaCaT cells stimulated by LL-37.

Techniques: Expressing, Quantitative RT-PCR, Irradiation, Western Blot, Control

Journal: ImmunoTargets and Therapy

Article Title: UVB Upregulates Inflammatory Cytokines in Rosacea Cell Model by Promoting the Expression of TRPVs and TLR2

doi: 10.2147/ITT.S571037

Figure Lengend Snippet: The effects of TRPV1, TRPV4 and TLR2 receptor antagonists on the expression of inflammatory factors in vitro experimental model for rosacea that underwent or did not undergo UVB irradiation. ( A-C ) The levels of inflammatory factors in the rosacea keratinocyte model were determined by ELISA after the treatment with 10 μM CAP, 20 μM RN-1734 and 50 μM TLR-IN-C29. ( D-F ) The levels of inflammatory factors in the rosacea keratinocyte model were detected by ELISA after 25 mJ/cm² UVB irradiation and treatment with 10 μM CAP, 20 μM RN-1734, and 50 μM TLR-IN-C29. (n=6, *P < 0.05, **P < 0.01, ****P < 0.0001.) CAP: capsazepine.

Article Snippet: The TRPV1 receptor antagonist capsazepine (10 μM, Selleck, China), TRPV4 receptor antagonist RN-1734 (20 μM, Selleck, China) and TLR2 receptor antagonist TLR2-IN-C29 (50 μM, Selleck, China) were used to treat HaCaT cells stimulated by LL-37.

Techniques: Expressing, In Vitro, Irradiation, Enzyme-linked Immunosorbent Assay

Journal: ImmunoTargets and Therapy

Article Title: UVB Upregulates Inflammatory Cytokines in Rosacea Cell Model by Promoting the Expression of TRPVs and TLR2

doi: 10.2147/ITT.S571037

Figure Lengend Snippet: The epigenetic alterations of TRPV1, TRPV4 and TLR2 promoters in rosacea cell model. ( A ) MeDIP was used to assess the relative methylation modification levels of the promoters of TRPV1, TRPV4 and TLR2 genes in the rosacea keratinocyte model after 25 mJ/cm² UVB irradiation. ( B ) ChIP was applied to assess the modification levels of H3K4me3, H3K9me3 and H3K27me3 in the promoters of TRPV1, TRPV4 and TLR2 genes in the rosacea keratinocyte model after 25 mJ/cm² UVB irradiation. (n = 3, *P < 0.05.).

Article Snippet: The TRPV1 receptor antagonist capsazepine (10 μM, Selleck, China), TRPV4 receptor antagonist RN-1734 (20 μM, Selleck, China) and TLR2 receptor antagonist TLR2-IN-C29 (50 μM, Selleck, China) were used to treat HaCaT cells stimulated by LL-37.

Techniques: Methylated DNA Immunoprecipitation, Methylation, Modification, Irradiation

Journal: Molecular Pain

Article Title: Evodiamine attenuates chemotherapy-induced peripheral neuropathy by mediating macrophage M2 polarization and inhibiting the upregulation of the p38 MAPK-TRPV1 axis in rat dorsal root ganglia

doi: 10.1177/17448069251392037

Figure Lengend Snippet: Establishment and characterization of the paclitaxel-induced chemotherapy-induced peripheral neuropathy (CIPN) rat model. (a) Schematic representation of the experimental timeline showing paclitaxel administration (2.0 mg/kg, i.p.), behavioral testing schedule, and tissue collection timepoints. (b) Development of mechanical allodynia as measured by paw withdrawal threshold (g) in blank (PBS), vehicle (DMSO) and paclitaxel-treated (PTX) rats over a 21-day period. (c) Development of thermal hyperalgesia as measured by paw licking latency (s) in blank, vehicle and PTX-treated rats. (d) Relative mRNA expression of TRPV channel subtypes (TRPV1, TRPV2, TRPV3, and TRPV4) in dorsal root ganglia (DRG) of blank, vehicle (DMSO) and PTX-treated rats at day 21. Data are presented as mean ± standard deviation (SD), n = 6 rats per group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 compared to vehicle group. ns, no significant, PTX + Vehicle group compared to PTX group.

Article Snippet: The TRPV1 antagonist capsazepine (MCE, HY-15640) was dissolved in DMSO and then diluted with PBS to the dosing concentration.

Techniques: Expressing, Standard Deviation

Journal: Molecular Pain

Article Title: Evodiamine attenuates chemotherapy-induced peripheral neuropathy by mediating macrophage M2 polarization and inhibiting the upregulation of the p38 MAPK-TRPV1 axis in rat dorsal root ganglia

doi: 10.1177/17448069251392037

Figure Lengend Snippet: Evodiamine selectively inhibits the upregulation of TRPV1 but not TRPV4 in the DRG of paclitaxel-induced CIPN rats. (a) Relative mRNA expression levels of Trpv1 in dorsal root ganglia (DRG) tissues from rats treated with PTX, PTX + vehicle (DMSO) and PTX + evodiamine (0.3, 1.0, or 3.0 mg/kg, daily) for 21 days. Expression was normalized to Gapdh. (b) Relative mRNA expression levels of Trpv4 in DRG tissues from the same experimental groups, normalized to Gapdh. Data are presented as mean ± standard deviation (SD), n = 6 rats per group. ** p < 0.01, **** p < 0.0001 compared to PTX + vehicle group. ns, no significant, PTX + Vehicle group compared to PTX group.

Article Snippet: The TRPV1 antagonist capsazepine (MCE, HY-15640) was dissolved in DMSO and then diluted with PBS to the dosing concentration.

Techniques: Expressing, Standard Deviation

Journal: Molecular Pain

Article Title: Evodiamine attenuates chemotherapy-induced peripheral neuropathy by mediating macrophage M2 polarization and inhibiting the upregulation of the p38 MAPK-TRPV1 axis in rat dorsal root ganglia

doi: 10.1177/17448069251392037

Figure Lengend Snippet: Evodiamine alleviates paclitaxel-induced mechanical allodynia and thermal hyperalgesia in rats in a TRPV1-dependent manner. (a, b) Damage effects of TRPV1 on the development of mechanical allodynia (a) and thermal hyperalgesia (b) in CIPN rats. Animals received daily intraperitoneal injections of evodiamine (3.0 mg/kg) or CAZ following paclitaxel (2 mg/kg) administration, and pain behaviors were assessed over a 21-day period. Data are presented as mean ± standard deviation (SD), n = 6 rats per group. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to PTX + Evo 3 mg/kg group; ns, no significant, PTX + CAZ + Evo 3.0 mg/kg group compared to PTX + CAZ group.

Article Snippet: The TRPV1 antagonist capsazepine (MCE, HY-15640) was dissolved in DMSO and then diluted with PBS to the dosing concentration.

Techniques: Standard Deviation

Journal: Molecular Pain

Article Title: Evodiamine attenuates chemotherapy-induced peripheral neuropathy by mediating macrophage M2 polarization and inhibiting the upregulation of the p38 MAPK-TRPV1 axis in rat dorsal root ganglia

doi: 10.1177/17448069251392037

Figure Lengend Snippet: Evodiamine reduces TRPV1 expression in DRG neurons by inhibiting paclitaxelinduced M1 polarization of macrophages. (a) Flow cytometry analysis shows the percentage of macrophages marked by CD86 and F4/80 in RAW264.7 cells of different treatment groups. Quadrants Q2 (upper left quadrant) represent the F4/80+CD86+ macrophage population, respectively. n = 3 per group. (b) Flow cytometry analysis shows the percentage of macrophages marked by CD206 and F4/80 in RAW264.7 cells of different treatment groups. n = 3 per group. (c) Bar graphs show the relative expression levels of TRPV1 mRNA in different treatment groups. n = 6 per group. (d) WB analysis shows the protein expression levels of TRPV1 in different treatment groups. n = 3 per group. Compared with the corresponding control, * p < 0.0001, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: The TRPV1 antagonist capsazepine (MCE, HY-15640) was dissolved in DMSO and then diluted with PBS to the dosing concentration.

Techniques: Expressing, Flow Cytometry, Control

Journal: Molecular Pain

Article Title: Evodiamine attenuates chemotherapy-induced peripheral neuropathy by mediating macrophage M2 polarization and inhibiting the upregulation of the p38 MAPK-TRPV1 axis in rat dorsal root ganglia

doi: 10.1177/17448069251392037

Figure Lengend Snippet: Evodiamine inhibits the p38 MAPK signaling pathway in DRG neurons to downregulate TRPV1 expression. (a) Representative Western blot images showing protein expression of TRPV1 (95 kDa), phosphorylated p38 MAPK (p-p38MAPK, 43 kDa), total p38 MAPK (40 kDa), and β-actin (42 kDa) in primary DRG neurons treated with different conditioned media. n = 3 per group. (b) Quantitative analysis of TRPV1 protein expression relative to β-actin. n = 3 per group. (c) Quantitative analysis of the phosphorylated p38 MAPK to total p38 MAPK ratio. Primary DRG neurons were treated with control medium (DMSO), macrophage-conditioned medium from paclitaxeltreated cells (MCM-PTX), macrophage-conditioned medium from evodiamine-treated cells (MCMEvo), or MCM-PTX plus the selective p38 MAPK inhibitor SB203580 (10 μM). n = 3 per group. (d) The constructed plasmid of sustained phosphorylation overexpression of p38MAPK (OE-p-p38MAPK) and the empty vector plasmid (OE-NC) were transfected into HEK 293T cells. The protein expression levels of p-p38MAPK in HEK 293T cells between the OE-NC group and OE-p-p38MAPK group were detected by WB. (e) The effect of p-p38MAPK overexpression on TRPV1 transcription in HEK 293T cells was detected by dual-luciferase reporter gene assay. n = 6 per group. Data are presented as mean ± SD ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. ns, no significant.

Article Snippet: The TRPV1 antagonist capsazepine (MCE, HY-15640) was dissolved in DMSO and then diluted with PBS to the dosing concentration.

Techniques: Expressing, Western Blot, Control, Construct, Plasmid Preparation, Phospho-proteomics, Over Expression, Transfection, Luciferase, Reporter Gene Assay

Journal: Molecular Pain

Article Title: Evodiamine attenuates chemotherapy-induced peripheral neuropathy by mediating macrophage M2 polarization and inhibiting the upregulation of the p38 MAPK-TRPV1 axis in rat dorsal root ganglia

doi: 10.1177/17448069251392037

Figure Lengend Snippet: Depletion of macrophages with clodronate liposomes inhibition of the p38 MAPK pathway and TRPV1 expression in DRG tissue. (a) Representative Western blot images showing protein expression of TRPV1, phosphorylated p38 MAPK (p-p38MAPK), total p38 MAPK, and β-actin in DRG tissues from different treatment groups. (b) Quantitative analysis of TRPV1 protein expression relative to β-actin. (c) Quantitative analysis of the phosphorylated p38 MAPK to total p38 MAPK ratio. Treatment groups include vehicle (DMSO), paclitaxel alone (PTX), paclitaxel plus evodiamine (PTX+Evo), and paclitaxel plus evodiamine and clodronate liposomes (PTX+CL). Data are presented as mean ± SD ( n = 3 per rats group). * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The TRPV1 antagonist capsazepine (MCE, HY-15640) was dissolved in DMSO and then diluted with PBS to the dosing concentration.

Techniques: Liposomes, Inhibition, Expressing, Western Blot

Journal: Journal of Neuroimmune Pharmacology

Article Title: Hyperalgesic Effect Evoked by il-16 and its Participation in Inflammatory Hypernociception in Mice

doi: 10.1007/s11481-024-10145-7

Figure Lengend Snippet: A-E Local inhibition of the hyperalgesia evoked by IL-16 (30 ng/kg, s.c., 1 h before testing) following the i.pl administration into the right paw (black bars) of the non-selective cyclooxygenase (COX) inhibitor diclofenac ( A ; 1–10 µg, 1 h before testing), the selective COX-1 inhibitor SC-560 ( B ; 0.1–1 µg, 1 h before testing,), the selective COX-2 inhibitor celecoxib ( C ; 1–5 µg, 1 h before testing), the TRPV1 channel inhibitor capsazepine ( D ; 0.03–0.3 µg, 1 h before testing) or the TRPA1 channel inhibitor HC030031 ( E ; 10–50 µg, 1 h before testing). Means and corresponding standard errors are represented ( n = 5–7 per group). •• p < 0.01 compared with the control group, ** p < 0.01 compared with the group treated with IL-16 (30 ng/kg), Tukey’s test. F ) Local hyperalgesic effect induced after the i.pl. administration of IL-16 (0.1–1 ng, 1 h before testing) in the injected paws (right, black bars) measured by the unilateral hot plate test. Means and corresponding standard errors are represented ( n = 6 per group). * p < 0.05, ** p < 0.01 compared with the control group, Tukey’s test

Article Snippet: The TRPV1 antagonist capsazepine (Tocris) and the TRPA1 antagonist HC030031 (Tocris) were initially dissolved in DMSO and further diluted in saline up to a maximal DMSO concentration of 10%.

Techniques: Inhibition, Control, Injection, Hot Plate Test

Journal: Addiction biology

Article Title: Interrelated involvement of the endocannabinoid/endovanilloid (TRPV1) systems and epigenetic processes in anxiety- and working memory impairment-related behavioural effects of nicotine as a stressor.

doi: 10.1111/adb.13421

Figure Lengend Snippet: FIGURE 1 Mitigating effects of the HDAC inhibitors, CB1 agonist, or TRPV1 antagonist against anxiety-like behaviours. The parameter values of the EPM test (percentages of entries into open arms and time spent on open arms) at the 2-h time point after the last NC (0.8 mg/kg, sc) and/or IM (10 min) treatment are shown as means with standard deviation (SD) bars (n = 10) for each HDAC inhibitor (SB or VA), CB1 agonist (AC), or TRPV1 antagonist (CZ) cotreatment group (with each ip dose [mg/kg]), and statistical significance in posthoc tests is denoted using the symbols as defined below. The detailed data and statistical results have been included in Table S1. (A) SB (100 mg/kg, ip) cotreatment groups (SB groups); (B) VA (300 mg/kg, ip) cotreatment groups (VA groups); (C) AC (0.2 mg/kg, ip) cotreatment groups (AC groups); (D) CZ (1 mg/kg, ip) cotreatment groups (CZ groups). **P < 0.01: significant attenuation as compared with the control group; ++P < 0.01: significant increase as compared with the NC, IM, or NC-IM group without any cotreatments; $$P < 0.01: significant attenuation as compared with the IM group without any cotreatments.

Article Snippet: See the T erm s and C onditions (https://onlinelibrary.w iley.com /term s-and-conditions) on W iley O nline L ibrary for rules of use; O A articles are governed by the applicable C reative C om m ons L icense 1H-pyrazole-3-carboxamide hydrochloride [SR]), the TRPV1 agonist olvanil (OL), and the TRPV1 antagonist capsazepine (CZ), which were all purchased from Tocris Cookson Inc. (Ellisville, Missouri, USA), the data were collected and shown for the following intraperitoneal (ip) doses: 50, 100, and 200 mg/kg for SB; 200, 300, and 400 mg/kg for VA; 0.05, 0.2, and 1 mg/kg for AC; 0.5, 1, and 2 mg/kg for SR; 0.1, 1, and 2.5 mg/kg for OL; and 0.1, 1, and 5 mg/kg for CZ, based on previous data and preliminary experiments.25,42–50 As ligands related to the ECB system, ligands for the CB1 receptors, the representative CB receptors expressed in the central nervous system, were selected.25,38,42,48–50 The doses were selected from those that induced no toxic behavioural alterations (e.g., continuous suppression of locomotor activity) by themselves at the prescribed time point even when combined administration was repeated.

Techniques: Standard Deviation, Control

Journal: Addiction biology

Article Title: Interrelated involvement of the endocannabinoid/endovanilloid (TRPV1) systems and epigenetic processes in anxiety- and working memory impairment-related behavioural effects of nicotine as a stressor.

doi: 10.1111/adb.13421

Figure Lengend Snippet: FIGURE 3 Interacting effects between the CB1 antagonist and mitigating (anxiolytic-like) drug (i.e., HDAC inhibitor, CB1 agonist, or TRPV1 antagonist) against anxiety-like behavioural alterations caused by NC and/or IM. The parameter values of the EPM test at the 2-h time point after the last NC (0.8 mg/kg, sc) or IM (10 min) treatment are shown as means with SD bars (n = 10) for each mitigating drug plus CB1 antagonist group (with each ip dose [mg/kg]), and statistical significance in post hoc tests is denoted using the symbols as defined below. The detailed data and statistical results have been included in Table S3. (A) SB (100 mg/kg, ip) plus SR (1 mg/kg, ip) groups (SB + SR groups); (B) VA (300 mg/kg, ip) plus SR (1 mg/kg, ip) groups (VA + SR groups); (C) AC (0.2 mg/kg, ip) plus SR (1 mg/kg, ip) groups (AC + SR groups); (D) CZ (1 mg/kg, ip) plus SR (1 mg/kg, ip) groups (CZ + SR groups). **P < 0.01: significant attenuation as compared with the control group; ++P < 0.01: significant increase as compared with the NC, IM, or NC-IM group without any cotreatments; $$P < 0.01: significant attenuation as compared with the IM group without any cotreatments; ##P < 0.01: significant attenuation as compared with the NC, IM, or NC-IM group cotreated with the efficacious HDAC inhibitor, CB1 agonist, or TRPV1 antagonist.

Article Snippet: See the T erm s and C onditions (https://onlinelibrary.w iley.com /term s-and-conditions) on W iley O nline L ibrary for rules of use; O A articles are governed by the applicable C reative C om m ons L icense 1H-pyrazole-3-carboxamide hydrochloride [SR]), the TRPV1 agonist olvanil (OL), and the TRPV1 antagonist capsazepine (CZ), which were all purchased from Tocris Cookson Inc. (Ellisville, Missouri, USA), the data were collected and shown for the following intraperitoneal (ip) doses: 50, 100, and 200 mg/kg for SB; 200, 300, and 400 mg/kg for VA; 0.05, 0.2, and 1 mg/kg for AC; 0.5, 1, and 2 mg/kg for SR; 0.1, 1, and 2.5 mg/kg for OL; and 0.1, 1, and 5 mg/kg for CZ, based on previous data and preliminary experiments.25,42–50 As ligands related to the ECB system, ligands for the CB1 receptors, the representative CB receptors expressed in the central nervous system, were selected.25,38,42,48–50 The doses were selected from those that induced no toxic behavioural alterations (e.g., continuous suppression of locomotor activity) by themselves at the prescribed time point even when combined administration was repeated.

Techniques: Control

Journal: Addiction biology

Article Title: Interrelated involvement of the endocannabinoid/endovanilloid (TRPV1) systems and epigenetic processes in anxiety- and working memory impairment-related behavioural effects of nicotine as a stressor.

doi: 10.1111/adb.13421

Figure Lengend Snippet: FIGURE 6 Counteraction caused by the CB1 antagonist against attenuating effects of the TRPV1 antagonist on HDAC inhibitor- or TRPV1 agonist-induced working memory improving-like behavioural alterations in the NC and/or IM treatment groups. The parameter values of the Y-maze test at the 2-h time point after the last NC (0.8 mg/kg, sc) and/or IM (10 min) treatment are shown as means with SD bars (n = 10) for each working memory improving-like drug (HDAC inhibitor or TRPV1 agonist) plus TRPV1 antagonist cotreatment group with or without additional CB1 antagonist (with each ip dose [mg/kg]), and statistical significance in post hoc tests is denoted using the symbols as defined below. The detailed data and statistical results have been included in Table S6. (A) SB (100 mg/kg, ip) plus CZ (1 mg/kg, ip) cotreatment groups with (or without) additional SR (1 mg/kg, ip) (SB + CZ + SR groups); (B) VA (300 mg/kg, ip) plus CZ (1 mg/kg, ip) cotreatment groups with (or without) additional SR (1 mg/kg, ip) (VA + CZ + SR groups); (C) OL (1 mg/kg, ip) plus CZ (1 mg/kg, ip) cotreatment groups with (or without) additional SR (1 mg/kg, ip) (OL + CZ + SR groups). **P < 0.01: significant attenuation as compared with the control group; ++P < 0.01: significant increase as compared with the NC, IM, or NC-IM group without any cotreatments; @@P < 0.01: significant attenuation as compared with the NC group without any cotreatments; $$P < 0.01: significant attenuation as compared with the IM group without any cotreatments; ##P < 0.01: significant attenuation as compared with the NC, IM, or NC-IM group cotreated with the efficacious (working memory improving-like) HDAC inhibitor or TRPV1 agonist; &&P < 0.01: significant increase as compared with the NC, IM, or NC-IM group cotreated with the mitigating drug (HDAC inhibitor or TRPV1 agonist) plus CZ.

Article Snippet: See the T erm s and C onditions (https://onlinelibrary.w iley.com /term s-and-conditions) on W iley O nline L ibrary for rules of use; O A articles are governed by the applicable C reative C om m ons L icense 1H-pyrazole-3-carboxamide hydrochloride [SR]), the TRPV1 agonist olvanil (OL), and the TRPV1 antagonist capsazepine (CZ), which were all purchased from Tocris Cookson Inc. (Ellisville, Missouri, USA), the data were collected and shown for the following intraperitoneal (ip) doses: 50, 100, and 200 mg/kg for SB; 200, 300, and 400 mg/kg for VA; 0.05, 0.2, and 1 mg/kg for AC; 0.5, 1, and 2 mg/kg for SR; 0.1, 1, and 2.5 mg/kg for OL; and 0.1, 1, and 5 mg/kg for CZ, based on previous data and preliminary experiments.25,42–50 As ligands related to the ECB system, ligands for the CB1 receptors, the representative CB receptors expressed in the central nervous system, were selected.25,38,42,48–50 The doses were selected from those that induced no toxic behavioural alterations (e.g., continuous suppression of locomotor activity) by themselves at the prescribed time point even when combined administration was repeated.

Techniques: Control

Journal: Archives of toxicology

Article Title: Cannabidivarin and cannabigerol induce unfolded protein response and angiogenesis dysregulation in placental trophoblast HTR-8/SVneo cells.

doi: 10.1007/s00204-024-03781-8

Figure Lengend Snippet: Fig. 2 CBDV and CBG increase the expression of ER-stress mark- ers. HTR-8/SVneo cells were treated with CBDV and CBG (5 μM) for 48 h, with or without the TRPV1 antagonist CPZ (0.2 µM). A-D Expression of the HSPA5, sXBP1, ATF4 and DDIT3 genes was analyzed through RT-PCR. Results show transcript levels normal- ized against ACTB. E The protein expression of p-eIF2α and CHOP

Article Snippet: HTR-8/SVneo cells were seeded in 6-well plates (4 × 105 cells/well) and treated with CBDV and CBG at 5 μM, with or without the transient receptor potential vanilloid 1 (TRPV1) antagonist capsazepine (CPZ, 0.2 μM, 0464, Tocris Bioscience, Bristol, UK), the IRE1 inhibitor 4μ8c (1 μM, SML0949, Sigma-Aldrich Co, Saint Louis, MO, USA) or the selective inhibitor of PERK, GSK 2656157 (GSK, 0.5 μM, sc-490341, Santa Cruz Biotechnology, CA, USA), which were added 30 min before the co-incubation with cannabinoids.

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction

Journal: Archives of toxicology

Article Title: Cannabidivarin and cannabigerol induce unfolded protein response and angiogenesis dysregulation in placental trophoblast HTR-8/SVneo cells.

doi: 10.1007/s00204-024-03781-8

Figure Lengend Snippet: Fig. 3 Effects of CBDV and CBG on caspase activation, ROS/RNS generation and mitochondrial membrane potential. A, B Evaluation of the activity of the initiator caspases-8 and -9 (48 h); C ROS/RNS generation (0 h) and D of Δψm (48 h). CBDV and CBG-treated cells (5 µM) were pre-incubated with CPZ (0.2 µM), 4µ8c (1 µM) or GSK (0.5 µM), to study the dependence of TRPV1 and UPR pathways. CCCP (30 µM) and PMA (50 ng/mL) were used as positive controls for Δψm and ROS generation, respectively. STS (10 µM) was used

Article Snippet: HTR-8/SVneo cells were seeded in 6-well plates (4 × 105 cells/well) and treated with CBDV and CBG at 5 μM, with or without the transient receptor potential vanilloid 1 (TRPV1) antagonist capsazepine (CPZ, 0.2 μM, 0464, Tocris Bioscience, Bristol, UK), the IRE1 inhibitor 4μ8c (1 μM, SML0949, Sigma-Aldrich Co, Saint Louis, MO, USA) or the selective inhibitor of PERK, GSK 2656157 (GSK, 0.5 μM, sc-490341, Santa Cruz Biotechnology, CA, USA), which were added 30 min before the co-incubation with cannabinoids.

Techniques: Activation Assay, Membrane, Activity Assay, Incubation