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Effects of hellebrigenin on apoptosis in NPC cells and in an NPC xenograft model. (A, B) <t>MAPK</t> protein expression was assessed using a Western blot assay following hellebrigenin treatment (0, 5, 10 and 20 nM). β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Cells were treated with 10 nM hellebrigenin with or without the ERK inhibitor <t>U0126.</t> β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (E, F) Cells were treated with 10 nM of hellebrigenin with or without the JNK inhibitor JNK‐in‐8. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (G) Tumour volumes of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The seventh day following tumour injection was identified as Day 0. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (H) Body weights of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (I) Immunohistochemical analysis of Ki67 and CHCHD2 expression in the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. Scale bar = 50 μm.
Mitogen Activated Protein Kinase Mapk Inhibitors, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Effects of hellebrigenin on apoptosis in NPC cells and in an NPC xenograft model. (A, B) <t>MAPK</t> protein expression was assessed using a Western blot assay following hellebrigenin treatment (0, 5, 10 and 20 nM). β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Cells were treated with 10 nM hellebrigenin with or without the ERK inhibitor <t>U0126.</t> β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (E, F) Cells were treated with 10 nM of hellebrigenin with or without the JNK inhibitor JNK‐in‐8. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (G) Tumour volumes of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The seventh day following tumour injection was identified as Day 0. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (H) Body weights of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (I) Immunohistochemical analysis of Ki67 and CHCHD2 expression in the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. Scale bar = 50 μm.
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Effects of hellebrigenin on apoptosis in NPC cells and in an NPC xenograft model. (A, B) <t>MAPK</t> protein expression was assessed using a Western blot assay following hellebrigenin treatment (0, 5, 10 and 20 nM). β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Cells were treated with 10 nM hellebrigenin with or without the ERK inhibitor <t>U0126.</t> β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (E, F) Cells were treated with 10 nM of hellebrigenin with or without the JNK inhibitor JNK‐in‐8. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (G) Tumour volumes of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The seventh day following tumour injection was identified as Day 0. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (H) Body weights of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (I) Immunohistochemical analysis of Ki67 and CHCHD2 expression in the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. Scale bar = 50 μm.
Mapk Inhibitor, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mapk inhibitors u0126  (Cell Signaling Technology Inc)
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Effects of hellebrigenin on apoptosis in NPC cells and in an NPC xenograft model. (A, B) <t>MAPK</t> protein expression was assessed using a Western blot assay following hellebrigenin treatment (0, 5, 10 and 20 nM). β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Cells were treated with 10 nM hellebrigenin with or without the ERK inhibitor <t>U0126.</t> β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (E, F) Cells were treated with 10 nM of hellebrigenin with or without the JNK inhibitor JNK‐in‐8. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (G) Tumour volumes of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The seventh day following tumour injection was identified as Day 0. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (H) Body weights of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (I) Immunohistochemical analysis of Ki67 and CHCHD2 expression in the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. Scale bar = 50 μm.
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erk1 2 mapk inhibitor u0126  (MedChemExpress)
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Effects of hellebrigenin on apoptosis in NPC cells and in an NPC xenograft model. (A, B) <t>MAPK</t> protein expression was assessed using a Western blot assay following hellebrigenin treatment (0, 5, 10 and 20 nM). β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Cells were treated with 10 nM hellebrigenin with or without the ERK inhibitor <t>U0126.</t> β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (E, F) Cells were treated with 10 nM of hellebrigenin with or without the JNK inhibitor JNK‐in‐8. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (G) Tumour volumes of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The seventh day following tumour injection was identified as Day 0. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (H) Body weights of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (I) Immunohistochemical analysis of Ki67 and CHCHD2 expression in the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. Scale bar = 50 μm.
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Effects of hellebrigenin on apoptosis in NPC cells and in an NPC xenograft model. (A, B) MAPK protein expression was assessed using a Western blot assay following hellebrigenin treatment (0, 5, 10 and 20 nM). β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Cells were treated with 10 nM hellebrigenin with or without the ERK inhibitor U0126. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (E, F) Cells were treated with 10 nM of hellebrigenin with or without the JNK inhibitor JNK‐in‐8. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (G) Tumour volumes of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The seventh day following tumour injection was identified as Day 0. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (H) Body weights of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (I) Immunohistochemical analysis of Ki67 and CHCHD2 expression in the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. Scale bar = 50 μm.

Journal: Journal of Cellular and Molecular Medicine

Article Title: The Efficacy of Hellebrigenin Against Nasopharyngeal Carcinoma Cells: The Molecular and Bioinformatic Analysis

doi: 10.1111/jcmm.70624

Figure Lengend Snippet: Effects of hellebrigenin on apoptosis in NPC cells and in an NPC xenograft model. (A, B) MAPK protein expression was assessed using a Western blot assay following hellebrigenin treatment (0, 5, 10 and 20 nM). β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Cells were treated with 10 nM hellebrigenin with or without the ERK inhibitor U0126. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (E, F) Cells were treated with 10 nM of hellebrigenin with or without the JNK inhibitor JNK‐in‐8. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. # p < 0.05 compared with hellebrigenin 10 nM. (G) Tumour volumes of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The seventh day following tumour injection was identified as Day 0. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (H) Body weights of the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. The results are presented as mean ± SE, n = 3. * p < 0.05 compared with vehicle. (I) Immunohistochemical analysis of Ki67 and CHCHD2 expression in the vehicle group and NPC xenograft mice treated with 4 mg/kg of hellebrigenin. Scale bar = 50 μm.

Article Snippet: Hellebrigenin (purity ≥ 99%, Figure ) and mitogen‐activated protein kinase (MAPK) inhibitors (U0126 and JNK‐in‐8) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, Western Blot, Control, Injection, Immunohistochemical staining