hellebrigenin (MedChemExpress)

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MedChemExpress hellebrigenin

Cytotoxic effects of <t>hellebrigenin</t> on NPC cell lines. (A) Chemical structure of hellebrigenin. (B) Viability of NPC‐039 and NPC‐BM cells was measured using the MTT assay following treatment of the cells with hellebrigenin (0, 5, 10 and 20 nM) for 24, 48 or 72 h. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Colony formation in NPC cell lines treated with hellebrigenin was assessed using a colony formation assay. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (E) Viability of human normal nasopharyngeal primary cells was measured using the MTT assay following treatment with hellebrigenin (0, 5, 10 and 20 nM) for 24 h. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (F, G) Cells treated with 0, 5, 10 and 20 nM of hellebrigenin for 24 h were collected and analysed through flow cytometry. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (H, I) Cell cycle proteins CDC2, CDK2, cyclin A2 and cyclin B1 were measured using a Western blot assay. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM.

Hellebrigenin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "The Efficacy of Hellebrigenin Against Nasopharyngeal Carcinoma Cells: The Molecular and Bioinformatic Analysis"

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

Journal: Journal of Cellular and Molecular Medicine

doi: 10.1111/jcmm.70624

Cytotoxic effects of hellebrigenin on NPC cell lines. (A) Chemical structure of hellebrigenin. (B) Viability of NPC‐039 and NPC‐BM cells was measured using the MTT assay following treatment of the cells with hellebrigenin (0, 5, 10 and 20 nM) for 24, 48 or 72 h. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Colony formation in NPC cell lines treated with hellebrigenin was assessed using a colony formation assay. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (E) Viability of human normal nasopharyngeal primary cells was measured using the MTT assay following treatment with hellebrigenin (0, 5, 10 and 20 nM) for 24 h. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (F, G) Cells treated with 0, 5, 10 and 20 nM of hellebrigenin for 24 h were collected and analysed through flow cytometry. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (H, I) Cell cycle proteins CDC2, CDK2, cyclin A2 and cyclin B1 were measured using a Western blot assay. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM.

Figure Legend Snippet: Cytotoxic effects of hellebrigenin on NPC cell lines. (A) Chemical structure of hellebrigenin. (B) Viability of NPC‐039 and NPC‐BM cells was measured using the MTT assay following treatment of the cells with hellebrigenin (0, 5, 10 and 20 nM) for 24, 48 or 72 h. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Colony formation in NPC cell lines treated with hellebrigenin was assessed using a colony formation assay. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (E) Viability of human normal nasopharyngeal primary cells was measured using the MTT assay following treatment with hellebrigenin (0, 5, 10 and 20 nM) for 24 h. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (F, G) Cells treated with 0, 5, 10 and 20 nM of hellebrigenin for 24 h were collected and analysed through flow cytometry. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (H, I) Cell cycle proteins CDC2, CDK2, cyclin A2 and cyclin B1 were measured using a Western blot assay. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM.

Techniques Used: MTT Assay, Colony Assay, Flow Cytometry, Western Blot

Apoptotic effects of hellebrigenin on NPC cell lines. (A, B) Chromatin condensation was assessed using DAPI staining following treatment of cells with hellebrigenin (0, 5, 10 and 20 nM) for 24 h. Scale bar = 50 μm. White arrows denote chromatin condensation. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Cells treated with 0, 5, 10 or 20 nM of hellebrigenin were analysed using annexin V and PI staining through flow cytometry. The FITC (+) cells are identified as apoptotic cells. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (E, F) Cells treated with 0, 5, 10 or 20 nM of hellebrigenin were analysed using JC‐1 staining through flow cytometry. The monomers are identified as depolarized cells. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM.

Figure Legend Snippet: Apoptotic effects of hellebrigenin on NPC cell lines. (A, B) Chromatin condensation was assessed using DAPI staining following treatment of cells with hellebrigenin (0, 5, 10 and 20 nM) for 24 h. Scale bar = 50 μm. White arrows denote chromatin condensation. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (C, D) Cells treated with 0, 5, 10 or 20 nM of hellebrigenin were analysed using annexin V and PI staining through flow cytometry. The FITC (+) cells are identified as apoptotic cells. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (E, F) Cells treated with 0, 5, 10 or 20 nM of hellebrigenin were analysed using JC‐1 staining through flow cytometry. The monomers are identified as depolarized cells. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM.

Techniques Used: Staining, Flow Cytometry

Effects of hellebrigenin on the intrinsic and extrinsic apoptotic pathways in NPC cells. (A, B) Death receptor proteins (DR5, FAS and RIP), (C, D) mitochondrial‐related proteins (Bcl‐xL, Mcl‐1 and Bak), (E, F) caspases (c‐caspase‐3, ‐8 and ‐9) and c‐PARP were measured using a Western blot assay following hellebrigenin treatment (0, 5, 10 and 20 nM). β‐Actin was used as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM.

Figure Legend Snippet: Effects of hellebrigenin on the intrinsic and extrinsic apoptotic pathways in NPC cells. (A, B) Death receptor proteins (DR5, FAS and RIP), (C, D) mitochondrial‐related proteins (Bcl‐xL, Mcl‐1 and Bak), (E, F) caspases (c‐caspase‐3, ‐8 and ‐9) and c‐PARP were measured using a Western blot assay following hellebrigenin treatment (0, 5, 10 and 20 nM). β‐Actin was used as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM.

Techniques Used: Western Blot, Control

The proteomics analysis of NPC cell lines treated with hellebrigenin and bioinformatic analysis of clinical data. (A) Volcano plots illustrating DEGs identified using a cut‐off of adjusted p < 0.05 and log2 fold change ≥ 0.6 or ≤ −0.6. Ninety‐eight genes were identified to be downregulated, and 40 genes were identified to be upregulated in the NPC‐039 cell line. By contrast, in the NPC‐BM cell line, 106 genes were downregulated, and 37 genes were upregulated. (B) Venn diagram illustrating the overlap of DEGs between the two cell lines. (C) GO analysis of hellebrigenin‐regulated genes. Top 10 DEGs associated with biological processes, cellular components and molecular function were selected. Numbers above each bar denote the number of genes identified. (D) Enrichment analysis by using KEGG pathway annotations. DEGs associated with environmental information processing, cellular processing and human disease were selected. (E) Venn diagram illustrating the overlap of DEGs between the GSE53819 data set of NPC patients and downregulated genes of two NPC cell lines. (F) Heatmap presenting the 17 downregulated genes in the NPC‐039, NPC‐BM cell lines and GSE data set. (G) Comparison of CHCHD2 mRNA expression levels in normal tissues versus tumour tissues of NPC from the GSE53819 data set. (H) Comparison of CHCHD2 mRNA expression levels in normal tissues versus tumour tissues of HNSCC patients from the TCGA database. (I) Comparison of CHCHD2 mRNA expression levels in earlier versus advanced stages of HNSCC patients from the TCGA database. (J) Comparison of CHCHD2 mRNA expression levels in different tumour sizes of HNSCC patients from the TCGA database. (K) Comparison of CHCHD2 mRNA expression levels in patients with low versus high CHCHD2 expression in terms of overall survival from the TCGA database.

Figure Legend Snippet: The proteomics analysis of NPC cell lines treated with hellebrigenin and bioinformatic analysis of clinical data. (A) Volcano plots illustrating DEGs identified using a cut‐off of adjusted p < 0.05 and log2 fold change ≥ 0.6 or ≤ −0.6. Ninety‐eight genes were identified to be downregulated, and 40 genes were identified to be upregulated in the NPC‐039 cell line. By contrast, in the NPC‐BM cell line, 106 genes were downregulated, and 37 genes were upregulated. (B) Venn diagram illustrating the overlap of DEGs between the two cell lines. (C) GO analysis of hellebrigenin‐regulated genes. Top 10 DEGs associated with biological processes, cellular components and molecular function were selected. Numbers above each bar denote the number of genes identified. (D) Enrichment analysis by using KEGG pathway annotations. DEGs associated with environmental information processing, cellular processing and human disease were selected. (E) Venn diagram illustrating the overlap of DEGs between the GSE53819 data set of NPC patients and downregulated genes of two NPC cell lines. (F) Heatmap presenting the 17 downregulated genes in the NPC‐039, NPC‐BM cell lines and GSE data set. (G) Comparison of CHCHD2 mRNA expression levels in normal tissues versus tumour tissues of NPC from the GSE53819 data set. (H) Comparison of CHCHD2 mRNA expression levels in normal tissues versus tumour tissues of HNSCC patients from the TCGA database. (I) Comparison of CHCHD2 mRNA expression levels in earlier versus advanced stages of HNSCC patients from the TCGA database. (J) Comparison of CHCHD2 mRNA expression levels in different tumour sizes of HNSCC patients from the TCGA database. (K) Comparison of CHCHD2 mRNA expression levels in patients with low versus high CHCHD2 expression in terms of overall survival from the TCGA database.

Techniques Used: Comparison, Expressing

Involvement of CHCHD2 in hellebrigenin‐induced apoptosis in NPC cells. (A, B) CHCHD2 protein expression in hellebrigenin‐treated NPC cells. 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) mRNA levels of CHCHD2 in NPC cells treated with hellebrigenin. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (D) mRNA levels of CHCHD2 in NPC cells treated with hellebrigenin with or without CHCHD2 siRNA. 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 treated with hellebrigenin, CHCHD2 plasmid or CHCHD2 siRNA were analysed using annexin V and PI staining through flow cytometry. The FITC (+) cells are identified as apoptotic cells. The results are presented as mean ± SD, n = 3. * p < 0.05. (G, H) Protein levels of c‐caspase‐3, ‐8 and ‐9, and PARP were assessed in cells treated with hellebrigenin, CHCHD2 plasmid or CHCHD2 siRNA through a Western blot assay. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05.

Figure Legend Snippet: Involvement of CHCHD2 in hellebrigenin‐induced apoptosis in NPC cells. (A, B) CHCHD2 protein expression in hellebrigenin‐treated NPC cells. 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) mRNA levels of CHCHD2 in NPC cells treated with hellebrigenin. The results are presented as mean ± SD, n = 3. * p < 0.05 compared with 0 nM. (D) mRNA levels of CHCHD2 in NPC cells treated with hellebrigenin with or without CHCHD2 siRNA. 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 treated with hellebrigenin, CHCHD2 plasmid or CHCHD2 siRNA were analysed using annexin V and PI staining through flow cytometry. The FITC (+) cells are identified as apoptotic cells. The results are presented as mean ± SD, n = 3. * p < 0.05. (G, H) Protein levels of c‐caspase‐3, ‐8 and ‐9, and PARP were assessed in cells treated with hellebrigenin, CHCHD2 plasmid or CHCHD2 siRNA through a Western blot assay. β‐Actin was identified as the internal control. The results are presented as mean ± SD, n = 3. * p < 0.05.

Techniques Used: Expressing, Control, Plasmid Preparation, Staining, Flow Cytometry, Western Blot

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.

Figure Legend 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.

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

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

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