scholarly journals Antimelanogenic Effects of Polygonum tinctorium Flower Extract from Traditional Jeju Fermentation via Upregulation of Extracellular Signal-Regulated Kinase and Protein Kinase B Activation

2018 ◽  
Vol 19 (10) ◽  
pp. 2895 ◽  
Author(s):  
You Chung ◽  
Ji-Hye Ko ◽  
Hyun-Kyu Kang ◽  
Seoyeon Kim ◽  
Choon Kang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
High Performance ◽  
Protein Kinase B ◽  
Skin Irritation ◽  
Akt Inhibitor ◽  
Western Blot Assay ◽  
Extracellular Signal Regulated Kinase ◽  
Flower Extract ◽  
Extracellular Signal ◽  
Polygonum Tinctorium

This study was carried out to investigate the antimelanogenic effects of a Polygonum tinctorium flower extract obtained using red nuruk, a traditional Jeju barley-based fermentation starter. We also studied the mechanism of action of the P. tinctorium fermented flower extract (PTFFE) in mouse melanoma cells (B16F10). Cells were treated with various concentrations (62.5, 125 and 250 μg/mL) of PTFFE and the results showed that PTFFE significantly decreased the melanin content and tyrosinase activity without being cytotoxic. In addition, PTFFE strongly inhibited the expression of tyrosinase and tyrosinase-related protein 2 by decreasing the expression of the microphthalmia-associated transcription factor, as shown by a western blot assay. Furthermore, PTFFE inhibited melanogenesis via upregulation of the phosphorylation of extracellular signal-regulated kinase (ERK) and protein kinase B, also known as AKT. We also used inhibitors such as PD98059 (a specific ERK inhibitor) or LY294002 (an AKT inhibitor) to determine whether the signaling pathways are involved. High-performance liquid chromatography fingerprinting showed the presence of a quercetin glucoside (isoquercitrin) and quercetin in PTFFE. To test the potential for PTFFE application as a cosmetic material, we also performed a primary skin irritation test on human skin. In this assay, PTFFE did not induce any adverse reactions at the treatment dose. Based on these results, we suggest that PTFFE may be considered a potential antimelanogenesis candidate for topical applications.

scholarly journals Protein Kinase B and Extracellular Signal-Regulated Kinase Inactivation is Associated with Regorafenib-Induced Inhibition of Osteosarcoma Progression In Vitro and In Vivo

2019 ◽  
Vol 8 (6) ◽  
pp. 900 ◽  
Author(s):  
Po-Jung Pan ◽  
Yu-Chang Liu ◽  
Fei-Ting Hsu
Keyword(s):  
Protein Kinase ◽  
Kinase Inhibitor ◽  
Protein Kinase B ◽  
Akt Inhibitor ◽  
Inhibitory Protein ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Apoptosis Protein

Osteosarcoma is the most common type of bone cancer. Multimodality treatment involving chemotherapy, radiotherapy and surgery is not effective enough to control osteosarcoma. Regorafenib, the oral multi-kinase inhibitor, has been shown to have positive efficacy on disease progression delay in chemotherapy resistant osteosarcoma patients. However anti-cancer effect and mechanism of regorafenib in osteosarcoma is ambiguous. Thus, the aim of this study is to investigate the efficacy and molecular mechanism of regorafenib on osteosarcoma in vitro and in vivo. Human osteosarcomas U-2 OS or MG-63 were treated with regorafenib, miltefosine (protein kinase B (AKT) inhibitor), or PD98059 (mitogen-activated protein/extracellular signal-regulated kinase (MEK) pathway inhibitor) for 24 or 48 h. Cell viability, apoptotic signaling transduction, tumor invasion, expression of tumor progression-associated proteins and tumor growth after regorafenib treatment were assayed by MTT 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, transwell assay, Western blotting assay and in vivo animal experiment, respectively. In these studies, we also indicated that regorafenib suppressed cell growth by prompting apoptosis of osteosarcoma cells, which is mediated through inactivation of ERK and AKT signaling pathways. After regorafenib treatment, downregulation of related genes in invasion (vascular endothelial growth factor (VEGF) and matrix metallopeptidase 9 (MMP-9)), proliferation (CyclinD1) and anti-apoptosis (X-linked inhibitor of apoptosis protein (XIAP), myeloid cell leukemia-1 (MCL-1), and cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein (C-FLIP)) were found. Moreover, upregulation of caspase-3 and caspase-8 cleavage were also observed. In sum, we suggest that regorafenib has potential to suppress osteosarcoma progression via inactivation of AKT and ERK mediated signaling pathway.

scholarly journals Anti-Melanogenic Effects of Bergamottin via Mitogen-Activated Protein Kinases and Protein Kinase B Signaling Pathways

2019 ◽  
Vol 14 (7) ◽  
pp. 1934578X1986210
Author(s):  
You Chul Chung ◽  
Yun Beom Kim ◽  
Bong Seok Kim ◽  
Chang-Gu Hyun
Keyword(s):  
Protein Kinase ◽  
Protein Kinases ◽  
Protein Kinase B ◽  
Positive Control ◽  
Akt Inhibitor ◽  
Mitogen Activated Protein Kinases ◽  
Melanocyte Stimulating Hormone ◽  
B16f10 Cells ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

In this study, we examined the inhibitory effects of bergamottin on melanogenesis in B16F10 murine melanoma cells, together with its effects on the mechanism of melanin synthesis. α-Melanocyte stimulating hormone-stimulated B16F10 cells were treated with various concentrations of bergamottin, with arbutin as a positive control. Bergamottin significantly decreased the melanin content and tyrosinase activity without showing any cytotoxicity. In addition, bergamottin treatment significantly downregulated the expression of tyrosinase-related protein-1,2 and tyrosinase by suppressing the expression of microphthalmia-associated transcription factor. The phosphorylation status of mitogen-activated protein kinases (MAPKs) and protein kinase B (AKT) was examined to determine the mechanism underlying the antimelanogenic effects of bergamottin. Bergamottin treatment increased the phosphorylation of extracellular signal-regulated kinase (ERK) and AKT, but decreased the phosphorylation of p38 and c-Jun N-terminal kinase in the B16F10 cells. Moreover, the use of PD98059 (ERK inhibitor) and LY294002 (AKT inhibitor) corroborated these findings, indicating that bergamottin inhibits melanogenesis via the MAPKase and AKT signaling pathway. Thus, bergamottin has potential for treating hyperpigmentation disorders and can be a promising chemical for skin-whitening in the cosmetic industry.

scholarly journals Hinokitiol reduces tumor metastasis by inhibiting heparanase via extracellular signal-regulated kinase and protein kinase B pathway

2020 ◽  
Vol 17 (3) ◽  
pp. 403-413
Author(s):  
Yueh-Jung Wu ◽  
Wei-Jie Hsu ◽  
Li-Hsien Wu ◽  
Huei-Pu Liou ◽  
Christian Ronquillo Pangilinan ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Tumor Metastasis ◽  
Protein Kinase B ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal
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