7
edits
Changes
Jump to navigation
Jump to search
mLine 15:
Line 15: − + Line 25:
Line 25: − + + + + + + + + + + +
added info
'''Anti-Inflammatory'''
'''Anti-Inflammatory'''
Hinokitiol revealed a modulatory effect on the production of tumor necrosis factor (TNF)-alpha, a factor that influences skin inflammation and hair follicle apoptosis. This is achieved at the transcription level by disrupting mRNA synthesis of TNF-alpha. Additionally, it suppresses phosphorylation of PDK1, Akt/PKB, and ERK, as a result diminishing the nuclear factor (NF)-kappaB activation, hence restoring hair loss.[[(https://www.sigmaaldrich.com/catalog/papers/18537078)|[15]]] In a recent study, Hinokitiol also revealed notable protection against ocular surface inflammation in dry eye syndrome (DES by inhibiting the NF-κB pathway [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4506343/ [16<nowiki>]</nowiki>].
Hinokitiol revealed a modulatory effect on the production of tumor necrosis factor (TNF)-alpha, a factor that influences skin inflammation and hair follicle apoptosis. This is achieved at the transcription level by disrupting the mRNA synthesis of TNF-alpha. Additionally, it suppresses phosphorylation of PDK1, Akt/PKB, and ERK, as a result diminishing the nuclear factor (NF)-kappaB activation, hence restoring hair loss.[[(https://www.sigmaaldrich.com/catalog/papers/18537078)|[15]]] In a recent study, Hinokitiol also revealed notable protection against ocular surface inflammation in dry eye syndrome (DES by inhibiting the NF-κB pathway [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4506343/ [16<nowiki>]</nowiki>].
'''Other activities'''
'''Other activities'''
This study indicates the inhibitory effect of hinokitiol on the migration of human adenocarcinoma A549 cells. The anticancer properties of hinokitiol are supported by the evaluation of results in the present study, including an increase of Bax/p53 and cytochrome c, and further activation of caspases-9/-3 and antioxidant enzymes CAT and SOD. Moreover, we discovered the inhibitory impact of hinokitiol on the A549 cell migration was accompanied through the downregulation of MMPs-9 and MMP-2. These outcomes can also illustrate a new therapeutic value of hinokitiol in anticancer therapy.
This study indicates the inhibitory effect of hinokitiol on the migration of human adenocarcinoma A549 cells. The anticancer properties of hinokitiol are supported by the evaluation of results in the present study, including an increase of Bax/p53 and cytochrome c, and further activation of caspases-9/-3 and antioxidant enzymes CAT and SOD. Moreover, we discovered the inhibitory impact of hinokitiol on the A549 cell migration was accompanied through the downregulation of MMPs-9 and MMP-2. These outcomes can also illustrate a new therapeutic value of hinokitiol in anticancer therapy.
Furthermore, another research showed strong anticancer characteristics of Hinokitiol by increasing the cytotoxicity against cervical cancer cells and non-small cell lung cancer (NSCLC) cells. Most cancers cell deaths are medicated through caspase-3 in apoptosis and consequently enlarged lysosomes which are regarded as possession of anticancer compounds and that can possibly result in lysosomal injury and increased autophagy followed by severe cell death. The choice of therapeutic to hinokitiol, a herbal product derivative, can be concluded to have a mechanism of action against NSCLC with minimum cytotoxic and maximized therapeutic effects.[http://www.kjcls.org/journal/view.html?doi=10.15324/kjcls.2019.51.2.221 [19<nowiki>]</nowiki>]
Furthermore, another research showed strong anticancer characteristics of Hinokitiol by increasing the cytotoxicity against cervical cancer cells and non-small cell lung cancer (NSCLC) cells. Most cancers cell deaths are medicated through caspase-3 in apoptosis and consequently enlarged lysosomes which are regarded as the possession of anticancer compounds and that can possibly result in lysosomal injury and increased autophagy followed by severe cell death. The choice of therapeutic to hinokitiol, a herbal product derivative, can be concluded to have a mechanism of action against NSCLC with minimum cytotoxic and maximized therapeutic effects.[http://www.kjcls.org/journal/view.html?doi=10.15324/kjcls.2019.51.2.221 [19<nowiki>]</nowiki>]
'''Further Cancer research'''
Hinokitiol has shown an established mechanism to antagonize epidermal growth factor receptor (EGFR) protein expression in mammosphere production breast cancer stem/progenitor cells (BCSCs) without altering the messenger RNA expression. Hinokitiol also decreased the stability of EGFR in BCSCs. The stable protein expression of EGFR and vasculogenic mimicry (VM) production capability of hinokitiol treated BCSCs were restored by combination treatment with a proteasome antagonist, MG132. It can be concluded that hinokitiol may antagonize the VM activity of BCSCs by stimulating proteasome-mediated EGFR break-down. Hinokitiol may be considered as a novel breast cancer therapeutic agent, by acting as an anti-VM. [https://www.spandidos-publications.com/10.3892/ol.2016.4300#:~:text=Hinokitiol%20dose%2Ddependently%20inhibits%20VM,anti%2Dinflammatory%20and%20antitumor%20activity [20<nowiki>]</nowiki>]
Further study demonstrated Hinokitiol regulates estrogen receptor signaling and also antagonize the proliferation breast cancer cells in humans. Hence, it can be considered as a promising agent against the treatment of hormone sensitive mammary tumorigenesis.[https://www.tandfonline.com/doi/full/10.1080/09168451.2015.1008978 [21<nowiki>]</nowiki>]
'''Hinokitiol with Curcumin'''
A potent effect was observed against NSCLC and gefitinib resistant NSCLC cells, when Hinokitiol was used in combination with Curcumin. This treatment indicated minimal cytotoxicity to healthy cells. [https://journals.sagepub.com/doi/10.1177/1934578X1801301223 [22<nowiki>]</nowiki>]