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1.
Int J Mol Sci ; 20(14)2019 Jul 17.
Article in English | MEDLINE | ID: mdl-31319552

ABSTRACT

Acne is an inflammatory skin disorder in puberty with symptoms including papules, folliculitis, and nodules. Propionibacterium acnes (P. acnes) is the main anaerobic bacteria that cause acne. It is known to proliferate within sebum-blocked skin hair follicles. P. acnes activates monocytic cell immune responses to induce the expression of proinflammatory cytokines. Although the anti-inflammatory function of the Laurus nobilis (L. nobilis) extract (LNE) on several immunological disorders have been reported, the effect of LNE in P. acnes-mediated skin inflammation has not yet been explored. In the present study, we examined the ability of the LNE to modulate the P. acnes-induced inflammatory signaling pathway, and evaluated its mechanism. LNE significantly suppressed the expression of P. acnes-mediated proinflammatory cytokines, such as IL-1ß, IL-6, and NLRP3. We also found that LNE inhibited the inflammatory transcription factor NF-κB in response to P. acnes. In addition, eucalyptol, which is the main constituent of LNE, consistently inhibited P. acnes-induced inflammatory signaling pathways. Moreover, LNE significantly ameliorated P. acnes-induced inflammation in a mouse model of acne. We suggest for the first time that LNE hold therapeutic value for the improvement of P. acnes-induced skin inflammation.


Subject(s)
Acne Vulgaris/drug therapy , Anti-Inflammatory Agents/pharmacology , Eucalyptol/pharmacology , Gram-Positive Bacterial Infections/drug therapy , Laurus/chemistry , Plant Extracts/pharmacology , Propionibacterium acnes/growth & development , Acne Vulgaris/metabolism , Acne Vulgaris/microbiology , Acne Vulgaris/pathology , Animals , Anti-Inflammatory Agents/chemistry , Cell Line , Eucalyptol/chemistry , Gram-Positive Bacterial Infections/metabolism , Gram-Positive Bacterial Infections/microbiology , Gram-Positive Bacterial Infections/pathology , Inflammation/drug therapy , Inflammation/metabolism , Inflammation/microbiology , Inflammation/pathology , Mice , Plant Extracts/chemistry
2.
Mol Med Rep ; 17(1): 877-883, 2018 Jan.
Article in English | MEDLINE | ID: mdl-29115465

ABSTRACT

Ultraviolet B (UVB) radiation induces DNA damage, oxidative stress and inflammation, and suppresses the immune system in the skin, which collectively contribute to skin aging and carcinogenesis. The DNA damage response, including DNA repair, can be regulated by the circadian clock and microRNA (miRNA) expression. The aim of the present study was to evaluate the reparative action of Trichosanthes kirilowii extract (TKE) against UVB irradiation­induced DNA damage in human keratinocytes. TKE demonstrated low cytotoxicity in normal HaCaT keratinocytes at low doses (up to 100 µg/ml). The results of a comet assay revealed that TKE enhanced the repair of UVB­induced DNA damage. TKE significantly upregulated the expression of the core clock protein, brain and muscle aryl hydrocarbon receptor nuclear translocator­like protein­1 (BMAL1), and downregulated the expression of miRNA (miR)­142­3p, as demonstrated using western blotting and the reverse transcription­quantitative polymerase chain reaction. Furthermore, the suppression of miR­142­3p by a specific inhibitor positively correlated with the repair activity. Overall, the data obtained demonstrated that TKE enhanced the repair of UVB­induced DNA damage by regulating the expression of BMAL1 and miR­142­3p. Consequently, TKE can be considered a potential candidate for the treatment of skin diseases associated with UVB­induced damage.


Subject(s)
ARNTL Transcription Factors/genetics , DNA Damage/radiation effects , DNA Repair/drug effects , Keratinocytes/drug effects , Keratinocytes/metabolism , MicroRNAs/genetics , Plant Extracts/pharmacology , Trichosanthes/chemistry , Ultraviolet Rays , Cell Line , Gene Expression Profiling , Gene Expression Regulation
3.
Oncol Rep ; 35(2): 779-84, 2016 Feb.
Article in English | MEDLINE | ID: mdl-26554741

ABSTRACT

In the present study, we investigated the roles and molecular mechanism of 10-gingerol, a phenolic compound isolated from Zingiber officinale, in regulating cell proliferation and invasion of MDA­MB­231 breast cancer cells. 10-gingerol treatment inhibited cell proliferation through downregulation of cell cycle regulatory proteins such as cyclin-dependent kinases and cyclins, and subsequent induction of G1 phase arrest. In addition, 10­gingerol treatment blocked cell invasion in response to mitogenic stimulation. These antitumor activities of 10­gingerol were mediated through inactivation of Akt and p38MAPK activity, and suppression of epidermal growth factor receptor expression. Collectively, these findings demonstrate the pharmacological roles of 10-gingerol in regulating breast cancer cell growth and progression, and suggest further evaluation and development as a potential therapeutic agent for the prevention and treatment of breast cancer.


Subject(s)
Antineoplastic Agents, Phytogenic/pharmacology , Breast Neoplasms/pathology , Catechols/pharmacology , Cell Proliferation/drug effects , Fatty Alcohols/pharmacology , Proto-Oncogene Proteins c-akt/metabolism , p38 Mitogen-Activated Protein Kinases/metabolism , Blotting, Western , Cell Line, Tumor , Female , Humans , Magnetic Resonance Spectroscopy , Neoplasm Invasiveness/pathology , Proto-Oncogene Proteins c-akt/drug effects , p38 Mitogen-Activated Protein Kinases/drug effects
4.
Am J Chin Med ; 42(2): 453-63, 2014.
Article in English | MEDLINE | ID: mdl-24707874

ABSTRACT

Siegesbeckia glabrescens (SG) Makino (Compositae) has been used as a traditional medicine for the treatment of allergic and inflammatory diseases. In the present study, we examined the effects and molecular mechanism of the ethanol extract of SG on cell proliferation and invasion in p53 wild-type A549 and p53-deficient H1299 non-small cell lung cancer (NSCLC) cells. SG treatment markedly inhibited the proliferation and invasion in both cell lines, independently of p53 expression. The anti-proliferative effect of SG on A549 cells was mediated by the inactivation of Akt and p70(S6K) as evidenced by treatment with LY294002 and rapamycin, respectively. In addition, anti-invasive activity of SG in A549 cells was found to be associated with the inhibition of p70(S6K). In contrast, in H1299 cells the inactivation of p38(MAPK) appeared to be involved in SG-mediated inhibition of cell proliferation and invasion. Collectively, these findings suggest that SG modulates cellular fates such as proliferation and invasion by differential regulation of signaling pathways, depending on the status of p53 expression in NSCLC, and support the development of SG as a potent therapeutic agent for the treatment of NSCLC.


Subject(s)
Antineoplastic Agents, Phytogenic , Asteraceae/chemistry , Carcinoma, Non-Small-Cell Lung/pathology , Cell Proliferation/drug effects , Cell Transformation, Neoplastic/drug effects , Lung Neoplasms/pathology , Plant Extracts/pharmacology , Carcinoma, Non-Small-Cell Lung/drug therapy , Carcinoma, Non-Small-Cell Lung/genetics , Cell Line, Tumor , Ethanol , Gene Expression/drug effects , Gene Silencing/drug effects , Humans , Lung Neoplasms/drug therapy , Lung Neoplasms/genetics , Molecular Targeted Therapy , Neoplasm Invasiveness , Phytotherapy , Plant Extracts/therapeutic use , Proto-Oncogene Proteins c-akt/metabolism , Ribosomal Protein S6 Kinases, 70-kDa/metabolism , Tumor Suppressor Protein p53/metabolism , p38 Mitogen-Activated Protein Kinases/metabolism
5.
Oncol Rep ; 29(2): 662-8, 2013 Feb.
Article in English | MEDLINE | ID: mdl-23233127

ABSTRACT

Integrin α3ß1 is expressed on many types of cancer cells and can regulate tumor growth and progression. In the present study, we examined the roles and molecular mechanism of integrin α3ß1 in modulating cell proliferation and migration of p53-deficient non-small cell lung cancer (NSCLC) cells. Reduced expression of integrin α3 by RNA silencing clearly induces cell proliferation and migration in H1299 cells, compared with those in control cells. Enhanced proliferation in integrin α3-silenced cells is mediated by upregulation and nuclear localization of cyclin-dependent kinases, and these effects require the activation of Akt and ERK as evidenced by treatment with LY294002 and PD98059, respectively. Furthermore, suppression of integrin α3 expression induces the expression of nuclear factor-κB and Bcl-2 as well as epidermal growth factor receptor, which are positively correlated with cell proliferation and survival. In contrast, increase in cell migration of integrin α3-silenced cells is found to be independent of Akt or ERK signaling pathways. Collectively, these findings suggest that integrin α3ß1 plays pivotal roles in regulating cell proliferation and migration that enhance the invasive type of p53-deficient NSCLC cells.


Subject(s)
Carcinoma, Non-Small-Cell Lung/genetics , Cell Movement/genetics , Cell Proliferation , Integrin alpha3beta1/genetics , Lung Neoplasms/genetics , Carcinoma, Non-Small-Cell Lung/metabolism , Cyclin-Dependent Kinases , ErbB Receptors/metabolism , Humans , Integrin alpha3beta1/metabolism , Lung Neoplasms/metabolism , MAP Kinase Signaling System , Matrix Metalloproteinase 2/metabolism , Matrix Metalloproteinase 9/metabolism , NF-kappa B/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Proto-Oncogene Proteins c-bcl-2/metabolism , RNA Interference , RNA, Small Interfering , Transfection , Tumor Suppressor Protein p53/deficiency , Up-Regulation
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