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[Display omitted] • Soft sea buckthorn oil capsules improved skin condition. • Soft sea buckthorn oil capsules enhanced catalase activity and decrease TNF-α secretion. • Soft sea buckthorn oil capsules increased HDL-C level. • Soft sea buckthorn oil capsules reduce dryness of eyes and vaginal problems. Sea buckthorn have been used for centuries as food and traditional medicine in Asia and Europe. This study evaluated the effects of a nutraceutical consisting of sea buckthorn oil as a functional supplement (Omegia™ sea buckthorn oil). Subjects were randomly divided into two groups and were given capsules containing or without sea buckthorn oil. Skin elasticity, color, collagen, pore, and redness were measured using skin assessment instruments. Blood samples were taken to assess serum antioxidant levels by using ELISA (enzyme-linked immunosorbent assay) kit. Additionally, a questionnaire survey was conducted to gather information on subjects' experiences in eye discomfort and vaginal dryness issues. After 12 weeks, skin parameters showed improvement, and participants reported relief from dry eyes and vulvar issues. This study highlights the potential of Omegia™ supplements demonstrating the ability to delay skin aging, increase high-density lipoprotein cholesterol, and antioxidant enzyme activity when used continuously for a period of 12 weeks. [ABSTRACT FROM AUTHOR]

[Display omitted] • Vegan collagen is an innovative plant-based collagen biomimetic. • Vegan collagen significantly increased collagen density and elasticity by 4.7% and 5.1% compared to the placebo group. • Vegan collagen significantly decreased wrinkles, texture, and pores by 27.5%, 20.1%, and 12.3% compared to the placebo group. • Vegan collagen significantly increased hydration and lightness by 4.3% and 2.3% compared to the placebo group. Vegan collagen is an innovative plant-based collagen biomimetic that contains a variety of plant extracts, including asiaticoside, ginsenoside, and through fermented amino acids, which stimulates the natural process for type I collagen synthesis. In this study, using vegan collagen (Corpowell BV, Schilde, Belgium) to explore the skin beautifying effects in the human body. 90 subjects were recruited and divided into a placebo group (n = 30), a vegan collagen group (n = 30), and a fish collagen group (n = 30). Subjects were informed to consume 1 sachet of the sample daily for 8 weeks. Skin conditions were measured at week 0, week 4 and week 8. The results showed that vegan collagen significantly increased collagen density and elasticity by 4.7% and 5.1% and decreased wrinkles, texture, and pores by 27.5%, 20.1%, and 12.3% compared to the placebo group. In addition, the hydration and lightness were increased by 4.3% and 2.3% compared to the placebo group. Vegan collagen has the potential to improve skin collagen density, elasticity, texture, wrinkles, pores, hydration, and lightness. [ABSTRACT FROM AUTHOR]

Highlights: [•] Physical properties and cytotoxicity of PC/LIL vesicles are studied. [•] LIL plays a key role in influencing physicochemical proper. [•] The apoptotic characteristic is found for PC/LIL vesicles. [ABSTRACT FROM AUTHOR]

Abstract: Background: Skin cancers are reportedly increasing worldwide. Developing novel anti-skin cancer drugs with minimal side effects is necessary to address this public health issue. Sinuleptolide has been demonstrated to possess anti-cancer cell activities; however, the mechanisms underlying the anti-skin cancer effects of 5-epi-sinuleptolide and sinuleptolide remain poorly understood. Methods: Apoptosis cell, cell-cycle-related regulatory factors, and mitochondria- and death receptor-dependent caspase pathway in 5-epi-sinuleptolide-induced cell apoptosis were examined using SCC25 cells. Results: 5-epi-Sinuleptolide inhibited human skin cancer cell growth more than did sinuleptolide. Treatment of SCC25 cells with 5-epi-sinuleptolide increased apoptotic body formation, and induced cell-cycle arrest during the G2/M phase. Notably, 5-epi-sinuleptolide up-regulated p53 and p21 expression and inhibited G2/M phase regulators of cyclin B1 and cyclin-dependent kinease 1 (CDK1) in SCC25 cells. Additionally, 5-epi-sinuleptolide induced apoptosis by mitochondria-mediated cytochrome c and Bax up-expression, down-regulated Bcl-2, and activated caspase-9 and -3. 5-epi-Sinuleptolide also up-regulated tBid, which is associated with up-regulation of tumor necrosis factor-α (TNF-α) and Fas ligand (FasL) and their cognate receptors (i.e., TNF-RI, TNF-R2 and Fas), downstream adaptor TNF-R1-associated death domain (TRADD) and Fas-associated death domain (FADD), and activated caspase-8 in SCC25 cells. Conclusions: The analytical results indicate that the death receptor- and mitochondria-mediated caspase pathway is critical in 5-epi-sinuleptolide-induced apoptosis of skin cancer cells. General significance: This is the first report suggesting that the apoptosis mediates the anti-tumor effect of 5-epi-sinuleptolide. The results of this study might provide useful suggestions for designing of anti-tumor drugs for skin cancer patients. [Copyright &y& Elsevier]

Abstract: Background: The Solanum species herbs have been used to treat cancer for centuries; however, the underlying mechanisms and effectiveness in vivo remain unclear. Objectives: SR-T100, extracted from the Solanum incanum, contains solamargine alkaloid as the main active ingredient. Here, we investigated the apoptosis-inducing effects of SR-T100 for targeting squamous cell carcinoma (SCC) in vitro and in vivo. Methods: We elucidated the mechanism by which SR-T100 induces apoptosis of human SCCs (A431, SCC4, SCC9, and SCC25) cells. The efficacy and safety issues were addressed regarding topical treatment of SR-T100 on UVB-induced cutaneous SCC of hairless mice and actinic keratoses (AKs) of human. Results: SR-T100 induces apoptosis in human SCCs cell lines by up-regulating the expressions of tumor necrosis factor receptors (TNFRs) and Fas, and downstream adaptors FADD/TRADD of the TNF-α and Fas ligand signaling cascades. SR-T100 also triggered the mitochondrial apoptotic pathway, as up-regulated cytochrome c and Bax, down-regulated Bcl-XL. Animal experiments showed that all papillomas (35/35) and 27 of 30 UVB-induced microinvasive SCCs in hairless mice disappeared within 10 weeks after once-daily application of topical SR-T100. Furthermore, 13 patients, who suffered with 14 AKs, were treated with once-daily topical SR-T100 gel and 10 AKs cured after 16 weeks, showing negligible discomforts. Conclusion: Our studies indicate that SR-T100 induces apoptosis of SCC cells via death receptors and the mitochondrial death pathway. The high efficacy of SR-T100 in our preclinical trial suggests that SR-T100 is a highly promising herb for AKs and related disorders. [Copyright &y& Elsevier]

Abstract: Background: Natural and synthetic substances are becoming increasingly utilized as tyrosinase inhibitors of depigmentation and developed cosmetics industry. However, few have been employed as skin-whitening agents, primarily because of numerous safety concerns. Objective: A novel compound was found, and then its safe concentrations and inhibition effect of hyperpigmentation by the regulation of the tyrosinase family of proteins were examined. Methods: A novel phenolic glucoside, origanoside (1), was isolated from Origanum vulgare. The structure of the origanoside (1) was established on the basis of spectral evidence and the safe concentrations were determined by MTT assay. Skin-whitening capacity in skin fibroblast Hs68 and melanoma B16 cells and in vivo animal test for origanoside (1) were investigated. Results: Origanoside (1) is non-toxic in concentrations of 0–100μg/ml in both cells. The ability of origanoside (1) to inhibit cellular tyrosinase and DOPA oxidase in B16 cells was investigated. Origanoside (1) significantly reduced expressions of microphthalmia-associated transcription factor (MITF), tyrosinase and tyrosinase-related proteins 2 (TRP-2) in vitro and in vivo, suggesting that origanoside (1) is responsible for the antimelanogenic effect. Smearing origanoside (1)-gel samples on 12 mice for 10 days increased L*, reduced a* and erythema-melanin (E/M), and b* was almost unchanged compared with those of samples and untreated groups, indicating that the skin lightened. Conclusion: Experimental data demonstrate that origanoside (1) causes depigmentation and may be useful for novel food additives and skin-whitening cosmetics. [Copyright &y& Elsevier]

Abstract: This study investigated the physicochemical characteristics of cationic vesicles that were prepared from two phosphatidylcholines and three dialkyldimethylammonium bromides (DXDAB) with differing in dialkyl chain lengths, ranging from 2-C14 to 2-C18, by measuring particle size and zeta potential. The dependence of particle size, zeta potential and short-storage stability of mixed phosphatidylcholine/DXDAB vesicles on the chain length and composition were also elucidated. Transmission electron microscopy analysis verified that vesicles were formed as a phosphatidylcholine film to which DXDAB was added in a phosphate buffer saline (PBS, pH 7.4). Furthermore, the toxicity to the human keratinocytes (HaCaT) and squamous cell carcinomas (SCC25) cells that were incubated with these vesicles, evaluated by a cell viability assay, increased with the percentage of DXDAB that was incorporated and was inversely proportional to the chain length of DXDAB. The morphological features (round shape, chromatin condensation and apoptosis bodies) and results of flow cytometry analysis (increased sub-G1 fraction) confirmed the induction of apoptosis in HaCaT and SCC25 cells by cationic vesicles. Apoptosis caused by cationic vesicles without the addition of any drugs was observed for the first time in HaCaT and SCC25 cells. The results of this investigation suggest that cytotoxicity is related to the zeta potential of the cationic vesicles. [Copyright &y& Elsevier]

Background: 8-Hydroxyquinoline derivatives have highly sensitive fluorescent chemosensors for metal ions, which are associated with anti-oxidant, anti-tumor and anti-HIV-1 properties. Head and neck squamous cell carcinoma (HNSCC) is associated with a high rate of mortality and novel anti-HNSCC drugs must be developed. Therefore, effective chemotherapy agents are required to address this public health issue.Hypothesis/purpose: The aim of this study was to investigate the inhibitory effect of tris(8-hydroxyquinoline)iron (Feq3) on the HNSCC and the underlying mechanism.Study Design/methods: A novel 8-hydroxyquinoline derivative, Feq3, was synthesized. The cell viabilities were analyzed using MTT reagent. Apoptosis and the cell cycle distributions were determined by flow cytometer. Reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence, western blot, MitoSOX and CellROX stain assay were used to study the mechanism of Feq3. Feq3 combined with antioxidants NAC (N-acetylcysteine) and BSO (buthionine sulfoximine) measured the cell viability and intracellular ROS.Results: Feq3 induced the death of HNSCC cells and caused them to exhibit the morphological features of apoptosis. Feq3 also induced apoptosis of SCC9 cells by cell cycle arrest during the G2/M phase and the induced arrest of SCC25 cells in the G0/G1 and G2/M phases, which was associated with decreased cyclin B1/cdc2 and cyclin D/cdk4 expressions. Feq3 increases reactive oxygen species (ROS) and reduces glutathione (GSH) levels, and responds to increased p53 and p21 expressions. Feq3 induced apoptosis by mitochondria-mediated Bax and cytochrome c up-expression and down-expression Bcl-2. Feq3 also up-regulated tBid, which interacts with the mitochondrial pathway and tumor necrosis factor-α (TNF-α)/TNF-Rs, FasL/Fas, and TNF-related apoptosis inducing ligand receptors (TRAIL-Rs)/TRAIL-dependent caspases apoptotic signaling pathway in HNSCC cells. However, Feq3 activates Fas but not FasL in SCC25 cells. Feq3 arrests the growth of HNSCC cells and is involved in the mitochondria- and death receptor (DR)-mediated caspases apoptotic pathway.Conclusion: This study is the first to suggest that apoptosis mediates the anti-HNSCC of Feq3. Feq3 has potential as a cancer therapeutic agent against HNSCC. [ABSTRACT FROM AUTHOR]

Abstract: Mdivi-1 is an inhibitor of dynamin related protein 1- (drp1)-mediated mitochondrial fission. However, the mechanisms through which this compound interacts directly with ion currents in heart cells remain unknown. In this study, its effects on ion currents and membrane potential in murine HL-1 cardiomyocytes were investigated. In whole-cell recordings, the addition of mdivi-1 decreased the amplitude of tail current (I tail) for the rapidly activating delayed-rectifier K+ current (I Kr) in a concentration-dependent manner with an IC50 value at 11.6μM, a value that resembles the inhibition requirement for mitochondrial division. It shifted the activation curve of I tail to depolarized voltages with no change in the gating charge. However, mdivi-1 did not alter the rate of recovery from current inactivation. In cell-attached configuration, mdivi-1 inside the pipette suppressed the activity of acetylcholine-activated K+ channels without modifying the single-channel conductance. Mdivi-1 (30μM) slightly depressed the peak amplitude of Na+ current with no change in the overall current–voltage relationship. Under current-clamp recordings, addition of mdivi-1 resulted in prolongation for the duration of action potentials (APs) and to increase the firing of spontaneous APs in HL-1 cells. Similarly, in pituitary GH3 cells, mdivi-1 was effective in directly suppressing the amplitude of ether-à-go-go-related gene-mediated K+ current. Therefore, the lengthening of AP duration and increased firing of APs caused by mdivi-1 can be primarily explained by its inhibition of these K+ channels enriched in heart cells. The observed effects of mdivi-1 on ion currents were direct and not associated with its inhibition of mitochondrial division. [Copyright &y& Elsevier]

Abstract: Aims: PF573228 is an inhibitor of focal adhesion kinase (FAK) and recognized to affect cell adhesion and migration in many types of cells. Its effects on ion currents and membrane potential have been investigated in this study. Main method: Electrophysiological studies of PF573228 actions on ion currents were performed in pituitary tumor (GH3) cells, in GH3 cells transfected with KCa1.1 siRNAs and in human embryonic kidney (HEK) cells expressing α-human slowpoke (α-hSlo). Key findings: In whole-cell experiments, PF573228 reversibly increased the amplitude of Ca2+-activated K+ currents (I K(Ca)) in GH3 cells. In inside-out recordings, this compound added to the bath did not modify single-channel conductance but stimulated large-conductance Ca2+-activated K+ (BKCa) channels with an EC50 value of 3.2μM. As BKCa-channel activity was stimulated by PF573228 (3μM), subsequent application of BMS191011 (3μM) did not further increase channel activity. PF573228 shifted the activation curve of BKCa channels to less positive membrane potential. Change in the kinetic behavior of BKCa channels caused by this compound is a result of the increased backward rate constants between closed states. PF573228 depressed the firing of action potentials in GH3 cells. However, in GH3 cells transfected with KCa1.1 siRNAs, PF573228-stimulated I K(Ca) was abolished. In HEK293T cells expressing α-hSlo, PF573228 enhanced BKCa-channel activity. Significance: In addition to an inhibition of FAK phosphorylation, PF573228 is effective in activating BKCa channels. The direct stimulation of these channels by this compound may contribute to the underlying mechanism through which it influences cell behavior. [Copyright &y& Elsevier]

Abstract: Rosmarinic acid methyl ester (Ov-8) was isolated form Origanum vulgare. The antioxidant activities of Ov-8 were evaluated by measuring radical-scavenging activities, reducing power, and inhibition of lipid peroxidation, using liposomes and mice tissue. The percentage inhibition, by Ov-8, of the activities of reactive oxygen species (ROSs) in H2O2-treated BNLCL2 cells was about 116.0–82.3% of that in H2O2-treated cells. The ability of Ov-8 to reduce tyrosinase, DOPA oxidase and melanin contents in B16 cells exceeded those of arbutin and l-ascorbic acid. Ov-8 reduced the expressions of the melanocortin-1 receptor (MC1R), microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related proteins-2 (TRP-2) and TRP-1 in B16 cells. Applying Ov-8-gel to mice increased L ∗ and reduced the erythema (E ∗) and melanin (M ∗) indices in relation to those of the base-gel and untreated groups. These results suggest that Ov-8 exhibits antioxidant and depigmentation activities that may be useful in food additives and in the control of skin pigmentation. [Copyright &y& Elsevier]

Squamous cell carcinoma (SCC) is the most common malignant tumor of the head and neck and generally detected in the late stages when the cancer has advanced, and therefore has a poor prognosis and survival rate. A high expression of growth-related oncogene alpha (Groα) is associated with tumor metastasis and invasion and the poor survival rate of patients. Microarray reveals that Groα exhibits a cancer-specific response in HNSCC. Quantitative real-time PCR (qRT-PCR) results concerning the mRNA expression of Groα in HNSCC tissues; indicate that Groα was more highly expressed in HNSCC than in non-cancerous matched tissue (NCMT). The serum of HNSCC patients and healthy subjects demonstrates that the expression of Groα in the HNSCC patients significantly exceeded than in healthy subjects. Furthermore, exposure Groα to stimulated the proliferation, clonogenicity and migration with HNSCC cells (SCC4, SCC9, SCC25 and OECM-1), yielding a stronger response than in non-malignant HaCaT and DOK cells. A high expression of Groα and its receptors CXCR1/2 (chemokine (C-X-C motif) receptor) in HNSCC tissues are highly correlated with tumor progression stage and metastasis. Following the treatment of SCC25 and OECM-1 cells with Groα, β-catenin, matrix metalloproteinases (MMP)-2, MMP-7 and MMP-9 expressions significantly increased but E -cadherin expression was slightly decreased, suggesting that the EMT and metastasis processes were activated by Groα. These findings constitute the first evidence that Groα promotes epithelial mesenchymal transition (EMT) and MMPs expressions in HNSCC via activating CXCR1/2, suggesting a role for Groα in mediating metastasis and its potential as a therapeutic target. [ABSTRACT FROM AUTHOR]

Abstract: Background: Apigenin, a natural plant flavone, may have chemopreventive and therapeutic potentials for anti-inflammatory, antioxidant, and anti-cancer. Nevertheless, the anti-tumor effect of apigenin on human head and neck squamous cell carcinoma (HNSCC) is not fully understood. Methods: The antioxidant capacity and protective effects of apigenin against oxidative stress in murine normal embryonic liver BNLCL2 cells are examined. Cell viability, morphologic change, clonogenic survival, cell cycle distribution, reactive oxygen species (ROS) production, glutathione formation, and death receptors- and Bcl-2-mediated caspase pathways of HNSCC SCC25 cells and A431 cells with apigenin are investigated. Results: Apigenin inhibits the growth of SCC25 and A431 cells and induces cell cycle arrest in the G2/M phase. Apigenin has an antioxidant capacity as well as the ability to inhibit lipid peroxidation. It protects BNLCL2 cells against oxidative damage, and is potentially able to prevent cancer. Apigenin increases intracellular ROS levels and reduces levels of glutathione; it also induces cell apoptosis via tumor necrosis factor receptor (TNF-R)-, TNF-related apoptosis-inducing ligand receptor (TRAIL-R)-, and Bcl-2-mediated caspase-dependent cell death pathways in SCC25 cells. The combination of apigenin with 5-fluorouracil (5-Fu) or cisplatin induces the dramatic death of SCC25 cells. Conclusions: Apigenin induces SCC25 cell apoptosis via the up-regulation of both TNF-R and TRAIL-R signaling pathways, and has a synergistic effect on the inhibition of cell proliferation in combination with 5-Fu or cisplatin. General significance: These analytical findings suggest that apigenin may be a good therapeutic agent against HNSCC cells. [Copyright &y& Elsevier]

Abstract: Our previous research demonstrated that a novel phenolic glucoside, origanoside, isolated from Origanum vulgare, exhibits significant antimelanogenesis activity. The present study was designed to investigate whether origanoside may serve as a quencher of oxidative insults and is involved in antimelanogenesis. It is found that origanoside exhibit the radical-scavenging capacity of 2,2-diphenyl-1-picrylhydrazyl (DPPH2032;-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS +) and superoxide anion radical (O2 −), the reducing power, and the inhibition ability of lipid peroxidation (LP). Pretreatment with origanoside in hydrogen peroxide (H2O2)-treated BNLCL2 and HaCaT cells increased the activities of catalase (CAT) and glutathione peroxidase (GPx), potentially reducing the amount of reactive oxygen species (ROS) generation. These findings confirm the cytoprotective effect of origanoside in hepatocytes and keratinocytes, suggesting that origanoside exhibits antioxidant activities and may be a useful food additive. [Copyright &y& Elsevier]