Effects of 445 nm, 520 nm, and 638 nm Laser Irradiation on the Dermal Cells.

Background: The invention of non-ionizing emission devices revolutionized science, medicine, industry, and the military. Currently, different laser systems are commonly used, generating the potential threat of excessive radiation exposure, which can lead to adverse health effects. Skin is the organ most exposed to laser irradiation; therefore, this study aims to evaluate the effects of 445 nm, 520 nm, and 638 nm non-ionizing irradiation on keratinocytes and fibroblasts. Methods: Keratinocytes and fibroblasts were exposed to a different fluency of 445 nm, 520 nm, and 638 nm laser irradiation. In addition, viability, type of cell death, cell cycle distribution, and proliferation rates were investigated. Results: The 445 nm irradiation was cytotoxic to BJ-5ta (≥58.7 J/cm2) but not to Ker-CT cells. Exposure influenced the cell cycle distribution of Ker-CT (≥61.2 J/cm2) and BJ-5ta (≥27.6 J/cm2) cells, as well as the Bj-5ta proliferation rate (≥50.5 J/cm2). The 520 nm irradiation was cytotoxic to BJ-5ta (≥468.4 J/cm2) and Ker-CT (≥385.7 J/cm2) cells. Cell cycle distribution (≥27.6 J/cm2) of Ker-CT cells was also affected. The 638 nm irradiation was cytotoxic to BJ-5ta and Ker-CT cells (≥151.5 J/cm2). The proliferation rate and cell cycle distribution of BJ-5ta (≥192.9 J/cm2) and Ker-CT (13.8 and 41.3 J/cm2) cells were also affected. Conclusions: At high fluences, 455 nm, 520 nm, and 638 nm irradiation, representing blue, green, and red light spectra, are hazardous to keratinocytes and fibroblasts. However, laser irradiation may benefit the cells at low fluences by modulating the cell cycle and proliferation rate.

In Vitro Examinations of Cell Death Induction and the Immune Phenotype of Cancer Cells Following Radiative-Based Hyperthermia with 915 MHz in Combination with Radiotherapy.

Multimodal tumor treatment settings consisting of radiotherapy and immunomodulating agents such as immune checkpoint inhibitors are more and more commonly applied in clinics. In this context, the immune phenotype of tumor cells has a major influence on the anti-tumor immune response as well as the composition of the tumor microenvironment. A promising approach to further boost anti-tumor immune responses is to add hyperthermia (HT), i.e., heating the tumor tissue between 39 °C to 45 °C for 60 min. One key technique is the use of radiative hyperthermia systems. However, knowledge is limited as to how the frequency of the used radiative systems affects the immune phenotype of the treated tumor cells. By using our self-designed in vitro hyperthermia system, we compared cell death induction and expression of immune checkpoint molecules (ICM) on the tumor cell surface of murine B16 melanoma and human MDA-MB-231 and MCF-7 breast cancer cells following HT treatment with clinically relevant microwaves at 915 MHz or 2.45 GHz alone, radiotherapy (RT; 2 × 5 Gy or 5 × 2 Gy) alone or in combination (RHT). At 44 °C, HT alone was the dominant cell death inductor with inactivation rates of around 70% for B16, 45% for MDA-MB-231 and 35% for MCF-7 at 915 MHz and 80%, 60% and 50% at 2.45 GHz, respectively. Additional RT resulted in 5-15% higher levels of dead cells. The expression of ICM on tumor cells showed time-, treatment-, cell line- and frequency-dependent effects and was highest for RHT. Computer simulations of an exemplary spherical cell revealed frequency-dependent local energy absorption. The frequency of hyperthermia systems is a newly identified parameter that could also affect the immune phenotype of tumor cells and consequently the immunogenicity of tumors.

Combined Effect of Vaccinium nilgiriensis Bark Extract and 680nm Laser Irradiation in Inducing Breast Cancer Cell Death.

BACKGROUND: Cancer refers to a collection of diseases where cells begin to multiply uncontrollably. Breast cancer is the most predominant malignancy in women. Herbal medicine is one of the important health care systems in most developing countries. Many studies have shown that naturally occurring compounds may support the prevention and treatment of various diseases, including cancer. Some of the plant extracts and isolated compounds show photosensitizing activities and reduce cell proliferation whereas some have revealed photoprotective effects. OBJECTIVES: The biological properties and medicinal uses of extracts and bioactive compounds from V. nilgiriensis have not been investigated. This study aims to evaluate the cytotoxic effects of V. nilgiriensis in combination with 680nm laser irradiation on MCF-7 breast cancer cells. METHODS: The inverted microscopy, ATP and LDH assay were used to analyze the cellular morphology, proliferation, cytotoxicity respectively after the treatment with V. nilgiriensis bark extract. The diode laser of wavelength 680nm and 15 J/cm2 fluency has been used for laser irradiation. The activity of apoptotic proteins was studied using ELISA and nuclear damage by Hoechst staining. RESULTS: The exposure of V. nilgiriensis extracts with laser irradiation at 680nm increases the cytotoxicity and decreases the proliferation of MCF-7 cells. The results of the Hoechst stain indicated nuclear damage. Our study proved that V. nilgiriensis holds a strong cytotoxic effect on breast cancer cells alone and in combination with laser irradiation by upregulating the expression of apoptotic proteins such as caspase 3, p53 and Bax. CONCLUSION: The results from this study showed that the bark ethyl acetate of V. nilgiriensis and in combination with laser is effective in preventing breast cancer cell proliferation in vitro. Further work is warranted to isolate the bioactive compounds from V. nilgiriensis bark extract and study the effect of compounds in the cell death induction. Due to the cytotoxic properties, V. nilgiriensis can be considered as a potent therapeutic agent for the treatment of cancer.

In vitro anti-tumor effect of high-fluence low-power laser light on apoptosis of human colorectal cancer cells.

Colorectal cancer is the third most common malignancy all over the world, along with high morbidity and mortality. As a treatment, high-fluence low-power laser irradiation (HF-LPLI) has reported that its biostimulatory activity can suppress or even destruct tumor growth in neoplastic diseases. The aim of the present study is to examine a therapeutic capacity of HF-LPLI for colorectal cancer treatment by using human colon cancer cell (HT29) model. The in vitro cancer cell model was used to analyze the underlying mechanism of laser-induced apoptosis. Laser irradiation was performed five times (once a day for five consecutive days) with 635 nm laser light for 8 and 16 min (fluence = 128 and 256 J/cm2), respectively. The efficiency of the HF-LPLI treatment was evaluated by MTT, fluorescence staining, cell wound healing, and western blot test during the 5-day period. Experiment data showed that HF-LPLI had a dose-dependent stimulating effect on cell viability, migration, and apoptosis of HT29 cells. The inhibition effect of laser treatment at 256 J/cm2 on cell viability was statistically significant. Meanwhile, the wound healing and western blot tests also confirmed that HF-LPLI could inhibit cell migration and induce cell apoptosis. The current research results demonstrate that 635 nm HF-LPLI can be an alternative treatment option for colorectal cancer by increasing the expression of caspase-3 and inducing HT29 tumor cell apoptosis through activation of the mitochondrial pathway.

An overview of potential novel mechanisms of action underlying Tumor Treating Fields-induced cancer cell death and their clinical implications.

Traditional cancer therapy choices for clinicians are surgery, chemotherapy, radiation and immune therapy which are used either standalone therapies or in various combinations. Other physical modalities beyond ionizing radiation include photodynamic therapy and heating and the more recent approach referred to as Tumor Treating Fields (TTFields). TTFields are intermediate frequency, low-intensity, alternating electric fields that are applied to tumor regions and cells using noninvasive arrays. TTFields have revolutionized the treatment of newly diagnosed and recurrent glioblastoma (GBM) and unresectable and locally advanced malignant pleural mesothelioma (MPM). TTFields are thought to kill tumor cells predominantly by disrupting mitosis; however it has been shown that TTFields increase efficacy of different classes of drugs, which directly target mitosis, replication stress and DNA damage pathways. Hence, a detailed understanding of TTFields' mechanisms of action is needed to use this therapy effectively in the clinic. Recent findings implicate TTFields' role in different important pathways such as DNA damage response and replication stress, ER stress, membrane permeability, autophagy, and immune response. This review focuses on potentially novel mechanisms of TTFields anti-tumor action and their implications in completed and ongoing clinical trials and pre-clinical studies. Moreover, the review discusses advantages and strategies using chemotherapy agents and radiation therapy in combination with TTFields for future clinical use.

Red-Light (670 nm) Therapy Reduces Mechanical Sensitivity and Neuronal Cell Death, and Alters Glial Responses after Spinal Cord Injury in Rats.

Individuals with spinal cord injury (SCI) often develop debilitating neuropathic pain, which may be driven by neuronal damage and neuroinflammation. We have previously demonstrated that treatment using 670 nm (red) light irradiation alters microglia/macrophage responses and alleviates mechanical hypersensitivity at 7 days post-injury (dpi). Here, we investigated the effect of red light on the development of mechanical hypersensitivity, neuronal markers, and glial response in the subacute stage (days 1-7) following SCI. Wistar rats were subjected to a mild hemi-contusion SCI at vertebra T10 or to sham surgery followed by daily red-light treatment (30 min/day; 670 nm LED; 35 mW/cm2) or sham treatment. Mechanical sensitivity of the rat dorsum was assessed from 1 dpi and repeated every second day. Spinal cords were collected at 1, 3, 5, and 7 dpi for analysis of myelination, neurofilament protein NF200 expression, neuronal cell death, reactive astrocytes (glial fibrillary acidic protein [GFAP]+ cells), interleukin 1 ß (IL-1ß) expression, and inducible nitric oxide synthase (iNOS) production in IBA1+ microglia/macrophages. Red-light treatment significantly reduced the cumulative mechanical sensitivity and the hypersensitivity incidence following SCI. This effect was accompanied by significantly reduced neuronal cell death, reduced astrocyte activation, and reduced iNOS expression in IBA1+ cells at the level of the injury. However, myelin and NF200 immunoreactivity and IL-1ß expression in GFAP+ and IBA1+ cells were not altered by red-light treatment. Thus, red-light therapy may represent a useful non-pharmacological approach for treating pain during the subacute period after SCI by decreasing neuronal loss and modulating the inflammatory glial response.

A Comprehensive Analysis of Near-Contact Photobiomodulation Therapy in the Host-Bacteria Interaction Model Using 3D-Printed Modular LED Platform.

One well-studied bacterial factor recognized by the host immune system is lipopolysaccharides (LPS) that stimulate host cells, resulting in cell inflammation. Although photobiomodulation (PBM) therapy demonstrates its potency on anti-inflammatory activity, the complete mechanism of action in the host-bacteria interaction model is still elusive. In addition, many studies were performed regarding a distance between the light source and biological sample (non-contact therapy) that may result in disparate reports on the efficacy of PBM therapy. Thus, it is critical to clearly understand the effect of this approach to maximize efficacy and minimize side effects. Here, a custom-built light-emitting diode (LED) platform that mimics near-contact therapy is developed. The effect and mechanism of PBM therapy on epithelial cells in response to LPS is systematically investigated under various conditions (wavelength, irradiation-time, pulse-frequency). The data show that the irradiation of near-infrared (NIR-LED) significantly improves the viability of inflamed cells. It reveals that NIR-LED inhibits the production of reactive oxygen species by regulating the Nox4-NF-κB pathway. Interestingly, however, high-pulse frequency stimulus causes the collapse of the mitochondrial membrane potential (ΔΨm) of cells, resulting in cell death. These results suggest that the optimized "PBM condition" is critical to assist the healthy immune system of the host against bacterial invasion.

Gold Nanorods and Nanoprisms Mediate Different Photothermal Cell Death Mechanisms In Vitro and In Vivo.

Photothermal therapy (PTT) is an efficient method of inducing localized hyperthermia and can be achieved using gold nanoparticles as photothermal agents. However, there are many hurdles to get over before this therapy can safely reach the clinics, including nanoparticles' optimal shape and the accurate prediction of cellular responses. Here, we describe the synthesis of gold nanorods and nanoprisms with similar surface plasmon resonances in the near-infrared (NIR) and comparable photothermal conversion efficiencies and characterize the response to NIR irradiation in two biological systems, melanoma cells and the small invertebrate Hydra vulgaris. By integrating animal, cellular, and molecular biology approaches, we show a diverse outcome of nanorods and nanoprisms on the two systems, sustained by the elicitation of different pathways, from necrosis to programmed cell death mechanisms (apoptosis and necroptosis). The comparative multilevel analysis shows great accuracy of in vivo invertebrate models to predict overall responses to photothermal challenging and superior photothermal performance of nanoprisms. Understanding the molecular pathways of these responses may help develop optimized nanoheaters that, safe by design, may improve PTT efficacy for clinical purposes.

Polyphenolic-polysaccharide conjugates from medicinal plants of Rosaceae/Asteraceae family protect human lymphocytes but not myeloid leukemia K562 cells against radiation-induced death.

The aim of the study was to investigate whether the polyphenolic-polysaccharide conjugates (PPCs), isolated from flowers of Sanguisorba officinalis L. and Erigeron canadensis L., and from leaves of Fragaria vesca L. and Rubus plicatus Whe. Et N. E., can protect human peripheral blood mononuclear cells (PBMCs) against gamma-irradiation damage while maintaining the radiosensitivity of the myeloid leukemia K562 cell line. PPCs isolated from the four plant sources are water-soluble macromolecules (14-50 kDa) that were previously chemically and structurally characterized. Cells were incubated with PPCs (25 µg/ml, 1 h) prior exposure to 15 Gy gamma-irradiation, non-irradiated appropriate samples served as controls. It was found that the PPCs were able to increase the post-radiation viability of PBMCs by inhibiting apoptosis, while they did not protect the leukemic cells against radiation-induced apoptotic death. The PPCs offered an efficient protection of PBMCs through scavenging of intracellular ROS and decreasing DNA damage, while they provided no reduction of the oxidative stress and DNA damage in K562 cells. Our findings strongly suggest that the PPCs, especially these isolated from S. officinalis and E. canadensis, can selectively protect normal lymphocytes against radiation injury, therefore they meet the criteria of radioprotectors for potential use in radiotherapy.

Cell line-specific efficacy of thermoradiotherapy in human and canine cancer cells in vitro.

OBJECTIVE: Aims were to investigate sensitivity of various human and canine cancer cell lines to hyperthermia and the influence of particular treatment conditions, and to analyze the DNA-damage response and mode of cell death in cell line radiosensitized by hyperthermia. Additionally, we were interested in the involvement of HSP70 in radiosensitization. METHODS: Radiosensitization by hyperthermia was determined in a panel of human and canine cancer cell lines using clonogenic cell survival assay, as well as levels of heat shock proteins (HSPs) using immunoblotting. The influence of the hyperthermia-radiotherapy time gap, different temperatures and the order of treatments on clonogenicity of hyperthermia-sensitive A549 cells was investigated. Additionally, DNA damage and cell death were assessed by Comet assay and an apoptosis/necrosis assay. Further we induced transient knockdown in A549 cells to test HSP70's involvement in radiosensitization. RESULTS: Out of eight cell lines tested, only two (A549 and Abrams) showed significant decrease in clonogenic cell survival when pre-treated with hyperthermia at 42°C. Strong induction of HSP70 upon thermoradiotherapy (HT-RT) treatment was found in all cell lines. Transient knockdown of HSP70 in A549 cells did not result in decrease of clonogenic cell survival in response to HT-RT. CONCLUSION: Tumor cell-type, temperature and order of treatment play an important role in radiosensitization by hyperthermia. However, hyperthermia has limited potency to radiosensitize canine cancer cells grown in a 2D cell culture setting presented here. DNA damage and apoptosis/necrosis did not increase upon combined treatment and cytosolic levels of HSP70 appear not to play critical role in the radiosensitization of A549 cells.

The enhanced photo-thermal therapy of Surface improved photoactive cadmium sulfide (CdS) quantum dots entrenched graphene oxide nanoflakes in tumor treatment.

Cancer is one of the death causing disease is always being a public health concern due to its rapid increase in the world population. Hyperthermal therapy is an anticancer treatment mutually given with chemotherapy. In the present study, CdS/rGO nanocomposites were synthesized using simple and scalable solvothermal method and applied as an efficient material in anticancer treatment. The prepared nanocomposites were characterized from physicochemical characterization techniques. The surface morphology and the crystallographic details were obtained from TEM and XRD analyses respectively. The elemental composition was confirmed from XPS spectra. The phase purity and the functional group analysis were done using Raman and FTIR spectroscopies respectively. The morphological analysis has been displayed the spherical shaped CdS nanoparticles that are firmly attached on the rGO thin sheet matrix further confirmed the formation of CdS/rGO nanoflakes. The live-dead assay method (cancerous and normal cell lines) cytocompatibility study displayed the cell survival of the CdS/rGO nanomaterials exhibited that above 95%, which means materials highly appropriate for the cancer therapy. The temperature profile of the CdS/rGO nanoflakes has enhanced effectively under the NIR absorption property of CdS coated rGO nanoflakes, which influenced to the cancer cell death. The results shown the anticancer activity of the proposed nanocomposites could open a new avenue in biomedicine research and utilized as an efficient materials for practical applications.

Superficial synthesis of photoactive copper sulfide quantum dots loaded nano-graphene oxide sheets combined with near infrared (NIR) laser for enhanced photothermal therapy on breast cancer in nursing care management.

The purpose of this report was to progress the advancement of nanotechnology combined with near-infrared (NIR) laser-mediated treatment for enhancing efficiency against breast cancer (MCF-7) cells. The physic-chemical interactions and properties of the surface improved nano-Graphene oxide (nGO) sheets with Copper Sulfide (CuS) quantum dots were analyzed by selected exclusive analytical methods. The cytotoxicity effect of nGO was investigated by various in vitro assays. The surface activated nGO was exhibited its maximum absorption peak at 233 nm. The XRD analysis shows that the intensity of graphite was decreased and new peak arises around 2Ѳ=11.4o with an interlayer distance of 0.728 to 0.828 nm. In addition, microscopic studies demonstrated that the synthesized nGO was found as a transparent layer with the crispy structure as well as few layers appear as nanoflakes. The cell toxicity enhancement on MCF-7 breast cancer cells was highly influenced by the concentration of CuSQDs loaded nGO sheets with an assessed IC50 value was 100 µg/mL. The fluorescence microscopic visualization was confirmed the cells apoptotic morphological variations and cell death in CuSQDs-nGO treated breast cancer (MCF-7) cell line. Furthermore, the augmented level of Caspase-3, ROS and LDH activities of cancer cells were exhibited after CuSQDs-nGO treatment. Therefore, the present detailed biological investigations demonstrated that NIR-combined with surface activated CuSQDs-nGO presented a significant enhancement of cytotoxic effect against MCF-7 breast cancer cell lines by photothermal therapy (PTT).

Ultrastructural and optical characteristics of cancer cells treated by a nanotechnology based chemo-photothermal therapy method.

The current chemotherapy method demonstrates the need for improvement in terms of efficacy and safety. Given the beneficiary effect of heat in combination with chemotherapy, the purpose of this study is to develop a multifunctional nanoplatform by co-incorporating gold nanoparticles (AuNPs) as photothermal agent and cisplatin as anticancer drug into alginate hydrogel (named as ACA) to enable concurrent thermo-chemotherapy. The in vitro cytotoxicity experiment showed that the as-developed nanocomplex was able to induce greater cytotoxicity in KB human nasopharyngeal cancer cells compared to free cisplatin at the same concentration. Moreover, the interaction of ACA and laser irradiation acted synergistically and resulted in higher cell death rate compared to separate application of photothermal therapy and chemotherapy. The micrograph of KB cells also revealed that ACA was able to selectively accumulate into the mitochondria, so that laser irradiation of KB cells pre-treated with ACA resulted in intensive morphological damages such as plasma membrane disruption, chromatin condensation, autophagic vacuoles formation and organelle degeneration. Moreover, the sign and magnitude of optical nonlinear refractive index measured by Z-scan technique was shown to be significantly altered in cells exposed to ACA with and without laser irradiation. Consequently, the nanocomplex developed herein could be a promising platform to combine photothermal therapy and chemotherapy effectively, thereby achieving synergistic therapeutic outcome.

QUANTITATIVE ANALYSIS OF THE POTENTIAL ROLE OF BASAL CELL HYPERPLASIA IN THE RELATIONSHIP BETWEEN CLONAL EXPANSION AND RADON CONCENTRATION.

Applying the two-stage clonal expansion model to epidemiology of lung cancer among uranium miners, it has been revealed that radon acts as a promoting agent facilitating the clonal expansion of already mutated cells. Clonal expansion rate increases non-linearly by radon concentration showing a plateau above a given exposure rate. The underlying mechanisms remain unclear. Earlier we proposed that progenitor cell hyperplasia may be induced upon chronic radon exposure. The objective of the present study is to test whether the induction of hyperplasia may provide a quantitative explanation for the plateau in clonal expansion rate. For this purpose, computational epithelium models were prepared with different number of basal cells. Cell nucleus hits were computed by an own-developed Monte-Carlo code. Surviving fractions were estimated based on the number of cell nucleus hits. Cell division rate was computed supposing equilibrium between cell death and cell division. It was also supposed that clonal expansion rate is proportional to cell division rate, and therefore the relative increase in cell division rate and clonal expansion rate are the same functions of exposure rate. While the simulation results highly depend on model parameters with high uncertainty, a parameter set has been found resulting in a cell division rate-exposure rate relationship corresponding to the plateau in clonal expansion rate. Due to the high uncertainty of the applied parameters, however, further studies are required to decide whether the induction of hyperplasia is responsible for the non-linear increase in clonal expansion rate or not. Nevertheless, the present study exemplifies how computational modelling can contribute to the integration of observational and experimental radiation protection research.

The effect of low-level laser irradiation on hyperglycemia-induced inflammation in human gingival fibroblasts.

Hyperglycemia-induced inflammation can greatly increase the risk of periodontal disease in people with diabetes. Low-level laser irradiation (LLLI) has been used for wound healing and anti-inflammation in many cases, and LLLI is known to inhibit the lipopolysaccharide (LPS)-stimulated inflammatory response. However, the therapeutic effect of LLLI in diabetes patients with periodontitis remains unknown. In this study, we cultured human gingival fibroblasts (HGFs) in high-glucose medium (35 mM) to mimic a hyperglycemic environment, and then measured the anti-inflammatory effect of LLLI by assessing the expression of pro-inflammatory genes including tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, IL-6, and IL-8 by quantitative real-time polymerase chain reaction. The results demonstrated no significant inflammatory response in HGFs cultured in mannitol medium and in those treated only with LLLI. However, HGFs cultured only in high-glucose medium showed significantly higher expression of pro-inflammatory cytokine than in those treated together with LLLI. We then observed that LLLI reduced the expression of pro-inflammatory cytokines in HGFs cultured in high-glucose medium by modulating cAMP signaling. We also investigated whether antioxidant (vitamin C) treatment reduced the inflammatory effect of oxidative stress in HGFs cultured in high-glucose medium but found no additive effect upon co-treatment with LLLI, suggesting that LLLI may activate cAMP signaling, but not reactive oxygen species (ROS) signaling, to reduce the high glucose-induced inflammation. In conclusion, LLLI may have an anti-inflammatory effect on HGFs in a high glucose environment and may benefit the treatment of periodontal disease in diabetes patients.

Photobiomodulation for Global Cerebral Ischemia: Targeting Mitochondrial Dynamics and Functions.

Hypothermia is currently the only approved therapy for global cerebral ischemia (GCI) after cardiac arrest; however, it unfortunately has multiple adverse effects. As a noninvasive procedure, photobiomodulation (PBM) therapy has emerged as a potential novel treatment for brain injury. PBM involves the use of low-level laser light therapy to influence cell behavior. In this study, we evaluated the therapeutic effects of PBM treatment with an 808-nm diode laser initiated 6 h after GCI. It was noted that PBM dose-dependently protected against GCI-induced neuronal death in the vulnerable hippocampal CA1 subregion. Functional assessments demonstrated that PBM markedly preserved both short-term (a week) and long-term (6 months) spatial learning and memory function following GCI. Further mechanistic studies revealed that PBM post-treatment (a) preserved healthy mitochondrial dynamics and suppressed substantial mitochondrial fragmentation of CA1 neurons, by reducing the detrimental Drp1 GTPase activity and its interactions with adaptor proteins Mff and Fis1 and by balancing mitochondrial targeting fission and fusion protein levels; (b) reduced mitochondrial oxidative damage and excessive mitophagy and restored mitochondrial overall health status and preserved mitochondrial function; and (c) suppressed mitochondria-dependent apoptosome formation/caspase-3/9 apoptosis-processing activities. Additionally, we validated, in an in vitro ischemia model, that cytochrome c oxidase served as a key PBM target for mitochondrial function preservation and neuroprotection. Our findings suggest that PBM serves as a promising therapeutic strategy for the functional recovery after GCI, with mechanisms involving PBM's preservation on mitochondrial dynamics and functions and the inhibition of delayed apoptotic neuronal death in GCI.

The effects of electromagnetic fields on cultured human retinal pigment epithelial cells.

A great deal of evidence has confirmed that electromagnetic fields (EMFs) can affect the central nervous system. In this study, cultured neonatal human retinal pigment epithelial (hRPE) cells were exposed to pulsed EMF of 1 mT intensity and 50 Hz frequency 8 h daily for 3 days. In addition to cell proliferation and cell death assays, immunocytochemistry for RPE65, PAX6, nestin, and cytokeratin 8/18 proteins were performed. Real-time reverse transcriptase polymerase chain reaction (RT-PCR) was performed for NES, PAX6, RPE65, and ACTA2 gene expression. Exposed hRPE cells did not demonstrate significant change in terms of cytomorphology, cell proliferation, or cell death. Protein expression of PAX6 was decreased in treated cells compared to controls and remained unchanged for RPE65, cytokeratin 8/18, and nestin. Gene expressions of NES, RPE65, and PAX6 were decreased in treated cells as compared to controls. Gene expression of ACTA2 did not significantly change. In conclusion, viability of cultivated neonatal hRPE cells did not change after short exposure to a safe dose of pulsed EMF albeit that both gene and protein expressions of retinal progenitor cell markers were reduced. Whether longer exposure durations that are being constantly produced by widely-used electronic devices may induce significant changes in these cells, needs further investigation. Bioelectromagnetics. 39:585-594, 2018. © 2018 Wiley Periodicals, Inc.

Radiosensitivity enhancement of human thyroid carcinoma cells by the inhibitors of histone deacetylase sodium butyrate and valproic acid.

Radiotherapy is one of the leading treatments for clinical cancer therapy. External beam radiotherapy has been proposed as an adjuvant treatment for patients bearing differentiated thyroid cancer refractory to conventional therapy. Our purpose was to study the combined effect of HDAC inhibitors (HDACi) and ionizing irradiation in thyroid cancer cell lines (Nthy-ori 3-1, WRO, TPC-1 and 8505c). HDACi radiosensitized thyroid cancer cells as evidenced by the reduction of survival fraction, whereas they had no effect in the normal cells. HDACi enhanced radiation-induced cell death in WRO cells. Gamma-H2AX foci number increased and persisted long after ionizing exposure in the HDACi-treated cells (WRO and TPC-1). Moreover, the expression of the repair-related gene Ku80 was differentially modulated only in the cancer cells, by the compounds at the protein and/or mRNA levels. We present in vitro evidence that HDACi can enhance the radiosensitivity of human thyroid cancer cells.

Blue light emitting diodes irradiation causes cell death in colorectal cancer by inducing ROS production and DNA damage.

The light emitting diodes (LEDs) irradiation has been demonstrated to be potential therapeutic strategies for several diseases. However, the blue LED effects remain largely unknown in colorectal cancer (CRC), which is a major cause of morbidity and mortality throughout the world. In this study, we determined the effects of blue LED irradiation, the maximal light emission at 470 nm in wavelength, in human CRC cell lines SW620 and HT29. The cells were irradiated with blue LED light for 0 J/cm2, 72 J/cm2, 144 J/cm2, 216 J/cm2 and 288 J/cm2 respectively. We found that irradiation with blue LED light induced a marked decrease of live cells and an increase of dead cells. Additionally, lower cell proliferation and a remarkably increase of cell apoptosis were observed in blue LED-irradiated cells as compared with non-irradiated control group. The cell migration was significantly inhibited by blue LED irradiation 24, 48 and 72 h later compared with non-treated group. Blue LED-treated CRC cells further displayed a remarkably inhibition of EMT process in CRC cells. Finally, we found the accumulation of ROS production and DNA damage were induced by blue LED irradiation. These results indicated that blue LED irradiation inhibits CRC cell proliferation, migration and EMT process as well as induces cell apoptosis, which may result from increased ROS accumulation and induction of DNA damage.