The cytotoxicity of breast cancer mcf-7 cell line treated with different wavelength of low-level laser.

Breast cancer remains a significant global health challenge, spurring ongoing investigations into innovative treatment approaches. Low-level laser therapy (LLLT) has emerged as a promising non-invasive therapeutic avenue of interest. This research delves into the impact of LLLT on the cytotoxicity of the MCF-7 breast cancer cell line, employing lasers emitting various wavelengths. The objective is to assess whether diverse LLLT wavelengths elicit disparate cytotoxic responses, shedding light on LLLT's potential as a targeted breast cancer treatment. MCF-7 cell cultures were subjected to lasers of varying wavelengths, including blue (473 nm), red (660 nm), and near-infrared (780 nm). Each wavelength was delivered at four different power levels: 10, 25, 45, and 65 mW, with exposure durations of 60, 300, 600, and 900 s. Cellular responses, encompassing factors such as cell viability, and cytotoxicity were assessed using WST-1 assays technique. Statistical analysis was performed to discern the wavelength-specific impacts of low-level laser therapy (LLLT) on MCF-7 cells. The study revealed that the blue laser had the least noticeable adverse impact on MCF-7 breast cancer cell lines, leading to the highest cell survival rate of 107.62% after 24 h. The most severe toxicity occurred when the laser was used at 45 mW for 900 s, resulting in cell viability ranging from 81.85% to 107.62%. As for cell viability after exposure to the red laser, the mildest harmful effect was observed at 45 mW power for 60 s, resulting in a cell survival rate of 147.62%. Conversely, the most significant toxic response occurred at 10 mW power for 60 s, resulting in a cell viability of 91.56%. In contrast, when employing infrared laser irradiation, the least substantial cytotoxic effect on MCF-7 cells was observed at 10 mW power for 600 s, resulting in the highest cell viability of 109.37% after 24 h. The most pronounced cytotoxic effect was observed by infrared laser (780 nm) at 25 mW power for 900 s, leading to the lowest viability of 32.53%.

Blackthorn fruit peel polyphenol extracts and photodynamic effect under blue light against Listeria monocytogenes.

Photodynamic inactivation is an emerging antimicrobial treatment that can be enhanced by employing exogenous photosensitizers to eradicate foodborne pathogens. This study investigated a novel combinatory strategy to eradicate Listeria monocytogenes using blackthorn fruit peel (BFP) and blue light (BL). Extracts of BFP were characterized in terms of polyphenolic content, individual constituents, and antioxidant and antimicrobial activity. The concentration of phenolic compounds and antioxidant activity were both found to be determinants of antimicrobial activity. It was further speculated that flavonols, predominantly quercetin and rutin, were responsible for the activity of BFP against L. monocytogenes. A combination of BFP and BL resulted in a rapid inactivation of the pathogen by up to 4 log CFU/mL at 58.5 J/cm2, corresponding to 15 min BL illumination. Flow cytometry analysis revealed that the bacterial cells lost activity and suffered extensive membrane damage, exceeding 90% of the population. After photosensitizing L. monocytogenes with the BFP constituents quercetin and rutin, a 1.3-log reduction was observed. When applied together, these compounds could inflict the same damaging effect on cells as they did individually when effects were added. Therefore, the results indicate that BFP represents a natural source of (pro-)photosensitizers, which act additively to create inactivation effects. This study may help identify more effective plant-based photosensitizers to control L. monocytogenes in food-related applications.

Blue light photobiomodulation induced osteosarcoma cell death by facilitating ferroptosis and eliciting an incomplete tumor cell stress response.

To investigate the potential of blue light photobiomodulation (PBM) in inducing ferroptosis, a novel form of regulated cell death, in OS cells, considering its known effectiveness in various cancer models. In this investigation, we exposed human OS cell lines, HOS and MG63, to different wavelengths (420, 460 and 480 nm) of blue light at varying irradiances, and examined cellular responses such as viability, apoptosis, levels of reactive oxygen species (ROS), and mitochondrial membrane potential (MMP). Transcriptome sequencing was employed to unravel the molecular mechanisms underlying blue light-induced effects, with validation via quantitative real-time PCR (qRT-PCR). Our findings revealed a wavelength- and time-dependent decrease in cell viability, accompanied by increased apoptosis and oxidative stress. Transcriptomic analysis identified differential expression of genes associated with ferroptosis, oxidative stress, and iron metabolism, further validated by qRT-PCR. These results implicated ferroptosis as a significant mechanism in the blue light-induced death of OS cells, potentially mediated by ROS generation and disruption of iron homeostasis. Also, An incomplete stress response was observed in MG63 cells induced by blue light exposure. Hence, blue light PBM holds promise as a therapeutic approach in OS clinical investigations; however, additional exploration of its underlying mechanisms remains imperative.

A cellulose-based light-management film incorporated with benzoxazine resin/tannic acid exhibiting UV/blue light double blocking and enhanced mechanical property.

Cellulose, as a biomass resource, has attracted increasingly attention and extensive research by virtue of its widely sources, ideal degradability, good mechanical properties and easy modification due to its rich hydroxyl groups. Nevertheless, it is still a challenge to attain high performance cellulose-based composite film materials with diverse functional combinations. In this work, we developed a multifunctional cellulose-based film via a facile impregnation-curing strategy. Here, benzoxazine resin (BR) is used as an optically functional component to endow the microfibrillated cellulose (MFC) film with powerful light management capabilities including UV and blue light double shielding, high transmittance, and high haze. Meanwhile, the introduction of tannic acid (TA) substantially enhanced the mechanical properties of the film, including tensile strength and toughness, by constructing energy-sacrificial bonds. An effective self-healing of the film was achieved by controlling the degree of BR curing. The final films exhibited 98.24 % UV shielding and 89.98 % blue light blocking, good mechanical properties including a tensile strength of 202.21 MPa and tensile strain of 7.1 %, as well as desirable thermal healing properties supported by incompletely cured BR. This work may provide new insights into the high-value utilization of biomass resources.

Exploration of the Graphene Quantum Dots-Blue Light Combination: A Promising Treatment against Bacterial Infection.

Graphene Quantum Dots (GQDs) have shown the potential for antimicrobial photodynamic treatment, due to their particular physicochemical properties. Here, we investigated the activity of three differently functionalized GQDs-Blue Luminescent GQDs (L-GQDs), Aminated GQDs (NH2-GQDs), and Carboxylated GQDs (COOH-GQDs)-against E. coli. GQDs were administrated to bacterial suspensions that were treated with blue light. Antibacterial activity was evaluated by measuring colony forming units (CFUs) and metabolic activities, as well as reactive oxygen species stimulation (ROS). GQD cytotoxicity was then assessed on human colorectal adenocarcinoma cells (Caco-2), before setting in an in vitro infection model. Each GQD exhibits antibacterial activity inducing ROS and impairing bacterial metabolism without significantly affecting cell morphology. GQD activity was dependent on time of exposure to blue light. Finally, GQDs were able to reduce E. coli burden in infected Caco-2 cells, acting not only in the extracellular milieu but perturbating the eukaryotic cell membrane, enhancing antibiotic internalization. Our findings demonstrate that GQDs combined with blue light stimulation, due to photodynamic properties, have a promising antibacterial activity against E. coli. Nevertheless, we explored their action mechanism and toxicity on epithelial cells, fixing and standardizing these infection models.

The role of the SIRT1/NF-κB/NLRP3 pathway in the pyroptosis of lens epithelial cells under shortwave blue light radiation.

Cataracts are the world's number one blinding eye disease. Cataracts can only be effectively treated surgically, although there is a chance of surgical complications. One of the pathogenic processes of cataracts is oxidative stress, which closely correlated with pyroptosis. SIRT1 is essential for the regulation of pyroptosis. Nevertheless, the role of SIRT1 in formation of cataracts is unclear. In this work, we developed an in vitro model of shortwave blue light (SWBL)-induced scotomization in human lens epithelial cells (HLECs) and an in vivo model of SWBL-induced cataracts in rats. The study aimed to understand how the SIRT1/NF-κB/NLRP3 pathway functions. Additionally, the evaluation included cell death and the release of lactate dehydrogenase (LDH), a cytotoxicity marker, from injured cells. First, we discovered that SWBL exposure resulted in lens clouding in Sprague- Dawley (SD) rats and that the degree of clouding was positively linked to the duration of irradiation. Second, we discovered that SIRT1 exhibited antioxidant properties and was connected to the NF-κB/NLRP3 pathway. SWBL irradiation inhibited SIRT1 expression, exacerbated oxidative stress, and promoted nuclear translocation of NF-κB and the activation of the NLRP3 inflammasome, which caused LEC pyroptosis and ultimately led to cataract formation. Transient transfection to increase the expression of SIRT1 decreased the protein expression levels of NF-κB, NLRP3, caspase-1, and GSDMD, inhibited HLEC pyroptosis, and reduced the release of LDH, providing a potential method for cataract prevention and treatment.

Modified Hybrid Hydroxyapatite-Silver Nanoparticles Activated via a Blue Light Source in Various Concentrations in Two-Step Self-Etch Adhesive to Caries-Affected Primary Dentin.

Aims: To evaluate hydroxyapatite-silver (HA-Ag) hybrid nanoparticles (NPs), as an antibacterial agent when integrated in self-etch (SE) adhesive. Blue light activated HA-Ag hybrid NP incorporation on mechanical properties, degree of conversion (DC), and microtensile bond strength (µTBS). Method: Eighty primary molar teeth have carious lesions reaching the dentin but not involving the pulp. The infected dentin was removed and carious-affected dentin (CAD) was preserved. Forty samples were inoculated with Streptococcus mutans. All primary teeth (n = 80) were allocated into four groups based on the incorporation of HA-Ag hybrid NPs in different concentrations (0%, 1%, 5%, and 10%). Group 1: 0% HA-Ag hybrid NPs + Clearfil SE bond primer, group 2: 1% HA-Ag hybrid NPs + Clearfil SE bond primer, group 3: 5 wt% HA-Ag NPs + Clearfil SE bond primer, and group 4: 10 wt% HA-Ag NPs + Clearfil SE bond primer. The survival rate assessment of S. mutans was conducted on 40 inoculated samples. On the remaining primary teeth (n = 40), Clearfil SE bonding agent was applied uniformly via a blue light source. The composite buildup was performed on the samples and µTBS and failure analysis assessed. Fourier transform infrared spectroscopy was performed to assess DC. Survival rates of S. mutans and µTBS among the tested groups were compared using ANOVA and Tukey post hoc analysis. Results: 10 wt % HA-Ag NPs + Clearfil SE bond primer exhibited the highest level of antibacterial efficacy (0.14 ± 0.02 CFU/mL) against S. mutans. The highest µTBS (18.38 ± 0.78 MPa) at the composite/CAD interface was in group 2 (1 wt % HA-Ag NPs + Clearfil SE bond primer + Clearfil SE bonding agent + activation with a blue light source). The highest DC was observed in the control group with Clearfil SE bond primer + Clearfil SE bonding agent + activation with a blue light source. Conclusion: 1 wt% HA-Ag hybrid NPs showed enhanced antibacterial effectiveness, DC, and bond strength of the SE adhesive to the primary CAD.

Blue Light Compromises Bacterial ß-Lactamases Activity to Overcome ß-Lactam Resistance.

OBJECTIVE: In this study, we evaluated the effectiveness of antimicrobial blue light (aBL; 410 nm wavelength) against ß-lactamase-carrying bacteria and the effect of aBL on the activity of ß-lactamases. METHODS: Pseudomonas aeruginosa, Escherichia coli, and Klebsiella pneumoniae strains carrying ß-lactamases as well as a purified ß-lactamase enzymes were studied. ß-lactamase activity was assessed using a chromogenic cephalosporin hydrolysis assay. Additionally, we evaluated the role of porphyrins in the photoreaction, as well as protein degradation by sodium dodecyl-sulfate polyacrylamide gel electrophoresis (SDS-PAGE). Finally, we investigated the bactericidal effect of combined aBL-ceftazidime exposure against a metallo-ß-lactamase expressing P. aeruginosa strain. RESULTS: Our study demonstrated that aBL effectively killed ß-lactamase-producing bacteria and reduced ß-lactamase activity. After an aBL exposure of 1.52 J/cm2, a 50% reduction in enzymatic activity was observed in P. aeruginosa. Additionally, we found a 40% decrease in the photoreaction activity of porphyrins following an aBL exposure of 64.8 J/cm2. We also revealed that aBL reduced ß-lactamase activity via protein degradation (after 136.4 J/cm2). Additionally, aBL markedly improved the bactericidal effect of ceftazidime (by >4-log10) in the metallo-ß-lactamase P. aeruginosa strain. CONCLUSION: Our results provide evidence that aBL compromises bacterial ß-lactamase activity, offering a potential approach to overcome ß-lactam resistance in bacteria.

Synergistic Effect of Doxorubicin and Blue Light Irradiation on the Antitumor Treatment of HepG2 Cells in Liver Cancer.

Doxorubicin (DOX) has been an effective antitumor agent for human liver cancer cells; however, an overdose might lead to major side effects appearing in clinical applications. In this work, we present a strategy of combining DOX and blue light (BL) irradiation for the antitumor treatment of HepG2 cells (one typical human liver cancer cell line). It is demonstrated that synergetic DOX and BL can significantly reduce cell proliferation and increase the apoptotic rate of HepG2 cells in comparison to individual DOX treatment. The additional BL irradiation is further helpful for enhancing the inhibition of cell migration and invasion. Analyses of reactive oxygen species (ROS) level and Western blotting reveal that the strategy results in more ROS accumulation, mitochondrial damage, and the upregulation of proapoptotic protein (Bcl-2) and downregulation of antiapoptotic protein (Bax). In addition to the improved therapeutic effect, the non-contact BL irradiation is greatly helpful for reducing the dosage of DOX, and subsequently reduces the side effects caused by the DOX drug. These findings offer a novel perspective for the therapeutic approach toward liver cancer with high efficiency and reduced side effects.

Protective effect and mechanism of Lycium ruthenicum Murray anthocyanins against retinal damage induced by blue light exposure.

Lycium ruthenicum Murray (LR) is a medicine and edible plant in Northwest China, and L. ruthenicum Murray anthocyanins (LRA) are green antioxidants with various pharmacological activities, such as antioxidant and anti-inflammatory activities. However, the protective effect and mechanism of LRA against retinal damage induced by blue light exposure are poorly understood. This study explored the protective effects and potential mechanisms of LRA on retinal damage induced by blue light exposure in vitro and in vivo. The results showed that LRA could ameliorate oxidative stress injury by activating the antioxidant stress nuclear factor-related factor 2 pathway, promoting the expression of phase II detoxification enzymes (HO-1, NQO1) and endogenous antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase), and reducing reactive oxygen species and malondialdehyde levels. Additionally, LRA could inhibit inflammatory response by decreasing the expression of blue light exposure-induced nuclear factor-κB (NF-κB) pathway-related proteins (NF-κB and p-IκBα), as well as interleukin (IL)-6, tumor necrosis factor-α, IL-1ß pro-inflammatory factors and pro-inflammatory chemokine VEGF, and increasing the expression of anti-inflammatory factor IL-10. Furthermore, LRA could ameliorate oxidative stress-induced apoptosis by upregulating Bcl-2 and downregulating Bax and Caspase-3 protein expression. All these results indicate that LRA can be used as an antioxidant dietary supplement for the treatment or prevention of retinal diseases.

Blue Light Effects on the Skin: A Post-2015 Update.

The debate surrounding the benefits versus harms of blue light have become a topic of interest recently due to increased exposure. Blue light therapy has been utilized with some success in a variety of dermatologic conditions. However, potential harms have also been documented. Currently, there is no evidence to suggest a necessity for blue light photoprotection, but there are products available with proven efficacy for those desiring protection. J Drugs Dermatol. 2024;23(6):472-476.     doi:10.36849/JDD.7665.

Effect of 460 nm blue light PBM on human MeWo melanoma cells.

Photobiomodulation (PBM) using 460 nm blue light has been shown to have an inhibitory effect on skin cancer cells. In this study, we used a continuous LED light source with a wavelength of 460 nm and designed various combinations of power density (ranging from 6.4 to 25.6 mW) and dose (ranging from 0.96 to 30.72 J/cm2) to conduct treatment experiments on MeWo cells to investigate the effects of blue light on MeWo melanoma cells. We are focusing on cell viability, cytotoxicity, mitochondrial function, oxidative stress, and apoptosis. We found that blue light inhibits these melanoma cells through oxidative stress and DNA damage, and this inhibition intensifies at higher irradiance levels. Although the cells initially attempt to resist the stress induced by the treatment, they eventually undergo apoptosis over time. These findings contribute to understanding melanoma's molecular response to blue light PBM, lay the groundwork for future clinical applications.

Blue light irradiation suppresses oral squamous cell carcinoma through induction of endoplasmic reticulum stress and mitochondrial dysfunction.

The therapeutic potential of blue light photobiomodulation in cancer treatment, particularly in inhibiting cell proliferation and promoting cell death, has attracted significant interest. Oral squamous cell carcinoma (OSCC) is a prevalent form of oral cancer, necessitating innovative treatment approaches to improve patient outcomes. In this study, we investigated the effects of 420 nm blue LED light on OSCC and explored the underlying mechanisms. Our results demonstrated that 420 nm blue light effectively reduced OSCC cell viability and migration, and induced G2/M arrest. Moreover, we observed that 420 nm blue light triggered endoplasmic reticulum (ER) stress and mitochondrial dysfunction in OSCC cells, leading to activation of the CHOP signal pathway and alterations in the levels of Bcl-2 and Bax proteins, ultimately promoting cell apoptosis. Additionally, blue light suppressed mitochondrial gene expression, likely due to its damage to mitochondrial DNA. This study highlights the distinct impact of 420 nm blue light on OSCC cells, providing valuable insights into its potential application as a clinical treatment for oral cancer.

High-Intensity Blue Light (450-460 nm) Phototherapy for Pseudomonas aeruginosa-Infected Wounds.

Background: Nosocomial wound infection with Pseudomonas aeruginosa (PA) is a serious complication often responsible for the septic mortality of burn patients. Objective: High-intensity antimicrobial blue light (aBL) treatment may represent an alternative therapy for PA infections and will be investigated in this study. Methods: Antibacterial effects of a light-emitting diode array (450-460 nm; 300 mW/cm2; 15/30 min; 270/540 J/cm2) against PA were determined by suspension assay, biofilm assay, and a human skin wound model and compared with 15-min topically applied 3% citric acid (CA) and wound irrigation solution (Prontosan®; PRT). Results: aBL reduced the bacterial number [2.51-3.56 log10 colony-forming unit (CFU)/mL], whereas PRT or CA treatment achieved a 4.64 or 6.60 log10 CFU/mL reduction in suspension assays. aBL reduced biofilm formation by 60-66%. PRT or CA treatment showed reductions by 25% or 13%. Here, aBL reduced bacterial number in biofilms (1.30-1.64 log10 CFU), but to a lower extend than PRT (2.41 log10 CFU) or CA (2.48 log10 CFU). In the wound skin model, aBL (2.21-2.33 log10 CFU) showed a bacterial reduction of the same magnitude as PRT (2.26 log10 CFU) and CA (2.30 log10 CFU). Conclusions: aBL showed a significant antibacterial efficacy against PA and biofilm formation in a short time. However, a clinical application of aBL in wound therapy requires effective active skin cooling and eye protection, which in turn may limit clinical implementation.

Differences between long- and short-wavelength light-induced retinal damage and the role of PARP-1 in retinal injury induced by blue light.

Photobiomodulation (PBM) therapy uses light of different wavelengths to treat various retinal degeneration diseases, but the potential damage to the retina caused by long-term light irradiation is still unclear. This study were designed to detect the difference between long- and short-wavelength light (650-nm red light and 450-nm blue light, 2.55 mW/cm2, reference intensity in PBM)-induced injury. In addition, a comparative study was conducted to investigate the differences in retinal light damage induced by different irradiation protocols (short periods of repeated irradiation and a long period of constant irradiation). Furthermore, the protective role of PARP-1 inhibition on the molecular mechanism of blue light-induced injury was confirmed by a gene knockdown technique or a specific inhibitor through in vitro and in vivo experiments. The results showed that the susceptibility to retinal damage caused by irradiation with long- and short-wavelength light is different. Shorter wavelength lights, such as blue light, induce more severe retinal damage, while the retina exhibits better resistance to longer wavelength lights, such as red light. In addition, repeated irradiation for short periods induces less retinal damage than constant exposure over a long period. PARP-1 plays a critical role in the molecular mechanism of blue light-induced damage in photoreceptors and retina, and inhibiting PARP-1 can significantly protect the retina against blue light damage. This study lays an experimental foundation for assessing the safety of phototherapy products and for developing target drugs to protect the retina from light damage.

Exposure of Bladder Cancer Cells to Blue Light (λ = 453 nm) in the Presence of Riboflavin Synergistically Enhances the Cytotoxic Efficiency of Gemcitabine.

Non-muscle invasive bladder cancer is a common tumour in men and women. In case of resistance to the standard therapeutic agents, gemcitabine can be used as off-label instillation therapy into the bladder. To reduce potential side effects, continuous efforts are made to optimise the therapeutic potential of drugs, thereby reducing the effective dose and consequently the pharmacological burden of the medication. We recently demonstrated that it is possible to significantly increase the therapeutic efficacy of mitomycin C against a bladder carcinoma cell line by exposure to non-toxic doses of blue light (453 nm). In the present study, we investigated whether the therapeutically supportive effect of blue light can be further enhanced by the additional use of the wavelength-specific photosensitiser riboflavin. We found that the gemcitabine-induced cytotoxicity of bladder cancer cell lines (BFTC-905, SW-1710, RT-112) was significantly enhanced by non-toxic doses of blue light in the presence of riboflavin. Enhanced cytotoxicity correlated with decreased levels of mitochondrial ATP synthesis and increased lipid peroxidation was most likely the result of increased oxidative stress. Due to these properties, blue light in combination with riboflavin could represent an effective therapy option with few side effects and increase the success of local treatment of bladder cancer, whereby the dose of the chemotherapeutic agent used and thus the chemical load could be significantly reduced with similar or improved therapeutic success.

Blue light irradiation inhibits the M2 polarization of the cancer-associated macrophages in colon cancer.

Recent studies have shown that blue light-emitting diode (LED) light has anti-tumor effects, suggesting the possibility of using visible light in cancer therapy. However, the effects of blue light irradiation on cells in the tumor microenvironment, including tumor-associated macrophages (TAMs), are unknown. Here, THP-1 cells were cultured in the conditioned medium (CM) of HCT-116 cells to prepare TAMs. TAMs were divided into LED-irradiated and control groups. Then, the effects of blue LED irradiation on TAM activation were examined. Expression levels of M2 macrophage markers CD163 and CD206 expression were significantly decreased in LED-irradiated TAMs compared with the control group. While control TAM-CM could induce HCT-116 cell migration, these effects were not observed in cells cultured in TAM-CM with LED irradiation. Vascular endothelial growth factor (VEGF) secretion was significantly suppressed in LED-exposed TAMs. PD-L1 expression was upregulated in HCT-116 cells cultured with TAM-CM but attenuated in cells cultured with LED-irradiated TAM-CM. In an in vivo model, protein expression levels of F4/80 and CD163, which are TAM markers, were reduced in the LED-exposed group. These results indicate that blue LED light may have an inhibitory effect on TAMs, as well as anti-tumor effects on colon cancer cells.

Effect of canal medicaments triple antibiotic paste, Bio-C Temp, and Nano-silver gel activated by visible blue light on canal dentin microhardness and extrusion bond strength of AH plus sealer: A SEM and EDX analysis.

AIM: Assessment of contemporary canal medicaments (Triple antibiotic paste (TAP), Bio-C Temp, and Nano silver gel activated by visible blue light on the dentin microhardness (MH) and push-out bond strength (PBS) of AH plus endodontic sealer. METHOD: Sixty extracted premolars were obtained and decontaminated. Canal cleaning and shaping were performed. The samples were randomly allocated into four groups based on the intracanal medicaments. Group 1= CH paste, Group 2= TAP, Group 3= Bio-C Temp, and Group 4= Nano-silver gel activated by visible blue light. MH assessment was performed using a Vickers Microhardness tester. Forty specimens, ten from each group underwent root canal obturation. PBS and failure mode evaluation were performed. ANOVA and Post Hoc Tukey test were utilized to conduct intra and inter-group comparisons. RESULTS: The maximum outcome of surface hardness was presented by Group-3 (Bio-C Temp®) specimens. However, minimum scores of MH were displayed by Group 1 (CH) treated teeth. The highest outcomes of EBS were exhibited by the cervical third of Group 3 (Bio-C Temp®) samples. The apical section of Group 4 Teeth with Nano Silver gel activated by visible blue light revealed the lowest scores of bond integrity. CONCLUSION: Bio-C Temp and TAP proved to be better intracanal medicament than other tested groups in terms of the push-out bond strength of the sealer. TAP displayed lower microhardness as compared to the Bio-C Temp.