جستجوی مقالات مرتبط با کلیدواژه "cell viability" در نشریات گروه "علوم پایه"

In recent years, significant efforts have been focused on advancements of novel biomaterials based on natural polymers and utilization of efficient methods such as skin tissue engineering for wound treatment. In this study, a 3D printed polycaprolactone (PCL) scaffold coated via immersion in a 1:4 blend of 40% silk fibroin from Bombyx mori cocoons and TEMPO-oxidized was developed. The pore size and the porosity were 180 µm and 85%, respectively. The results demonstrated an enhancement in exudate absorption (swelling and water uptake of 1342% and 80%, respectively), improvement in storage modulus (G’) from 500 to 4000 Pa, as well as viscoelasticity up to 60%, which all are favorable for wound dressing applications. Moreover, the wettability and biodegradability studies revealed an overall increase in contact angle and degradation rate of 19.9°±3, and 95%, respectively. Cell viability and migration studies on fibroblastic cells (L929) using MTT assay, DAPI/ Phalloidin staining, and scratch test showed over 90% viability up to 7 days and complete scratch repair within 24 hours. These findings show that 3D printed PCL scaffolds coated with silk fibroin and oxidized nanocellulose are promising for wound healing applications and might pave the way to natural polymer-based wound dressings.

Breast cancer is the most common cause of death from cancer among women. The triple-negative breast cancer (TNBC) is the most invasive subtype, and chemotherapy is the only therapy option. Cancer cells preferably utilize the glycolysis pathway even with proper oxygen availability, and this activation plays a great role in tumorigenesis. Therefore, glycolysis targeting can be an effective strategy for cancer treatment. Here, the apoptotic effect of a glycolysis inhibitor named dichloroacetate (DCA) on TNBC cells MDA-MB-231 was assessed, and the expression of anti-apoptotic genes and oncogenic miRNAs was evaluated. MTT assay showed that DCA reduces cell viability in a dose-dependent manner with the IC50 concentration of 50 mM. Annexin/PI assay demonstrated that DCA due to DCA treatment. Finally, the expression of anti-apoptotic genes Bcl2l1 and Mcl1 and oncogenic miRNAs miR21 and miR27a decreased due to DCA treatment. Our results confirmed that DCA, as a glycolysis inhibitor, leads to apoptosis induction in TNBC cells because of reducing expression of viability genes and miRNAs.

The worldwide incidence rate for cancer has been rising. However, the molecular mechanisms involved in tumor growth and metastasis are unclear. Autophagy is a cellular pathway that leads to cell death or survival depending on the specific condition of the tumor cells. The aim of this study was to evaluate the effects of activation or inhibition of the autophagy pathway using tunicamycin or N-acetylcysteine on cell viability in the MDA-MB-231 breast cancer cell line.

MDA-MB-231 cells were cultured in the presence of different doses of tunicamycin or N-acetylcysteine. Then, a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was performed for the evaluation of tumor cell viability. Real-time PCR was carried out to evaluate the expression of the genes encoding for Becline-1 and the mammalian target of rapamycin (mTOR) (as autophagy markers) in the MDA-MB-231 cell line. The LC3-II to LC3-I ratio and p62 were measured with western blotting.

Tunicamycin significantly increased autophagy markers and inhibited cell viability in a time- and dose-dependent manner. A negative significant correlation was observed between the expression of autophagy markers and cell viability. However, N-acetylcysteine resulted in decreased autophagy and increased cell viability just at a concentration of 2mM.

Tunicamycin leads to activation of the autophagy pathway, resulting in a decrease in cell viability in breast cancer cells (MDA-MB-231); and N-acetylcysteine, at a low concentration, can inhibit autophagy and increase cell viability. Thus, the autophagy pathway can be considered a target in cancer treatment.

Nanotechnology is one of the emerging and advanced sciences that has been highly developed in recent years and has caused environmental pollution. Therefore, in this study, the toxicity of silver nanoparticles on the green alga Chlorella vulgaris was investigated. Chlorella vulgaris cells were exposed to concentrations of 0, 0.005, 0.001, 0.05, 0.01, 0.5 and 0.1 mg / l silver nanoparticles over a period of 96 hours. The results showed that the cell density of Chlorella vulgaris decreased with increasing concentration of silver nanoparticles compared to the control group and even at the lowest concentration of 0.005 mg / l caused the cell growth inhibition (p<0.05). With increasing concentration of silver nanoparticles, the survival rate decreased compared to the control group and did not change during the 96-hour period. The amount of chlorophyll a, b and total pigments in the concentrations of 0.05 and 0.1 mg / l and the duration of 24 hours were the highest, but the values ​​of carotenoids showed the highest in 96 h and the concentration of 0.01 mg / l of silver nanoparticles. Silver nanoparticles are highly toxic to Chlorella vulgaris and if silver nanoparticles are released, the production, survival and chlorophyll content of this microalgae, as one of the main primary producers in freshwater ecosystems, is damaged.

Actinomycetes are a good resource to discover new drugs based on their abundant secondary metabolites. Because both fungal and human cells are eukaryotes, the metabolites of fungal antagonist actinomycetes may also inhibit the growth of cancer cells.

The antagonistic activity of 24 actinomycete strains that inhibited the growth of cells of a plant pathogen, Phytophthora capsici, was investigated against 4 other plant pathogens. The siderophores production of two selected strains that showed the highest antagonistic activity against pathogens was evaluated. The cytotoxicity effects of two strains on the SW480 cell line was measured using MTT assay in vitro and the IC50 percentage was determined.

Only two selected strains had 30 and 54% inhibitory effect against Phytophthora drechsleri, respectively. The strain 408 had no inhibitory effect against Pythium ultimum, while the strain 6010 completely prevented Pythium ultimum growth. The strain 6010, unlike the strain 408, controlled the growth of Rhizoctonia solani and Fusarium oxysporum pathogens about 70%. Only the strain 408 was able to produce siderophore. The significant effect of the treatment on colorectal cancer cells was observed at 2.47 and 2.71% (v/v) concentrations for both 408 and 6010 strains, respectively.

The results of this study confirmed our hypothesis that secondary metabolites of antagonistic actinomycetes can lead to cancer cells death. The use of fungal or oomycete cells is introduced as an easy, safe, and inexpensive method for screening actinomycetes that are candidates for the discovery of new anticancer drugs.

Lung carcinoma is the second most common type of cancer. Inefficiency of the current treatments and the undesirable side effects of chemotherapy drugs made the know-how of the treatment important. The purpose of this study is to investigate the synergic effect of curcumin and Cisplatin in comparison with the sole application of each treatment on Calu-6 cell line, an epithelial cell line of human lung carcinoma, and the expression of Cdc42 gene. The viability of Calu-6 was examined after 24- or 48-hour treatment with doses of 0.5 to 8 µg/ml of curcumin, 0.1 to 50 µg/ml of cisplatin and combined doses of curcumin and Cisplatin by MTT assay. To measure apoptosis and the expression of Cdc42 gene, flow cytometry and Real-Time PCR were utilized. Decrease of cell viability and induction of cell death were observed in the cells treated with 0.67 µg/ml of curcumin and 1.7 µg/ml of cisplatin (the lowest effective dose) and the combined treatment with the same doses of each drug after 24-hour treatments. The maximum rates of early and late apoptosis were related to treatment with curcumin and the combined treatment. The gene expression analysis results indicated that both Curcumin and Cisplatin decrease the expression of Cdc42 gene, moreover, their co-administration showed synergic effects. Therefore, Curcumin could be an appropriate option for complementary administration with other chemotherapy agents in order to reduce their efficient dose, and to reduce their side effects.