Adenosine receptor family especially A1 type is expressed in breast cancer cells in which P53 and caspase genes are wild-type. The aim of this study was to investigate the correlation between A1 receptor and either cell apoptosis or proliferation and also to recognize the relationship between this receptor and P53 and the expression of caspases 3, 8 and 9 in MCF-7 cell line. MCF-7 cells were treated intermittently with A1 receptor agonist N6-Cyclopentyladenosine (CPA) and A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) in different times to measure the expression of p53, caspase 3, 8 and 9 besides apoptosis and survival rate. Our findings indicated that DPCPX significantly induced apoptosis in MCF-7 cells while the cell viability was reduced specially 72 h after the treatment and the expression of p53 gene and caspase expressions was dramatically up-regulated. On the other hand, CPA increased the cell viability and reduced apoptosis in MCF-7 cells. Our results indicated a significant down-regulation in the MCF-7 mRNA expression of p53 and caspases 3, 8 and 9. Furthermore, DPCPX induced p53 and caspase 3, 8 and 9 expressions that consequently promotes the cell apoptosis in MCF-7 cells. Therefore, DPCPX can be considered as an anti-cancer drug.

Background and Aims: Tissue engineering is a relatively novel field that has been intensely developing during recent years and has shown to be excessively promising when used for cartilage regeneration. Scaffolds represent important components for tissue engineering. Materials and Methods: The Poly Lactic-Co-Glycolic Acid (PLGA) impregnated with fibrin and hyaluronic acid (HA) produce hybrid scaffolds. human adipose-derived stem cells (hADSCs) were seeded in scaffolds and cultured in chondrogenic media. The viability of cells in different groups was assessed by MTT. The expression of chondrogenic related genes [Sox9, type II collagen (Col II), Aggrecan(AGG)] and type X collagen (Col X) was quantified by real-time polymerase chain reaction. Results: The results of the real-time PCR showed SOX9, AGG and Col X gene expression in the control groups being significantly lower than the other groups (p≤0.05). It also demonstrated Col II gene expression in the control group being significantly lower than the PLGA/Fibrin and PLGA/Fibrin/HA groups (p≤0.05). The Col X gene expression of cells in PLGA/HA and PLGA/Fibrin/HA groups significantly decreased in comparison with the PLGA/Fibrin group (p≤0.05). Conclusions: These conclusions indicate that administration of PLGA/ Fibrin and PLGA/HA scaffolds, particularly PLGA/Fibrin/ HA, motivates chondrogenesis in hADSCs. This can be diminished by decreasing hypertrophic markers and increasing characteristic markers of hyaline cartilage.

The pandemic outbreak of coronavirus disease 2019 (COVID-19) has created health challenges in all parts of the world. Understanding the entry mechanism of this virus into host cells is essential for effective treatment of COVID-19 disease. This virus can bind to various cell surface molecules or receptors, such as angiotensin-converting enzyme 2 (ACE2), to gain cell entry. Respiratory failure and pulmonary edema are the most important causes of mortality from COVID-19 infections. Cytokines, especially proinflammatory cytokines, are the main mediators of these complications. For normal respiratory function, a healthy air–blood barrier and sufficient blood flow to the lungs are required. In this review, we first discuss airway epithelial cells, airway stem cells, and the expression of COVID-19 receptors in the airway epithelium. Then, we discuss the suggested molecular mechanisms of endothelial dysfunction and blood vessel damage in COVID-19. Coagulopathy can be caused by platelet activation leading to clots, which restrict blood flow to the lungs and lead to respiratory failure. Finally, we present an overview of the effects of immune and non-immune cells and cytokines in COVID-19-related respiratory failure.

Background: Adenosine receptor family, especially A1 type is-overexpressed in breast-derived tumor cells and the P53 gene is mutant in some of these cells while the casps gene is of wild type as well. The aim of this study was to evaluate the effect of the A1 receptor function on cell programmed death or proliferation, as well as the relationship between this receptor stimulation/inhibition and caspase 3 (casp3) expression in T47D cell line that has a mutant and non-functional P53 gene. Materials and Methods: The expression of casps3 was measured by real-time polymerase chain reaction and then flow cytometery and MTT assay were used to assess the apoptotic and proliferation cell rate after the treatment of T47D cells with specific agonist N6-cyclopentyladenosine (CPA) and antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) of this receptor 24, 48, and 72 hours after treatment. Result: Our results indicated that DPCPX significantly induces apoptosis in T47D cells and the rate of survival cell after the reduction of this treatment, especially 72 hours after treatment. Finally, the expression of casp3 was up-regulated by DPCPX treatment, especially in 72 hours while CPA treatment had opposite results (P>0.05). Conclusion: In general, DPCPX could up-regulate casp3 gene expression and subsequently increase the apoptosis rate in T47D cells with casp3 expression without the P53 gene interference. Therefore, adenosine A1 receptor antagonists may be introduced as anti-cancer agents.

Background: Sodium dodecyl sulfate (SDS) detergent is widely used in tissue decellularization to produce scaffolds for tissue engineering. Despite its strong decellularization, this substance has relatively high toxicity and causes changes in tissue composition. Sodium lauryl ether sulfate (SLES) is a new poly anionic detergent that is less toxic than SDS but weaker than it. The present study aimed to decellularize the intestinal tissue using SDS and SLES solutions, forming a cell scaffold, and examining scaffolds obtained from this tissue. Methods: Eighteen male Sprague-Dawley rats were divided into three groups. The intestines of all rats were removed after anesthesia. In the first group (controls), rats’ intestines were placed in a 10% formalin solution. In the second group, intestines were decellularized using an SLES solution. In the third group animals’ intestines were decellularized using an SDS solution. To evaluate decellularization, samples were stained with hematoxylin-eosin staining and Alcian blue staining for glycosaminoglycans (GAGs), and Masson’s trichrome for collagen fibers. A confocal Raman microscope was used to compare collagen, lipid, GAG, and genetic content. Results: Hematoxylin-eosin staining showed that the nucleus and DNA were removed in the decellularized scaffolds by SDS or SLES. The SLES group, compared to the SDS group, showed fewer changes in the epithelial tissue, and muscle layers in both scaffolds were well preserved. The results of confocal Raman microscopy showed that tryptophan, lipid, glycogen, and protein were broken down by both detergents; however, the residual amount of glycogen was the same in both substances, but disulfide bonds of proteins, hydroxyproline, and lipids in the decellularized intestine with SLES were mostly preserved. Conclusion: Both substances were suitable for intestinal decellularization and removed the overall structure of intestinal tissue, but SLES retained collagen and GAG content better than SDS.

Background: Every year, many people around the world die from cancers. Among all types of cancers, brain cancer has been recognized as one of the most deadly cancers due to the late detection and limitations of current therapies, and thus it remains an unresolved problem. Glioblastoma occurs in different parts of the central nervous system and is one of the most important causes of cancer death in people. In addition, there are many problems for the treatment of cancer cells. One of the limiting factors is the resistance of cancer cells to chemotherapy drugs. In this regard, the use of nanoparticles (NPs) is an effective method for overcoming this problem. Materials and Methods: In this study, iron oxide-NPs were synthesized and loaded on the folic and lomustine. Further, the size and morphology of NPs were assessed by transmission electron microscopy, X-ray photoelectron spectroscopy, and dynamic light scattering. Then, the U87-MG cell line was cultured in the Dulbecco’s Modified Eagle Medium and treated with nano, nano-folic, nano-lomustine (LUM), LUM, and complex, followed by evaluating 50% inhibitory concentration, tetrazolium assay, and caspase-6 activity. Results: Our results showed that cell viability decreased in LUM container groups by increasing the incubation time. Based on the caspase-6 activity analysis, the mortality rate increased in LUM container groups after 3 days. These findings indicated that LUM, complex, and nano-LUM increase cell death in U87MG. Conclusion: Finally, the results suggested that LUM in NPs could be applied as a safer form of drug delivery for targeting cancer.