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Atherosclerosis is considered as the most common cardiovascular disease and a leading cause of global mortality, which develops through consecutive steps. Various cellular and molecular biomarkers such as microRNAs are identified to be involved in atherosclerosis progression. MicroRNAs are a group of endogenous, short, non-coding RNAs, which are able to bind to specific sequences on target messenger RNAs and thereby modulate gene expression post-transcriptionally. MicroRNAs are key players in wide range of biological processes; thus, their expression level is regulated in pathophysiological conditions. Ample evidences including in vitro and in vivo studies approved a critical role of microRNAs in epigenetic and the sequential processes of atherosclerosis from risk factors to plaque formation, progression, and rupture. Based on these findings, miRNAs seems to be promising candidates for therapeutic approach. This review summarizes the role of miRNAs in atherosclerosis development, epigenetic, and therapy. Moreover, the application of exosomes in miRNA delivery, and/or their prognostic and diagnostic values are also discussed.

Hydrogen sulfide (H 2 S), a well-known toxic gas, is regarded as endogenous neuromodulator and plays multiple roles in the central nervous system under physiological and pathological states, especially in secondary neuronal injury. Recent studies have shown relatively high concentrations of hydrogen sulfide (H 2 S) in the brain and also cytoprotective effects of endogenous and exogenous H 2 S in models of in vitro and in vivo ischemic injury. H 2 S protects neurons by functioning as an anti-oxidant, anti-inflammatory, and anti-apoptotic mediator and by improving neurological function. Moreover, it protects neurons from glutamate toxicity. Therefore, the present study aimed to determine whether H 2 S provides protection in transient focal cerebral ischemia. Focal ischemia was induced by 60-min middle cerebral artery occlusion (MCAO), followed by 23-h reperfusion. Saline as a vehicle and NaHS (H 2 S donor; 1 and 5 mg) were intraperitoneally injected (IP) at the beginning of ischemia. Infarct volume, brain edema, and apoptosis were assessed 24 h after MCAO. Treatment with NaHS at doses of 1 and 5 mg markedly reduced total infarct volumes by 29 and 51 %, respectively ( P  < 0.001). In addition, NaHS at doses of 1 and 5 mg reduced brain edema ( P  < 0.05) and inhibited apoptosis by decreasing positive TUNEL cells ( P  < 0.001). The present study shows that treatment with H 2 S reduces brain injuries and postischemic cerebral edema in a dose-dependent manner likely through the blocking programmed cell death. We propose that H 2 S might be a promising therapeutic target for stroke, although more researches are necessary to take into account the potential therapeutic effects of H 2 S in stroke patients.

Brucella abortus vaccines help control bovine brucellosis. The RB51 strain is a live attenuated vaccine with low side effects compared with other live attenuated brucellosis vaccines, but it provides insufficient protective efficacy. Cell-mediated immune responses are critical in resistance against intracellular bacterial infections. Therefore, we hypothesized that the listeriolysin O (LLO) expression of Listeria monocytogenes, BAX, and SMAC apoptotic proteins in strain RB51 could enhance vaccine efficacy and safety. B. abortus RB51 was transformed separately with two broad-host-range plasmids (pbbr1ori-LLO and pBlu–mLLO-BAX-SMAC) constructed from our recent work. pbbr1ori-LLO contains LLO, and pBlu–mLLO-BAX-SMAC contains the mutant LLO and BAX-SMAC fusion gene. The murine macrophage-like cell line J774A.1 was infected with the RB51 recombinant strain containing pBlu-mLLO-BAX-SMAC, RB51 recombinant strain containing LLO, and RB51 strain. The bacterial cytotoxicity and survival and apoptosis of host cells contaminated with our two strain types—RB51 recombinants or the parental RB51—were assessed. Strain RB51 expressing mLLO and BAX-SMAC was tested in BALB/c mice and a cell line for enhanced modulation of IFN-γ production. LDH analysis showed that the RB51-mLLO-BAX-SMAC and RB51-LLO strains expressed higher cytotoxicity in J774A.1 cells than RB51. In addition, RB51 recombinants had lower macrophage survival rates and caused higher levels of apoptosis and necrosis. Mice vaccinated with the RB51 recombinant containing mLLO-BAX-SMAC showed an enhanced Th1 immune response. This enhanced immune response is primarily due to bacterial endosome escape and bacterial antigens, leading to improved apoptosis and cross-priming. This potentially enhanced TCD8+- and T cell-mediated immunity leads to the increased safety and potency of the RB51 recombinant (RB51 mLLO-BAX-SMAC) as a vaccine candidate against B. abortus.

The development of protective vaccines for spp. has been hampered by the difficulty in transformation of cells with foreign DNA for genetic manipulation. It seems that the formation of spheroplasts would increase the efficiency of transformation. The aim of this study was to devise an efficient method for the transformation of spp. At first, spheroplast of was prepared by glycine and ampicillin induction and transformed using optimized protocols of CaCl , electroporation, and lipofection methods. Then, the efficacy of transformation was compared between the three-mentioned methods. Ampicillin-induced spheroplasts from early-log phase culture of when incubated in a medium-containing 0.2 M sucrose during cell recovery had higher transformation efficiency in three different methods. Comparison of the transformation efficiency of RB51 using the CaCl , lipofection, and electroporation methods revealed that the transformation efficiency with the lipofection method was significantly higher than with other two methods ( < 0.05). Lipofection method by lipofectamine 2000 on ampicillin-induced spheroplasts can be a suitable approach for transformation.

Propolis is a natural product used in cancer treatment, which is produced by bees via different sources. The chemical composition of Propolis is determined based on the climatic and geographical conditions, as well as harvesting time and method. This compound has been the subject of numerous investigational endeavors due to its expansive therapeutic capacity which includes antibacterial, anti-fungal, anti-inflammatory, anti-oxidant, anti-viral, and anti-cancer effects. The growing incidence rate of different cancers necessitates the need for developing novel preventive and therapeutic strategies. Chemotherapy, radiotherapy, and stem cell therapy have proved effective in cancer treatment, regardless of the adverse events associated with these modalities. Clinical application of natural compounds such as Propolis may confer promise as an adjuvant therapeutic intervention, particularly in certain subpopulations of patients that develop adverse events associated with anticancer regimens. The diverse biologically active compounds of propolis are believed to confer anti-cancer potential by modulation of critical signaling cascades such as caffeic acid phenethyl ester, Galangin, Artepillin C, Chrysin, Quercetin, Caffeic acid, Nymphaeols A and C, Frondoside A, Genistein, p-coumaric acid, and Propolin C. This review article aims to deliver a mechanistic account of anti-cancer effects of propolis and its components. Propolis can prevent angiogenesis by downregulating pathways involving Jun-N terminal kinase, ERK1/2, Akt and NF-ƘB, while counteracting metastatic progression of cancer by inhibiting Wtn2 and FAK, and MAPK and PI3K/AKT signaling pathways. Moreover, propolis or its main components show regulatory effects on cyclin D, CDK2/4/6, and their inhibitors. Additionally, propolis-induced up-regulation of p21 and p27 may result in cell cycle arrest at G2/M or G0/G1. The broad anti-apoptotic effects of propolis are mediated through upregulation of TRAIL, Bax, p53, and downregulation of the ERK1/2 signaling pathway. Considering the growing body of evidence regarding different anti-cancers effects of propolis and its active components, this natural compound could be considered an effective adjuvant therapy aimed at reducing related side effects associated with chemotherapy and radiotherapy.

This study aimed to investigate the effect of Nano Propolis (NP) on cell viability, pro‐apoptotic gene expression, anti‐metastatic activity, and radiosensitization in the A‐375 skin cancer cell line. The IC50 values of 85 and 60 μg/mL were determined for propolis extract (PE) and NP, respectively, in cellular and molecular experiments using A‐375 melanoma cells and Vero normal cells. To assess apoptosis, the expression levels of Bax and Bcl‐2 genes were measured using quantitative reverse transcription polymerase chain reaction (qRT‐PCR). A scratch assay was used to assess the ability of NP and PE to reduce tumor cell migration. A cell cycle assay evaluated the effect of both formulations on cell proliferation after 48 h of incubation. An alkaline comet assay was used to measure DNA strand breaks after treatment with NP or Propolis Extract, combined with ionizing radiation. All statistical analyses were performed using SPSS v.20 and GraphPad Prism v.9. NP at its IC50 concentration showed a stronger ability to increase the apoptotic cell rate, inhibit cancer cell migration, suppress cancer cell growth through G1‐phase arrest, and increase radioprotective effects in the normal cell line, while also increasing radiosensitivity in the cancer cell line compared with PE. NP demonstrated better and more effective activity against A‐375 melanoma cells than PE. Iranian nano propolis stoppeded the cell cycle at G1 phase, increased the apoptosis and anti‐metastasis effect rather than propolis extract. The combination of Iranian nano propolis with ionizing radiataion significantly increased its anticancer properties on cancer cells and protected normal cells. The better and more effective performance of propolis nanoparticle was evident against melanoma cancer cells, A‐375, than propolis extract.