Sodium selenite preserves rBM-MSCs' stemness, differentiation potential, and immunophenotype and protects them against oxidative stress via activation of the Nrf2 signaling pathway.

BACKGROUND: The physiological level of reactive oxygen species (ROS) is necessary for many cellular functions. However, during the in-vitro manipulations, cells face a high level of ROS, leading to reduced cell quality. Preventing this abnormal ROS level is a challenging task. Hence, here we evaluated the effect of sodium selenite supplementation on the antioxidant potential, stemness capacity, and differentiation of rat-derived Bone Marrow MSCs (rBM-MSCs) and planned to check our hypothesis on the molecular pathways and networks linked to sodium selenite's antioxidant properties. METHODS: MTT assay was used to assess the rBM-MSCs cells' viability following sodium selenite supplementation (concentrations of: 0.001, 0.01, 0.1, 1, 10 µM). The expression level of OCT-4, NANOG, and SIRT1 was explored using qPCR. The adipocyte differentiation capacity of MSCs was checked after Sodium Selenite treatment. The DCFH-DA assay was used to determine intracellular ROS levels. Sodium selenite-related expression of HIF-1α, GPX, SOD, TrxR, p-AKT, Nrf2, and p38 markers was determined using western blot. Significant findings were investigated by the String tool to picture the probable molecular network. RESULTS: Media supplemented with 0.1 µM sodium selenite helped to preserve rBM-MSCs multipotency and keep their surface markers presentation; this also reduced the ROS level and improved the rBM-MSCs' antioxidant and stemness capacity. We observed enhanced viability and reduced senescence for rBM-MSCs. Moreover, sodium selenite helped in rBM-MSCs cytoprotection by regulating the expression of HIF-1 of AKT, Nrf2, SOD, GPX, and TrxR markers. CONCLUSIONS: We showed that sodium selenite could help protect MSCs during in-vitro manipulations, probably via the Nrf2 pathway.

A global systematic review and meta-analysis on correlation between biofilm producers and non-biofilm producers with antibiotic resistance in Uropathogenic Escherichiacoli.

Escherichia coli accounts for nearly 80% of community-acquired and 50% of hospital-acquired urinary tract infections (UTI). This study aimed to evaluate the correlation between biofilm producers and Non-biofilm producers with antibiotic resistance in Uropathogenic Escherichia coli (UPEC) isolated from patients with UTI globally. The search was conducted between 1st 2000 to 30th October 2021 in various databases (PubMed, Scopus, Web of sciences, and Google Scholar) with suitable MeSH terms, and text words. Then, after applying the appropriate inclusion and exclusion criteria on the studies for their selection, the data were analyzed by CMA software. Thirty-seven studies met the eligibility criteria to include. The pooled prevalence of ESBL and MDR isolates were reported 37.9%, and 65.8%, respectively. Biofilm formation varied between 13.3% and 99% all over the world. A total of 74.4% of all isolates were biofilm producers, out of which 28.6%, 35.2%, and 38.6% showed strong, moderate, and weak biofilm. The highest and lowest resistance was against Amoxicillin and Meropenem with the prevalence of 80.8%, and 13%, respectively. Fourteen out of 17(82.35%) studies reported a positive correlation between biofilm and antibiotic resistance. Findings showed high numbers of isolates were able to form biofilm, which is one of the factors of antibiotic resistance, and this has been confirmed by the positive significant correlation between biofilm formation and antibiotic resistance that has been reported by studies included. Therefore, due to the importance of biofilm in the etiology of UTI caused by UPEC, it should be prevented; consequently, bacterial resistance can be reduced and controlled.

Selectively targeting cancer stem cells: Current and novel therapeutic strategies and approaches in the effective eradication of cancer.

Cancer stem cells (CSCs) are a subgroup of cells in malignant cancers, which possess self-renewal capacity, tumor-initiating capability, and pluripotency, as well as being responsible for tumor maintenance, metastasis, relapse, and chemoresistance. The treatment modalities previously established for cancer included surgery, chemotherapy, and radiotherapy. The majority of tumor cells of non-CSCs could be eradicated using conventional chemotherapy and radiotherapy. Therefore, novel and promising therapeutic strategies that selectively target CSCs are of great importance. In this review, we described different therapeutic strategies such as immunotherapy, metabolism-based therapeutic strategies, and additional potential therapeutic approaches (targeting microRNAs [miRNAs], histone deacetylase, and DNA methyl transferase) against CSCs. Taken together, due to the inefficiency of anticancer single therapies, targeting CSCs through their metabolism and using immunotherapy and miRNAs besides classical chemo- and radiotherapy may exert better therapeutic effects.