Quercetin modulates expression of serum exosomal long noncoding RNA NEAT1 to regulate the miR-129-5p/BDNF axis and attenuate cognitive impairment in diabetic mice.

AIMS: Cognitive impairment poses a considerable health challenge in the context of type 2 diabetes mellitus (T2DM), emphasizing the need for effective interventions. This study delves into the therapeutic efficacy of quercetin, a natural flavonoid, in mitigating cognitive impairment induced by T2DM in murine models. MATERIALS AND METHODS: Serum exosome samples were obtained from both T2DM-related and healthy mice for transcriptome sequencing, enabling the identification of differentially expressed mRNAs and long noncoding RNAs (lncRNAs). Subsequent experiments were conducted to ascertain the binding affinity between mmu-miR-129-5p, NEAT1 and BDNF. The structural characteristics and dimensions of isolated exosomes were scrutinized, and the expression levels of exosome-associated proteins were quantified. Primary mouse hippocampal neurons were cultured for in vitro validation, assessing the expression of pertinent genes as well as neuronal vitality, proliferation, and apoptosis capabilities. For in vivo validation, a T2DM mouse model was established, and quercetin treatment was administered. Changes in various parameters, cognitive ability, and the expression of insulin-related proteins, along with pivotal signaling pathways, were monitored. KEY FINDINGS: Analysis of serum exosomes from T2DM mice revealed dysregulation of NEAT1, mmu-miR-129-5p, and BDNF. In vitro investigations demonstrated that NEAT1 upregulated BDNF expression by inhibiting mmu-miR-129-5p. Overexpression of mmu-miR-129-5p or silencing NEAT1 resulted in the downregulation of insulin-related protein expression, enhanced apoptosis, and suppressed neuronal proliferation. In vivo studies validated that quercetin treatment significantly ameliorated T2DM-related cognitive impairment in mice. SIGNIFICANCE: These findings suggest that quercetin holds promise in inhibiting hippocampal neuron apoptosis and improving T2DM-related cognitive impairment by modulating the NEAT1/miR-129-5p/BDNF pathway within serum exosomes.

Fat transplant: Amazing growth and regeneration of cells and rebirth with the miracle of fat cells.

BACKGROUNDS AND OBJECTIVE: During fat transplantation, adipose tissue is removed from the body and injected into different areas under the skin. The goal of this review article is to look into the efficacy and applicability of fat transplantation in regenerative medicine and rejuvenation, including Nanofat, Microfat, and Millifat. METHODS: As a search strategy and study selection, we searched the PubMed and Medline databases until 2023 using related keywords (e.g., Nanofat, Microfat and Millifat, Regenerative Medicine, and Rejuvenation). RESULTS: Autologous fat transplantation has no risk of an allergic reaction or rejection of the transplant by the individual. Autologous adipose tissue is considered an ideal filler for facial rejuvenation and is suggested as the most biocompatible and non-immunogenic skin filler. Adipose tissue transplant may have semi-permanent to permanent effects. According to recent reports, adipose tissues possess a high percentage of mature stem cells. The effect of regenerating adipose tissue and its intrinsic cells can be described as an obvious process. Variations in the sizes of adipose tissues can result in different results depending on the surgical site. Based on topographic assessment, graft fats are assigned depending on the anatomical locations and the size such as Millifat (2-2.5 mm), Microfat (1 mm), and Nanofat (500 µm or less). CONCLUSION: Some characteristics of fat tissue increase its effectiveness, such as increasing stem cells, growth factors, cytokines, and compounds effective in repair, regeneration, and rejuvenation.

Chitosan/Pectin Nanoparticles Encapsulated with Echinacea pallida: a Focus on Antibacterial and Antibiofilm Activity Against Multidrug-Resistant Staphylococcus aureus.

In recent years, the alarming spread of antibiotic resistance has posed a grave global threat to public health, resulting in millions of fatalities worldwide. Multidrug-resistant (MDR) microorganisms have emerged due to the broad spread of resistance and the sharing of resistance genes between various varieties of bacteria. A promising strategy for treating difficult-to-treat bacterial infections is the development of nanomaterial-based therapeutics that could circumvent existing pathways linked to acquire drug resistance. The objectives of this study were to prepare chitosan/pectin-encapsulated Echinacea pallida (E. pallida) extract and evaluate its efficacy against MDR isolates. E. pallida extract was encapsulated into chitosan (CS)/pectin (PN) nanoparticles (NPs) using the gelation technique in the present study. The synthesized NPs were analyzed using scanning electron microscopy (SEM), dynamic light scattering (DLS), transmission electron microscopes (TEM), and Fourier transform infrared (FT-IR) spectroscopy. Antibacterial and antibiofilm activity of the nanoparticles against S. aureus has been assessed and explored. In addition, the toxicity of synthetic NPs against HEK 93 cells was evaluated. The interactions between functional groups were confirmed by FT-IR spectroscopy. The CS/PN NPs were spherical with uniform surfaces, and their dimension ranged from 80 to 110 nm. The PDI of the E. pallida extract was 0.521, and its entrapment efficiency (EE%) was 84.35%. The synthesized CS/PN NPs exhibited antibacterial and antibiofilm activity against bacteria relevant to public health. In addition, the results demonstrated that the extract-containing NPs had no toxic impact on HEK-93 cells. The findings presented here should aid the development of novel plant extracts with enhanced stability and antibacterial activity, thereby reducing the need for antibiotics.

A thorough understanding of the role of lncRNA in prostate cancer pathogenesis; Current knowledge and future research directions.

In the entire world, prostate cancer (PCa) is one of the most common and deadly cancers. Treatment failure is still common among patients, despite PCa diagnosis and treatment improvements. Inadequate early diagnostic markers and the emergence of resistance to conventional therapeutic approaches, particularly androgen-deprivation therapy, are the causes of this. Long non-coding RNAs (lncRNAs), as an essential group of regulatory molecules, have been reported to be dysregulated through prostate tumorigenesis and hold great promise as diagnostic targets. Besides, lncRNAs regulate the malignant features of PCa cells, such as proliferation, invasion, metastasis, and drug resistance. These multifunctional RNA molecules interact with other molecular effectors like miRNAs and transcription factors to modulate various signaling pathways, including AR signaling. This study aimed to compile new knowledge regarding the role of lncRNA through prostate tumorigenesis in terms of their effects on the various malignant characteristics of PCa cells; in light of these characteristics and the significant potential of lncRNAs as diagnostic and therapeutic targets for PCa. AVAILABILITY OF DATA AND MATERIALS: Not applicable.