Immunometabolites in viral infections: Action mechanism and function.

The interplay between viral pathogens and host metabolism plays a pivotal role in determining the outcome of viral infections. Upon viral detection, the metabolic landscape of the host cell undergoes significant changes, shifting from oxidative respiration via the tricarboxylic acid (TCA) cycle to increased aerobic glycolysis. This metabolic shift is accompanied by elevated nutrient accessibility, which is vital for cell function, development, and proliferation. Furthermore, depositing metabolites derived from fatty acids, TCA intermediates, and amino acid catabolism accelerates the immunometabolic transition, facilitating pro-inflammatory and antimicrobial responses. Immunometabolites refer to small molecules involved in cellular metabolism regulating the immune response. These molecules include nutrients, such as glucose and amino acids, along with metabolic intermediates and signaling molecules adenosine, lactate, itaconate, succinate, kynurenine, and prostaglandins. Emerging evidence suggests that immunometabolites released by immune cells establish a complex interaction network within local niches, orchestrating and fine-tuning immune responses during viral diseases. However, our current understanding of the immense capacity of metabolites to convey essential cell signals from one cell to another or within cellular compartments remains incomplete. Unraveling these complexities would be crucial for harnessing the potential of immunometabolites in therapeutic interventions. In this review, we discuss specific immunometabolites and their mechanisms of action in viral infections, emphasizing recent findings and future directions in this rapidly evolving field.

Critical roles of long noncoding RNA H19 in cancer.

Long noncoding RNAs (lncRNAs) are a category of noncoding RNAs characterized by their length, often exceeding 200 nucleotides. There is a growing body of data that indicate the significant involvement of lncRNAs in a wide range of disorders, including cancer. lncRNA H19 was among the initial lncRNAs to be identified and is transcribed from the H19 gene. The H19 lncRNA exhibits significant upregulation in a diverse range of human malignancies, such as breast, colorectal, pancreatic, glioma, and gastric cancer. Moreover, the overexpression of H19 is frequently associated with a worse prognosis among individuals diagnosed with cancer. H19 has been shown to have a role in facilitating several cellular processes, including cell proliferation, invasion, migration, epithelial-mesenchymal transition, metastasis, and apoptosis. This article summarizes the aberrant upregulation of H19 in human malignancies, indicating promising avenues for future investigations on cancer diagnostics and therapeutic interventions.

A narrative review of the effects of dexamethasone on traumatic brain injury in clinical and animal studies: focusing on inflammation.

Traumatic brain injury (TBI) is a type of brain injury resulting from a sudden physical force to the head. TBI can range from mild, such as a concussion, to severe, which might result in long-term complications or even death. The initial impact or primary injury to the brain is followed by neuroinflammation, excitotoxicity, and oxidative stress, which are the hallmarks of the secondary injury phase, that can further damage the brain tissue. Dexamethasone (DXM) has neuroprotective effects. It reduces neuroinflammation, a critical factor in secondary injury-associated neuronal damage. DXM can also suppress the microglia activation and infiltrated macrophages, which are responsible for producing pro-inflammatory cytokines that contribute to neuroinflammation. Considering the outcomes of this research, some of the effects of DXM on TBI include: (1) DXM-loaded hydrogels reduce apoptosis, neuroinflammation, and lesion volume and improves neuronal cell survival and motor performance, (2) DXM treatment elevates the levels of Ndufs2, Gria3, MAOB, and Ndufv2 in the hippocampus following TBI, (3) DXM decreases the quantity of circulating endothelial progenitor cells, (4) DXM reduces the expression of IL1, (5) DXM suppresses the infiltration of RhoA + cells into primary lesions of TBI and (6) DXM treatment led to an increase in fractional anisotropy values and a decrease in apparent diffusion coefficient values, indicating improved white matter integrity. According to the study, the findings show that DXM treatment has neuroprotective effects in TBI. This indicates that DXM is a promising therapeutic approach to treating TBI.

Effects of L-ascorbic acid (C6H8O6: Vit-C) on collagen amino acids: DFT study.

Vitamin C plays a very important role in the repair of connective tissue, especially for sports whose training causes the most damage to this tissue. Therefore, many people believe that L-ascorbic acid (C6H8O6: vitamin C) reduces the recovery time between sports exercises. The most abundant form of structural protein in the body is collagen. Collagen is characterized by a high concentration of the three amino acids glycine (Gly), proline (Pro), and hydroxyproline (Hyp), which creates its characteristic triple helix structure. Therefore, in this study, the effect of vitamin C presence on the sequence, interaction, and orientation of amino acids for collagen formation is investigated using computational simulation. This study aimed to investigate the mechanism of action of vitamin C in terms of thermodynamics and structure of the reaction. The calculations are performed using density function theory (DFT) by the base set of B3LYP/6-311++G (p,d). The results show that the presence of vitamin C is effective in the formation of collagen protein for this interaction and the mechanism of amino acid sequence (Gly-Hyp-Pro) is better in the formation of collagen protein in the presence of vitamin C. The presence of Vit-C in the formation and direction of hydroxyproline (Hyp) causes its separation from the prolyl 5-hydroxylase enzyme. In the absence of vitamin C, the reaction stops at this stage and proline cannot be converted into hydroxyproline. The computational data shows vitamin C prevents unwanted interactions and directs amino acid reactions to repair connective tissue (collagen). Therefore, vitamin C acts as a cofactor in the Prolyl 5-Hydroxylase enzyme and causes it to convert proline to hydroxyl.