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The complex formation of uracil and cytosine with glycyl-L-glutamic acid (β-endorphin 30-31), γ-L-glutamyl-L-cysteinyl-glycine (glutathione reduced), α-L-alanyl-L-tyrosine, and α-L-alanyl-α-L-alanine in a buffered saline has been studied using dissolution calorimetry. The values of the reaction constant, the change in Gibbs energy, enthalpy, and entropy were obtained. It is shown that the ratio of the enthalpy and entropy factors depends on the charge of the peptide ion, and the number of H-bond acceptors in the peptide structure. The contributions of interaction between charged groups and polar fragments, hydrogen bonding, and stacking interaction are discussed, taking into account the effect of solvent reorganization around the reactant molecules.

Ulcerative colitis (UC), a subtype of inflammatory bowel disease, manifests with symptoms such as abdominal pain, diarrhea, and mucopurulent, bloody stools. The pathogenesis of UC is not fully understood. At present, the incidence of UC has increased significantly around the world. Conventional therapeutic arsenals are relatively limited, with often poor efficacy and many adverse effects. In contrast, traditional Chinese medicine (TCM) holds promise due to their notable effectiveness, reduced recurrence rates, and minimal side effects. In recent years, significant progress has been made in the basic research on TCM for UC treatment. It has been found that the inhibition of ferroptosis through the intervention of TCM can significantly promote intestinal mucosal healing and reverse UC. The mechanism of action involves multiple targets and pathways.

Csilla Enikő SzaboDepartment of Pediatrics I, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca, RomaniaEmail szabocsillaeniko@gmail.comIntroduction: Type 1 diabetes (T1DM) is a chronic autoimmune or idiopathic condition, featuring complex and unique interactions between proteins and enzyme systems. The purpose of the present study is to investigate the role of AdipoQ +276G>T, TNF-α-308G>A, GSTT1/GSTM1 polymorphic variants in the development of T1DM.Materials and methods: The study is designed as a cross-sectional study, involving 72 diabetic cases and 90 controls. Genotyping was carried out according to specific protocols for the above-mentioned polymorphic variants.Results: The G allele of AdipoQ was associated with the development of type 1 diabetes (OR 0.577, CI95% 0.336-0.802, p=0.001), similar to the GG and GA genotypes (OR 0.405, CI95% 0.156-0.654, p=0.001 and OR 0.623, CI95% 0.401-0.855, p=0.004). The G allele of TNF-α was marginally associated with the development of type 1 diabetes (OR 0.789, CI95% 0.579-0.956, p=0.005). The presence of the T1 genotype was a strong predictor for type 1 diabetes (OR 3.4, CI95% 1.433-6.243, p<0.001).Conclusion: The results of our study suggest that G alleles of AdipoQ and TNFα act as a protective factor in T1DM, while the T1 allele for GST could be considered a risk factor for the development of Type 1 diabetes in our study group.

Ischemia-reperfusion (I/R) injury is a critical contributor to adverse outcomes following stroke. During I/R injury, excessive production of reactive oxygen species (ROS) leads to various forms of neuronal cell death. Moreover, the blood-brain barrier (BBB) significantly hinders the delivery and efficacy of many neuroprotective agents. Given selenium’s crucial role in mitigating brain ischemia, we developed a selenium-based nanozyme encapsulated in glutathione (GSH)-conjugated liposomes to overcome these challenges. Specifically, we encapsulated selenium-doped carbon dot nanozymes (Se-CDs) within GSH-conjugated liposomes (Se-CD@LP-GSH) to enable targeted delivery and enhance therapeutic efficacy in ischemic stroke. This system demonstrates effective ROS scavenging capabilities both in vitro and in vivo, while also enhancing the biocompatibility of Se-CDs and their ability to cross the BBB. In the tMCAo model, Se-CD@LP-GSH reduces the neuronal death and infarct area following cerebral I/R injury, and promotes improvements in spatial learning ability and sensorimotor function. Mechanistically, Se-CD@LP-GSH promoted the upregulation of GPX4, an essential selenoprotein, thereby preserving mitochondrial function and suppressing ROS generation Consequently, the reduced ROS levels inhibit NLRP3/GSDMD-mediated neuronal pyroptosis during cerebral I/R injury. By improving the brain-targeting ability of Se-CDs via GSH-functionalized liposomal delivery, our work elucidates their neuroprotective efficacy and mechanistic basis, thus providing a translationally relevant strategy for ischemic stroke therapy.

Suicidal erythrocyte death or eryptosis contributes to or even accounts for anemia in a wide variety of clinical conditions, such as iron deficiency, dehydration, hyperphosphatemia, vitamin D excess, chronic kidney disease (CKD), hemolytic-uremic syndrome, diabetes, hepatic failure, malignancy, arteriitis, sepsis, fever, malaria, sickle-cell disease, beta-thalassemia, Hb-C and G6PD-deficiency, Wilsons disease, as well as advanced age. Moreover, eryptosis is triggered by a myriad of xenobiotics and endogenous substances including cytotoxic drugs and uremic toxins. Eryptosis is characterized by cell membrane scrambling with phosphatidylserine exposure to the erythrocyte surface. Triggers of eryptosis include oxidative stress, hyperosmotic shock, and energy depletion. Signalling involved in the regulation of eryptosis includes Ca 2+ entry, ceramide, caspases, calpain, p38 kinase, protein kinase C, Janus-activated kinase 3, casein kinase 1α, cyclin-dependent kinase 4, AMP-activated kinase, p21-activated kinase 2, cGMP-dependent protein kinase, mitogen- and stress-activated kinase MSK1/2, and ill-defined tyrosine kinases. Inhibitors of eryptosis may prevent anaemia in clinical conditions associated with enhanced eryptosis and stimulators of eryptosis may favourably influence the clinical course of malaria. Additional experimentation is required to uncover further clinical conditions with enhanced eryptosis, as well as further signalling pathways, further stimulators, and further inhibitors of eryptosis. Thus, a detailed description of the methods employed in the analysis of eryptosis may help those, who enter this exciting research area. The present synopsis describes the experimental procedures required for the analysis of phosphatidylserine exposure at the cell surface with annexin-V, cell volume with forward scatter, cytosolic Ca 2+ activity ([Ca 2+ ] i ) with Fluo3, oxidative stress with 2′,7′-dichlorodihydrofuorescein diacetate (DCFDA), glutathione (GSH) with mercury orange 1(4-chloromercuryphenyl-azo-2-naphthol), lipid peroxidation with BODIPY 581/591 C11 fluorescence, and ceramide abundance with specific antibodies. The contribution of kinases and caspases is defined with the use of the respective inhibitors. It is hoped that the present detailed description of materials and methods required for the analysis of eryptosis encourages further scientists to enter this highly relevant research area.

This review summarizes the current knowledge on the contribution of metals to the development of oxidative stress in fish. Metals are important inducers of oxidative stress in aquatic organisms, promoting formation of reactive oxygen species through two mechanisms. Redox active metals generate reactive oxygen species through redox cycling, while metals without redox potential impair antioxidant defences, especially that of thiol-containing antioxidants and enzymes. Elevated levels of reactive oxygen species lead to oxidative damage including lipid peroxidation, protein and DNA oxidation, and enzyme inactivation. Antioxidant defences include the enzyme system and low molecular weight antioxidants. Metal-binding proteins, such as ferritin, ceruloplasmin and metallothioneins, have special functions in the detoxification of toxic metals and also play a role in the metabolism and homeostasis of essential metals. Recent studies of metallothioneins as biomarkers indicate that quantitative analysis of mRNA expression of metallothionein genes can be appropriate in cases with elevated levels of metals and no evidence of oxidative damage in fish tissue. Components of the antioxidant defence are used as biochemical markers of oxidative stress. These markers may be manifested differently in the field than in results found in laboratory studies. A complex approach should be taken in field studies of metal contamination of the aquatic environment.

Background The aim of this study is to explore the effects of TGF-β1 on autophagy and apoptosis induced by exogenous hydrogen peroxide (H 2 O 2 ) in annulus fibrosus (AF) cells and possible signal pathways involved in this process. Methods AF cells were isolated from rat lumbar discs and subjected to different concentrations of exogenous H 2 O 2 (50, 100, 200 μmol/L) for different time periods (0.5, 1, 2, and 4 h). Cell viability was determined by CCK-8 assay, and the levels of autophagy and apoptosis were evaluated by Western blotting and caspase 3, 8, 9 activity assay. By administration with different concentrations of TGF-β1 (5, 10, 20 ng/mL), the effects of TGF-β1 on autophagy and apoptosis induced by H 2 O 2 were observed, and the possible signaling pathways were also investigated by using various apoptosis inhibitors or an autophagy inhibitor Bafilomycin A (Baf A) in AF cells. Results H 2 O 2 significantly impaired cell viability in a dose- and time-dependent manner. H 2 O 2 also induced a sudden and the highest level of autophagy at 1 h, and gradually increased apoptosis through ERK pathway. The mitochondrial pathway was involved in H 2 O 2 -induced apoptosis in AF cells. TGF-β1 reduced the expression of p-ERK and downregulated the expressions of Beclin-1, LC3 II/I, and mitochondrial-related apoptotic proteins (Bax/Bcl-2, caspase-9). Meanwhile, TGF-β1 downregulated the level of intracellular H 2 O 2 through upregulating the expression level of glutathione peroxidase-1 (GPx-1). Conclusions TGF-β1 reduced autophagy and apoptosis induced by exogenous H 2 O 2 through downregulating the expression of ERK in AF cells. TGF-β1 could downregulate the level of ERK and intracellular H 2 O 2 by upregulating GPx-1.

Fetal growth restriction (FGR) is a critical condition linked to various etiologies, increasing the risk of fetal complications and mortality. The study investigated the expression levels of angiogenic factors and inflammatory cytokines in peripheral blood mononuclear cells (PBMCs) from normal pregnancies and those affected by FGR. It also examined their association with maternal oxidative stress markers. messenger RNA (mRNA) expression was analyzed using real-time PCR in PBMCs, while oxidative stress (OS) markers were assessed via spectrophotometric assays and ELISA in the maternal blood of 75 cases of FGR and 75 healthy pregnancies. FGR cases exhibited disrupted angiogenic signaling, elevated oxidative and inflammatory responses, indicating a pathological interplay among these systems. Results showed significantly reduced vascular endothelial growth factor (VEGF) along with increased soluble FMS-like tyrosine kinase-1 (sFlt-1) and nuclear factor-kappa B (NF-κB) expression in FGR cases. A notable inverse relationship of sFlt-1 existed with both VEGF and placental growth factor (PlGF), while sFlt-1 positively correlated with OS markers like Malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG). Additionally, NF-κB expression was strongly linked to MDA, tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6). This understanding highlights the potential for targeted interventions, such as antioxidant therapies or strategies to modulate inflammatory pathways, to improve outcomes in FGR. Le retard de croissance foetale (RCF) est une pathologie grave liée à diverses étiologies, augmentant le risque de complications et de mortalité foetales. L'étude a examiné les niveaux d'expression des facteurs angiogéniques et des cytokines inflammatoires dans les cellules mononucléaires du sang périphérique (CMSP) issues de grossesses normales et de grossesses atteintes de RCF. Elle a également examiné leur association avec les marqueurs du stress oxydatif maternel. L'expression de l'ARN messager (ARNm) a été analysée par PCR en temps réel dans les CMSP, tandis que les marqueurs du stress oxydatif (SO) ont été évalués par spectrophotométrie et ELISA dans le sang maternel de 75 cas de RCF et de 75 grossesses saines. Les cas de RCF présentaient une perturbation de la signalisation angiogénique et des réponses oxydatives et inflammatoires élevées, indiquant une interaction pathologique entre ces systèmes. Les résultats ont montré une réduction significative du facteur de croissance de l'endothélium vasculaire (VEGF) ainsi qu'une augmentation de l'expression de la tyrosine kinase-1 soluble de type FMS (sFlt-1) et du facteur nucléaire kappa B (NF-κB) dans les cas de RCIU. Une relation inverse notable entre le sFlt-1 existait à la fois avec le VEGF et le facteur de croissance placentaire (PlGF), tandis que le sFlt-1 était positivement corrélé à des marqueurs de survie globale comme le malondialdéhyde (MDA) et la 8-hydroxy-2'-désoxyguanosine (8-OHdG). De plus, l'expression de NF-κB était fortement liée au MDA, au facteur de nécrose tumorale alpha (TNF-α) et à l'interleukine-6 (IL-6). Cette compréhension souligne le potentiel d'interventions ciblées, telles que les thérapies antioxydantes ou les stratégies de modulation des voies inflammatoires, pour améliorer les résultats dans le RCIU.

Background: India is an opulent provenance of medicinal plants used therapeutically to treat various disorders including depression. The present study was designed to scrutinize the antidepressant activity of Sharbat Ahmad Shahi (SAS) in swiss albino mice. Methods: The antidepressant activity was studied in swiss albino mice using two behavioural paradigms i.e forced swimming test (FST) and tail suspension test (TST). Sharbat ahmad shahi (6ml/kg), hydroalcoholic and aqueous extract of the ingredients of SAS (0.34mg/kg and 0.64mg/kg) respectively, was used as test drugs, Flauxatine (20mg/kg) was used as a standard drug and vehicle was distilled water (10ml/kg), orally for 14 days. Results: SAS, hydroalcoholic and aqueous extract of the ingredients of SAS produced a significant antidepressant effect in both FST and TST as they reduced the immobility time. A significant reduction in TBARS and an increased in GSH levels were observed in brains of mice exposed to FST and TST. Conclusion: The present study propound that SAS, hydroalcoholic and aqueous extract of the ingredients of SAS possess an antidepressant like effect.