Anti-inflammatory Functions Research Articles

Enhancement of Antioxidative and Anti-Inflammatory Activities of Corn Silk Polysaccharides After Selenium Modification.

This study aimed to study the effect of selenium modification on the bioactivity of corn silk polysaccharides, particularly its antioxidant and anti-inflammatory functions. HNO3-NaSeO3 was used to selenize degraded corn silk polysaccharides (DCSP). The structure and physicochemical properties of DCSP and selenized corn silk polysaccharides (Se-DCSP) were characterized by inductively coupled plasma emission spectroscopy, Fourier-transform infrared, ultraviolet-visible spectroscopy, nuclear magnetic resonance, nanometer, scanning electron microscopy, and thermogravimetric analysis. The protective effects of DCSP and Se-DCSP on HK-2 cells damaged by nano-calcium oxalate and the changes of inflammatory factors were detected by laser confocal microscopy, flow cytometry, and fluorescence microscopy. The selenium content of DCSP and Se-DCSP were 19.5 and 1226.7μg/g, respectively. Compared with DCSP, Se-DCSP showed significantly improved biological activity, including the scavenging ability of various free radicals (increased by about 2-3 times), the intracellular reactive oxygen content (decreased by about 1.5 times), and the mitochondrial membrane potential (decreased by about 2.5 times). Moreover, cell viability and morphological recovery ability were improved. Compared with DCSP, Se-DCSP significantly down-regulated HK-2 cell inflammatory factors MCP-1 (about 1.7 times), NLRP3, and NO (about 1.5 times). The antioxidant activity and the ability to down-regulate the expression of inflammatory factors of Se-DCSP were significantly enhanced compared with DCSP, and Se-DCSP can better protect HK-2 cells from oxidative damage, indicating that Se-DCSP has a stronger potential ability to inhibit kidney stone formation.

Vitamin D Deficiency as a Factor Associated with Cognitive Impairment in Patients with Type 2 Diabetes Mellitus

Objective: Vitamin D as an essential nutrient is increasingly being studied and reported to have roles in diabetes and cognitive function through its antioxidant, anti-inflammatory, and neuroprotective functions. This study aimed to investigate vitamin D deficiency as a factor associated with cognitive impairment in Type 2 Diabetes Mellitus patients. Materials and Methods: This case-control study was conducted at the diabetic center and neurology outpatient clinic at Prof. Dr. I.G.N.G Ngoerah Hospital in Denpasar, Indonesia between September and December 2022. Cases had a score of < 26 on the Montreal Cognitive Assessment questionnaire (Indonesian version) controls had a score ≥26. Vitamin D levels were assessed using serum 25-hydroxyvitamin D levels. The cut-off for vitamin D deficiency was obtained through the receiver operating curve characteristic. Results: In total 31 cases and 31 controls were included. The cut-off for vitamin D deficiency was <24.6 ng/ml. Patients with T2DM and vitamin D deficiency had an increased association with cognitive impairment (OR 3.8; 95% CI [1.1 to 13.4]) compared to patients without vitamin D deficiency. Other independent factors associated with cognitive impairment in T2DM were low education levels (OR 5.4; 95% CI [1.3 to 22.2]) and diabetes duration of more than 5 years (OR 4.1; 95% CI [1.1 to 14.4]). Conclusion: Vitamin D deficiency is one of the factors associated with cognitive impairment in T2DM patients.

Wheat peptide alleviates DSS-induced colitis by activating the Keap1-Nrf2 signaling pathway and maintaining the integrity of the gut barrier.

Inflammatory bowel disease (IBD) is difficult to cure, and formulating a dietary plan is an effective means to prevent and treat this disease. Wheat peptide contains a variety of bioactive peptides with anti-inflammatory and antioxidant functions. The results of this study showed that preventive supplementation with wheat peptide (WP) can significantly alleviate the symptoms of dextran sulfate sodium (DSS)-induced colitis in mice. WP can increase body weight, alleviate colon shortening, and reduce disease activity index (DAI) scores. In addition, WP improved intestinal microbial disorders in mice with colitis. Based on LC-MS, a total of 313 peptides were identified in WP, 4 of which were predicted to be bioactive peptides. The regulatory effects of WP and four bioactive peptides on the Keap1-Nrf2 signaling pathway were verified in Caco-2 cells. In conclusion, this study demonstrated that WP alleviates DSS-induced colitis by helping maintain gut barrier integrity and targeting the Keap1-Nrf2 axis; these results provided a rationale for adding WP to dietary strategies to prevent IBD.

Этапы становления микробиоты желудочно‑кишечного тракта и роль пробиотиков в коррекции кишечной колики у детей первых месяцев жизни

The physiologic microbiota of the GI tract performs many important functions that coordinate various processes, such as trophic, protective, anti-inflammatory, and immune functions. Transient enzymatic immaturity and immaturity of neuroendocrine regulation of GI motility in newborns creates prerequisites for gastrointestinal dysfunctions that increase with imbalance of the intestinal microbiome, represented by intestinal colic, increased gas formation, gastroesophageal and duodenogastric regurgitation. The objective of the study was to analyze the effectiveness of Probielle® Baby probiotic in the correction of intestinal colic and associated functional GI disorders in children of the first months of life. Patients and methods. The study included 88 children of the first 3 months of life, divided into 3 groups – two main groups receiving Probielle® Baby probiotic and a control group, in which only symptomatic therapy of intestinal colic was performed. The parameters of efficacy assessment included: daily monitoring of crying duration, assessment of stool frequency and consistency, severity of flatulence, frequency and nature of regurgitation, dynamics of intestinal microbiota composition. In order to determine the severity of the intestinal colic syndrome, a score was used. Results. In association with Probielle® Baby, the regression of intestinal colic was more pronounced, and fewer episodes of flatulence and proximal gastroesophageal regurgitation were also noted. Thus, the use of probiotics will significantly increase the effectiveness of complex therapy of gastrointestinal dysfunctions in newborns and children of the first months of life. Key words: microbiota, newborns, immunity, intestinal colic, Probielle Baby

The Role of Traditional Chinese Medicines in the Treatment of Osteoporosis.

Osteoporosis (OP) represents a substantial public health issue and is associated with increasing rates of morbidity and mortality. It is characterized by reduced bone mineral density, deterioration of bone tissue quality, disruption of the microarchitecture of bones, and compromised bone strength. These changes may be attributed to the following factors: intercellular communication between osteoblasts and osteoclasts; imbalanced bone remodeling; imbalances between osteogenesis and adipogenesis; imbalances in hormonal regulation; angiogenesis; chronic inflammation; oxidative stress; and intestinal microbiota imbalances. Treating a single aspect of the disease is insufficient to address its multifaceted nature. In recent decades, traditional Chinese medicine (TCM) has shown great potential in the treatment of OP, and the therapeutic effects of Chinese patent drugs and Chinese medicinal herbs have been scientifically proven. TCMs, which contain multiple components, can target the diverse pathogeneses of OP through a multitargeted approach. Herbs such as XLGB, JTG, GSB, Yinyanghuo, Gusuibu, Buguzhi, and Nvzhenzi are among the TCMs that can be used to treat OP and have demonstrated promising effects in this context. They exert their therapeutic effects by targeting various pathways involved in bone metabolism. These TCMs balance the activity of osteoblasts (bone-forming cells) and osteoclasts (bone-resorbing cells), and they exhibit anti-inflammatory, immunomodulatory, anti-oxidative, and estrogen-like functions. These multifaceted mechanisms underlie the efficacy of these herbs in the management and treatment of OP. Herein, we examine the efficacy of various Chinese herbs and Chinese patent drugs in treating OP by reviewing previous clinical trials and basic experiments, and we examine the potential mechanism of these therapies to provide evidence regarding the use of TCM for treating OP.

Therapeutic potential of elafin in airway inflammatory disease

Elafin, which is derived from trappin-2 or pre-elafin by proteolysis, is an endogenous serine protease inhibitor with a low molecular weight. Its inhibitory activity is dependent on anchoring to the extracellular matrix by forming covalent bonds with its distinctive N-terminal domain via tissue transglutaminases. In addition to inhibiting proteases, it also exhibits anti-inflammatory, antibiotic, antifungal, antiviral and immunomodulatory functions. Elafin plays an important role in inflammatory disease and is a promising candidate for the anti-inflammatory treatment of respiratory diseases. This review will discuss the therapeutic potential of elafin in airway inflammation and provide evidence and suggestions for the future treatment of airway inflammatory diseases. In addition, the therapeutic potential of elafin in lung cancer is also discussed.

Effects of yeast peptides on the growth, antioxidant and anti-inflammatory capacities, immune function, and diarrhea status of suckling calves.

Yeast peptides, which are small-molecule active peptides extracted from yeast proteins, are known for their antibacterial, antioxidant, and anti-inflammatory properties. However, the effects of yeast peptide on suckling calves remain unclear. In this study, the effects of yeast peptide supplementation on the growth, diarrhea incidence, and immune function of calves during the suckling period were determined. Thirty newborn calves were randomly divided into two groups: the control group (CON) and the treatment group (AP), which received fresh pasteurized milk supplemented with yeast peptides (5 g/day). The experiment lasted for 49 days (7-56 days of age). The dry matter intake, body weight, diarrhea status, immune function, antioxidant capacity, and anti-inflammatory activity of the calves were analyzed. The AP group had higher dry matter intake, daily weight gain, and feed efficiency than the CON group (P < 0.05). Moreover, the duration and frequency of diarrhea were significantly lower in the AP group than in the CON group (P < 0.05). Furthermore, the immune, antioxidant, and anti-inflammatory capabilities of the AP group were significantly higher than those of the CON group (P < 0.05). These findings provide valuable insights for the improvement of early health management during calf rearing.

Astaxanthin targets IL-6 and alleviates the LPS-induced adverse inflammatory response of macrophages.

Numerous natural compounds are recognized for their anti-inflammatory properties attributed to antioxidant effects and the modulation of key inflammatory factors. Among them, astaxanthin (AST), a potent carotenoid antioxidant, remains relatively underexplored regarding its anti-inflammatory mechanisms and specific molecular targets. In this study, human monocytic leukemia cell-derived macrophages (THP-1) were selected as experimental cells, and lipopolysaccharides (LPS) served as inflammatory stimuli. Upon LPS treatment, the oxidative stress was significantly increased, accompanied by remarkable cellular damage. Moreover, LPSs escalated the expression of inflammation-related molecules. Our results demonstrate that AST intervention could effectively alleviate LPS-induced oxidative stress, facilitate cellular repair, and significantly attenuate inflammation. Further exploration of the anti-inflammatory mechanism revealed AST could substantially inhibit NF-κB translocation and activation, and mitigate inflammatory factor production by hindering NF-κB through the antioxidant mechanism. We further confirmed that AST exhibited protective effects against cell damage and reduced the injury from inflammatory cytokines by activating p53 and inhibiting STAT3. In addition, utilizing network pharmacology and in silico calculations based on molecular docking, molecular dynamics simulation, we identified interleukin-6 (IL-6) as a prominent core target of AST anti-inflammation, which was further validated by the RNA interference experiment. This IL-6 binding capacity actually enabled AST to curb the positive feedback loop of inflammatory factors, averting the onset of possible inflammatory storms. Therefore, this study offers a new possibility for the application and development of astaxanthin as a popular dietary supplement of anti-inflammatory or immunomodulatory function.

Riboflavin ameliorates intestinal inflammation via immune modulation and alterations of gut microbiota homeostasis in DSS-colitis C57BL/6 mice.

While there have been advancements in understanding the direct and indirect impact of riboflavin (B2) on intestinal inflammation, the precise mechanisms are still unknown. This study focuses on evaluating the effects of riboflavin (B2) supplementation on a colitis mouse model induced with 3% dextran sodium sulphate (DSS). We administered three different doses of oral B2 (VB2L, VB2M, and VB2H) and assessed its impact on various physiological and biochemical parameters associated with colitis. Mice given any of the three doses exhibited relative improvement in the symptoms and intestinal damage. This was evidenced by the inhibition of the pro-inflammatory cytokines TNF-α, IL-1β, and CALP, along with an increase in the anti-inflammatory cytokine IL-10. B2 supplementation also led to a restoration of oxidative homeostasis, as indicated by a decrease in myeloperoxidase (MPO) and malondialdehyde (MDA) levels and an increase in reduced glutathione (GSH) and catalase (CAT) activities. B2 intervention showed positive effects on intestinal barrier function, confirmed by increased expression of tight junction proteins (occludin and ZO-1). B2 was linked to an elevated relative abundance of Actinobacteriota, Desulfobacterota, and Verrucomicrobiota. Notably, Verrucomicrobiota showed a significant increase in the VB2H group, reaching 15.03% relative abundance. Akkermansia exhibited a negative correlation with colitis and might be linked to anti-inflammatory function. Additionally, a remarkable increase in n-butyric acid, i-butyric acid, and i-valeric acid was reported in the VB2H group. The ameliorating role of B2 in gut inflammation can be attributed to immune system modulation as well as alterations in the gut microbiota composition, along with elevated levels of fecal SCFAs.

Effect of glucocorticoid blockade on inflammatory responses to acute sleep fragmentation in male mice.

The association between sleep and the immune-endocrine system is well recognized, but the nature of that relationship is not well understood. Sleep fragmentation induces a pro-inflammatory response in peripheral tissues and brain, but it also activates the hypothalamic-pituitary-adrenal (HPA) axis, releasing glucocorticoids (GCs) (cortisol in humans and corticosterone in mice). It is unclear whether this rapid release of glucocorticoids acts to potentiate or dampen the inflammatory response in the short term. The purpose of this study was to determine whether blocking or suppressing glucocorticoid activity will affect the inflammatory response from acute sleep fragmentation (ASF). Male C57BL/6J mice were injected i.p. with either 0.9% NaCl (vehicle 1), metyrapone (a glucocorticoid synthesis inhibitor, dissolved in vehicle 1), 2% ethanol in polyethylene glycol (vehicle 2), or mifepristone (a glucocorticoid receptor antagonist, dissolved in vehicle 2) 10 min before the start of ASF or no sleep fragmentation (NSF). After 24 h, samples were collected from brain (prefrontal cortex, hypothalamus, hippocampus) and periphery (liver, spleen, heart, and epididymal white adipose tissue (EWAT)). Proinflammatory gene expression (TNF-α and IL-1β) was measured, followed by gene expression analysis. Metyrapone treatment affected pro-inflammatory cytokine gene expression during ASF in some peripheral tissues, but not in the brain. More specifically, metyrapone treatment suppressed IL-1β expression in EWAT during ASF, which implies a pro-inflammatory effect of GCs. However, in cardiac tissue, metyrapone treatment increased TNF-α expression in ASF mice, suggesting an anti-inflammatory effect of GCs. Mifepristone treatment yielded more significant results than metyrapone, reducing TNF-α expression in liver (only NSF mice) and cardiac tissue during ASF, indicating a pro-inflammatory role. Conversely, in the spleen of ASF-mice, mifepristone increased pro-inflammatory cytokines (TNF-α and IL-1β), demonstrating an anti-inflammatory role. Furthermore, irrespective of sleep fragmentation, mifepristone increased pro-inflammatory cytokine gene expression in heart (IL-1β), pre-frontal cortex (IL-1β), and hypothalamus (IL-1β). The results provide mixed evidence for pro- and anti-inflammatory functions of corticosterone to regulate inflammatory responses to acute sleep loss.

Interferon-tau protects bovine endometrial epithelial cells against inflammatory injury by regulating the PI3K/AKT/β-catenin/FoxO1 signaling axis

Endometritis is one of the most common causes of infertility in dairy cows, and is histopathologically characterized by inflammation and damage of endometrial epithelium. Interferon-tau (IFN-τ) is a novel type I interferon secreted by ruminant trophoblast cells with low cytotoxicity even at high doses. Previous studies suggested that IFN-τ plays an important role in inflammation. However, the mechanisms whereby IFN-τ may modulate the inflammatory responses in the bovine endometrium are unknown. In the present study, primary bovine endometrial epithelial cells (BEEC) isolated from fresh and healthy uterine horns were used for in vitro studies. The integrity of BEEC was assessed by immunofluorescence staining for cytokeratin 18 (CK-18, a known epithelial marker). For the experiments, BEEC were stimulated with different concentrations of lipopolysaccharide (LPS; 0-20 µg/mL) for different times (0-24 h). Cell viability and apoptosis were assessed via CCK-8 and flow cytometry. In a preliminary study, we observed that compared with the control group without LPS, 10 µg/mL of LPS stimulation for 24 h induced apoptosis. In a subsequent study, 20 or 40 ng/mL of IFN-τ alleviated LPS-induced apoptosis. Relative to the LPS group, western blotting further revealed that IFN-τ inhibited the protein abundance of TLR4 and phosphorylated (p-) p65 (p-p65) and Bax/Bcl-2 ratio, suggesting that IFN-τ can protect BEEC against inflammatory injury. Furthermore, the protein abundance of p-phosphoinositide 3-kinase (p-PI3K), p-protein kinase B (p-AKT), p-glycogen synthase kinase-3β (p-GSK3β), β-catenin, and p-forkhead box O1 (p-FoxO1) was lower in the LPS group, whereas IFN-τ upregulated their abundance. The use of LY294002, a specific inhibitor of PI3K/AKT, attenuated the upregulation of p-PI3K, p-AKT p-GSK3β, β-catenin, and p-FoxO1 induced by IFN-τ, and also blocked the downregulation of TLR4, p-p65, and Bax/Bcl-2 ratio. This suggested that the inhibition of TLR4 signaling by IFN-τ was mediated by the PI3K/AKT pathway. Furthermore, compared with the LPS group, the β-catenin agonist SB216763 led to greater p-FoxO1 and lower p-p65 and cell apoptosis. In contrast, knockdown of β-catenin using small interfering RNA had the opposite effects. To explore the role of FoxO1 on the inhibition of TLR4 by IFN-τ, we employed LY294002 to inhibit the PI3K/AKT while FoxO1 was knocked down. Results revealed that the knockdown of FoxO1 blocked the upregulation of TLR4 and p-p65 induced by LY294002, and enhanced the inhibition of IFN-τ on TLR4, p-p65, and cell apoptosis. Overall, these findings confirmed that IFN-τ can protect endometrial epithelial cells against inflammatory injury via suppressing TLR4 activation through the regulation of the PI3K/AKT/β-catenin/FoxO1 axis. These represent new insights into the molecular mechanisms underlying the anti-inflammatory function of IFN-τ in BEEC, and also provide a theoretical basis for further studies on the in vivo application of IFN-τ to help prevent negative effects of endometritis.

Potentials of omega-3 fatty acids as therapeutic drugs and its obstacles in the pathway: A critical review

Context: Eicosapentaenoic acid, docosahexaenoic acid, and docosapentaenoic acid are the significant members of the ω-3 fatty acid group. Their beneficial pharmacological effects open new paths for therapeutics. Aims: To provide an updated overview of the source, chemical features, pharmacological effects, dosage forms, and patents of omega-3 fatty acids and analyze the limitations in visualizing them as an active drug for treatment. Methods: PubMed, Science Direct, Google Scholar, Springer Link, Google Patent, and Espacenet were used for the systematic search for articles from 2011–2023. Specific keywords were used for the search. For the screening process, articles related to the topic with full text in English were chosen. Two independent researchers analyzed, extracted, and summarized relevant data in Excel for data presentation. Results: 196 references were chosen for this review. In summary, lipid mediators from omega-3 fatty acids were found to exert anti-inflammatory functions, modulate signal transactions, regulate gene expression, and work as anti-microbial agents. These functions positively impact the cardiovascular, immune, metabolic, nerve, and optic systems. Despite abundant benefits, most products related to n-3 fatty acids were concentrated on utilizing as adjuvants and supplements. The source-related issues, complex extraction methods, oxidative instability, cost, side effects of formulations, complicated patent processes, and lenient regulation for supplements have been viewed as the reasons. Conclusions: Omega-3 fatty acids are a safe choice as a therapeutic drug for elderly patients, pregnant women, and children with disorders. Microbial production, low-energy formulation, and the use of natural emulsifiers can resolve the obstacles in this pathway.

SIRT1 inhibitors within Qing-Luo-Yin alleviated white adipose tissues-mediated inflammation in antigen-induced arthritis mice.

White adipose tissues (WAT) release large amounts of inflammatory mediators, which are responsible for the pathology of rheumatoid arthritis (RA). The current study investigated the involvement of WAT in the treatments of antigen-induced arthritis (AIA) mice with the herbal formula Qing-Luo-Yin (QLY). Cytokines and biochemical/metabolic indicators were determined by ELISA and colorimetry methods, respectively. Monocytes were analyzed by flow cytometry. Tissues were subjected to PCR, western-blot and histological analyses. Pre-adipocytes were cultured in the different mouse serum from the in vivo experiment, and some of them were treated by certain compounds or/and lipopolysaccharide. Afterwards, the catalytic activity and thermostability of SIRT1 were tested. Gene/protein expression and cytokine production were investigated too. NAMPT and SIRT1 were silenced in some cells by siRNA. AIA mice suffered from inflammatory adipokines-mediated metabolism and immune disorders. Besides joint protective effects, QLY therapies favored adipocyte differentiation and suppressed inflammatory adipokines release. The up-regulation of fatty acid oxidation and inflammatory monocyte polarization was therefore inhibited in peripheral tissues. PPARγ expression was generally promoted by QLY. Whereas, SIRT1 activity was always impaired, indicated by the declined NAD+ levels and the increased ace-p65 expression. QLY effectively inhibited eNAMPT release in AIA mouse serum-cultured pre-adipocytes. This effect was antagonized by resveratrol (a SIRT1 agonist) and overshadowed by NAMPT silencing. QLY-related compounds berberine, dioscin and sophocarpine showed high binding affinities to SIRT1, stabilized this protein, and inhibited its deacetylation activity in vitro. Their effects on ace-p65 expression were weakened when SIRT1 was silenced. SIRT1 inhibitors in QLY reduced eNAMPT production and up-regulated PPARγ in AIA mice, leading to inflammation remission. These clues show that except for the well-known anti-inflammatory functions, SIRT1 participates in inflammatory reactions too and could be a potential anti-rheumatic target.

Preventive and therapeutic effects of the peel powder of P. granatum in a rat sepsis model

The aim of the present study was to evaluate the treatment potential of Punica granatum L. peel powder in an experimentally induced sepsis model in rats. Sepsis was induced in 10-week-old, male, Wistar Albino (n=24) rats. The animals were divided into four groups: Sham-operated (S) Group, Control (C) Group, Treatment-1 (T1) Group, and Treatment-2 (T2) Group. To induce the sepsis model, the cecal ligation and puncture procedure was performed. The P. granatum peel powder (200 mg/kg; per os) was applied one hour before (T1) and 10 hours after (T2) surgery in a volume of 2 mL. At the end of the experimental procedure, microbial and histopathological analyses were performed. The histopathological scores on the liver, lungs, heart, kidney, spleen, and pancreas were evaluated. Escherichia coli, Staphylococcus aureus and E. coli + S. aureus were isolated from blood cultures. Severe bacteria were detected in the blood of the group C animals. It was found that there were fewer bacteria in groups T1 (n=2) and T2 (n=4) compared with group C. There were no lesions in the pancreas tissues of any groups. Vascular changes, degeneration, and necrosis were common in the organs in all cases of group C compared to group S. The findings in group T1 were similar to those in group C, however, it was seen in fewer animals. It was determined that there was a general improvement in group T2, and in addition the existing lesions were moderate in severity. In conclusion, P. granatum L. peel powder prevented CLP-induced lung injury in experimental rats. Thus, P. granatum L. peel powder may be an alternative therapeutic agent against lung tissue injury induced by sepsis. The recovery from inflammation was better in group T2 than in the other groups. According to the results of the current study, P. granatum peel powder was found to be effective in the treatment of sepsis with antimicrobial and anti-inflammatory functions.

APPLICATION OF SIMPLE INHALATION THERAPY IN PULMONARY TB PATIENTS TO OVERCOME THE INEFECTIVENESS OF BREATH WAY CLEANING

Background: Inadequate airway clearance is one of the nursing issues that arises during the pulmonary tuberculosis disease process. If untreated, ineffective airway clearance can result in hypoxemia, decreased consciousness, and even cell death. Objective: The purpose of this study is to see that simple inhalation therapy can help pulmonary tuberculosis patients at the Banyu Urip Community Health Center to overcome ineffective airway clearance. Methods: The research methodology combines a case study approach with a family nursing process approach, with one case as the unit of analysis, Mrs. K, a pulmonary tuberculosis patient who get treatment at the Banyu Urip Community Health Center working area. Data was gathered through interviews, physical examinations, supporting examinations, and a literature review. In the study, 350 ml of hot water steam and 5 drops of eucalyptus oil were applied twice a day for three days, for 10-15 minutes. Result: The research results of simple inhalation therapy proved to have a positive effect on Mrs. K, as evidenced by a reduction in verbal complaints, including ease in driving out secretions, respiratory frequency was within normal limits, and breathing became easier, because the cineol content of eucalyptus oil has mucolytic, bronchodilator, and anti-inflammatory functions. Conclusion: To overcome airway ineffectiveness and improve health status, simple inhalation therapy combined with eucalyptus oil can be used as an alternative. Non-pharmacological techniques that are simple, easy to use but provide numerous benefits in health care facilities, such as simple inhalation therapy, are expected of health care workers.

Regulation of miRNA-155-5p ameliorates NETosis in pulmonary fibrosis rat model via inhibiting its target cytokines IL-1β, TNF-α and TGF-β1

Idiopathic pulmonary fibrosis (IPF) is an age-related inflammatory disease with no cure up till now.It is accompanied by neutrophils infiltration as the main responders to inflammation and fibrosis. Importantly, neutrophils release neutrophil extracellular traps (NETs) through NETosis process. The function of microRNAs during inflammation became of great biological attention. Owing to microRNAs’ central role in immune system, microRNA-155-5p (miR-155-5p) is intensely involved in the inflammatory response. Capsaicin (Cap) is a bioactive compound that exhibits antioxidative and anti-inflammatory functions. Recent studies have shown its role in regulation of certain microRNAs’ expressions. Accordingly, the present study aims to investigate the effect of miR-155-5p regulation in suppressing NETs production via ameliorating its target inflammatory cytokines, IL-1ß, TNF-α and TGF-ß1, in bleomycin (BLM)-induced pulmonary fibrosis rat model treated by Cap. The obtained results demonstrated that miR-155-5p downregulation was associated with significant decrease in IL-1ß, TNF-α, TGF-β1, which consequently, reduced hydroxyproline (HYP), NETs activity markers as NE and PAD-4, and alleviated CTGF levels in lung tissues of animals treated by Cap. Furthermore, NETosis ultrastructure examination by transmission electron microscope (TEM), MPO immunohistochemical staining and histopathological studies confirmed an abolishment in NETs formation and an improvement in lung tissue architecture in Cap-treated rats. This study concluded that Cap quenched the inflammatory response through interrupting IL-1β, TNF-α and TGF-β1 pathway via modulating miR-155-5p expression. In addition, Cap was able to alleviate pulmonary NETosis markers by restraining NETs activity markers. These findings provide novel insight into the application of Cap-based treatment in ameliorating pulmonary damage in IPF.

Revitalizing mitochondrial function and empowering spinal cord recovery using copper-catalyzed Pdots

Spinal cord injury (SCI) inflicts devastating consequences for health. While drugs have been employed to alleviate SCI symptoms, their complex synthesis procedures and the need for specialized drug delivery raise concerns regarding administration. Herein, we utilize a green synthesis protocol to produce polymer quantum dots (Pdots) from polyvinylpyrrolidone precursors, empowered by the catalytic prowess of copper. These Copper-catalyzed Pdots (CPdots) not only offer enhanced improved fluorescence properties but also exhibit remarkable antioxidant, anti-inflammatory, and mitochondrial function repair effects. An intriguing finding emerged from our research as CPdots were observed to activate the AMPK/PGC-1α/Sirt3 pathway-a distinctive molecular mechanism that combats mitochondrial dysfunction, and mitigates calcium overload associated with acute SCI. Furthermore, the rapid metabolism and exceptional biocompatibility of our CPdots reinforce their safety and efficacy.

Antioxidant and Anti-Inflammatory Functions of High-Density Lipoprotein in Type 1 and Type 2 Diabetes.

(1) Background: high-density lipoproteins (HDLs) exhibit antioxidant and anti-inflammatory properties that play an important role in preventing the development of atherosclerotic lesions and possibly also diabetes. In turn, both type 1 diabetes (T1D) and type 2 diabetes (T2D) are susceptible to having deleterious effects on these HDL functions. The objectives of the present review are to expound upon the antioxidant and anti-inflammatory functions of HDLs in both diabetes in the setting of atherosclerotic cardiovascular diseases and discuss the contributions of these HDL functions to the onset of diabetes. (2) Methods: this narrative review is based on the literature available from the PubMed database. (3) Results: several antioxidant functions of HDLs, such as paraoxonase-1 activity, are compromised in T2D, thereby facilitating the pro-atherogenic effects of oxidized low-density lipoproteins. In addition, HDLs exhibit diminished ability to inhibit pro-inflammatory pathways in the vessels of individuals with T2D. Although the literature is less extensive, recent evidence suggests defective antiatherogenic properties of HDL particles in T1D. Lastly, substantial evidence indicates that HDLs play a role in the onset of diabetes by modulating glucose metabolism. (4) Conclusions and perspectives: impaired HDL antioxidant and anti-inflammatory functions present intriguing targets for mitigating cardiovascular risk in individuals with diabetes. Further investigations are needed to clarify the influence of glycaemic control and nephropathy on HDL functionality in patients with T1D. Furthermore, exploring the effects on HDL functionality of novel antidiabetic drugs used in the management of T2D may provide intriguing insights for future research.

Non-Invasive Study of Intracranial Pressure in Pre- and Post-Chemotherapy Patients for the Treatment of Breast Neoplasia

Introduction: Breast cancer is the most common type among women and brings to them significant organic changes. A new intracranial pressure monitorization method consists of an external system of sensors that detects micrometric deformations on the cranial bones and transmits, in real-time, electrical signals that are visualized on a monitor. Objective: To identify changes in intracranial pressure due to chemotherapy connections through non-invasive methodology. Methods: The present study was conducted at Hospital Santa Casa de Misericordia in the city of Ponta Grossa, PR, Brazil in 2017. The variables P2/P1 ratio (ICP morphological evaluation), laboratory parameters, comorbidities, and clinical aspects of the volunteers were evaluated. The vascular toxicity of chemotherapy often causes endothelial dysfunction, resulting in a loss of vasodilation effects and suppresses anti-inflammatory and vascular repair functions. Results: The values of the P2/P1 ratio before and after chemotherapy were also compared between groups. A statistically significant difference was observed in the pre-chemotherapy P2/P1 values compared to the post-chemotherapy values. Conclusion: Variations in ICP may occur in cancer patients. Further studies are necessary to evaluate if this change may contribute to the chemotherapy side effects occurrence.

Co-delivery of indomethacin and uricase as a new strategy for inflammatory diseases associated with high uric acid.

Uric acid is the final metabolite in humans. High level of uric acid chronically induces urate deposition, aggravates kidney damage, and concomitantly causes an increase in inflammatory factors. Alleviating acute inflammation and decreasing uric acid levels are the key points in the treatment of inflammatory diseases associated with high uric acid. However, a drug delivery system that combines anti-inflammatory and uric acid reduction functions at the same time remains a challenge to be settled. Here, we designed a nanocrystal-based co-delivery platform, IND Nplex, characterized by loading of indomethacin (IND) and uricase. Compared with free IND or uricase, IND Nplex possessed a better anti-inflammatory effect by restraining the release of inflammation-related factors in vitro. In addition, pharmacokinetic and biodistribution studies revealed that IND Nplex significantly prolonged the retention time in vivo and was more concentrated in the kidney. In acute gouty arthritis model rats, IND Nplex markedly relieved ankle joint swelling and mitigated synovial inflammation. In acute kidney injury model rats, IND Nplex indicated better biocompatibility and significant amelioration of renal fibrosis. Moreover, IND Nplex showed the effect of anti-inflammatory and improved renal function via determination of inflammatory factors and biochemical markers in the serum and kidney. In conclusion, these results indicate that IND Nplex exerts anti-inflammatory activity and uric acid-lowering effect and could become a promising candidate for the treatment of uric acid-related diseases.