Expression Of Interleukin Research Articles

Effects of dietary ginger (Zingiber officinale) polysaccharide on the growth, antioxidant, immunity response, intestinal microbiota, and disease resistance to Aeromonas hydrophila in crucian carp (Carassius auratus)

Ginger polysaccharides (GP) promote growth and development in fish. However, the effects of GP on crucian carp remain unclear. The present study investigated the effects of GP on the growth performance, immunity, intestinal microbiota, and disease resistance in crucian carp. Four treatment groups were established with different concentrations of GP (0.1 %, 0.2 %, 0.4 %, and 0.8 %). GP was not added as the control group, and the feeding period lasted for 56 d, followed by a 96-h anti-infection treatment using Aeromonas hydrophila. The results showed that dietary GP significantly improved growth performance, especially in the 0.4 % GP group. Furthermore, GP administration notably increased serum lysozyme (LMZ) activity, digestive enzyme performance, and antioxidant capacity of crucian carp. Moreover, dietary inclusion of GP up-regulated the expression of tumour necrosis factor-α (TNF-α), interleukin-8 (IL-8), interferon-γ (IFN-γ), and nuclear factor kappa-B (NF-κB) genes while down-regulating IL-10 and transforming growth factor-β (TGF-β) gene expressions, thus promoting liver health in crucian carp. Additionally, incorporating GP into the diet regulated both the diversity and composition of the intestinal microbiota in crucian carp, explicitly enhancing the relative abundance of beneficial bacteria, such as Fusobacteriota and Firmicutes. Therefore, GP reduces the mortality of crucian carp infected with A. hydrophila. In conclusion, this study provides novel insights into the application of dietary GP in cultured fish and evaluates the value of traditional Chinese medicinal polysaccharides against pathogenic bacteria.

Overview on the role of dietary Spirulina platensis on immune responses against Edwardsiellosis among Oreochromis niloticus fish farms

Edwardsiellosis is a bacterial fish disease that mostly occurs in freshwater farms and is characterized by a high mortality rate. Edwardsiella tarda strain was recovered from 17 fish out of 50 Nile tilapia, which were harboring clinical signs of systemic septicemia. The level of un-ionized ammonia (NH3) in the fish farm’s water was 0.11–0.15 mg/L, which was stressful for the Nile tilapia.Sequencing of the gyrB1 gene confirmed that the isolate was E. tarda JALO4, and it was submitted to NCBI under the accession number PP449014. The isolated E. tarda harbored the virulence gene edw1 AHL-synthase (quorum sensing). In addition, the isolate was sensitive to trimethoprim and sulfamethoxazole mean while it was intermediate to florfenicol. The median lethal dose (LD50) of E. tarda JALO4 was determined to be 1.7 × 105 CFU/mL in Nile tilapia.In the indoor experiment, Nile tilapia (45.05 ± 0.4 g), which received dietary Spirulina platensis (5 and 10 g/kg fish feed), showed optimum growth and feed utilization. Meanwhile, after receiving dietary S. platensis, the fish’s feed conversion ratio (FCR) was significantly enhanced compared to the control, which was 1.94, 1.99, and 2.88, respectively. The expression of immune-related genes interleukin (IL)-1β and tumor necrosis factor (TNF)-α were upsurged in E. tarda-challenged fish with higher intensity in S. platensis groups. Dietary S. platensis at a dose of 10 g/kg fish feed could provide a relative protection level (RPL) of 22.2% Nile tilapia challenged against E. tarda. Nile tilapia experimentally infected E. tarda, drastically altering their behavior: higher operculum movement, low food apprehension, and abnormal swimming dietary S. platensis (10 g/kg fish feed) could rapidly restore normal status.It was concluded that Edwardsiellosis could alter Nile tilapia behavior with a high loss in fish population. Fish received dietary-S. platensis could rapidly restore normal behavior after E. tarda infection. It is recommended the incorporation of S. platensis at doses of 10 g/kg into the Nile tilapia diet to boost their immunity and counteract E. tarda infection.

Seasonal Comparative Analysis of Follicular Interleukin Concentration and Expression of IL1RII, IL4 and IL1RA in Cystic Follicles Versus Normal Preovulatory Follicles in Buffalo

Seasonal Comparative Analysis of Follicular Interleukin Concentration and Expression of IL1RII, IL4 and IL1RA in Cystic Follicles Versus Normal Preovulatory Follicles in Buffalo

Anti-Inflammatory Effect of Atorvastatin and Rosuvastatin on Monosodium Urate-Induced Inflammation through IL-37/Smad3-Complex Activation in an In Vitro Study Using THP-1 Macrophages.

Objective: The pleiotropic effect of hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) is responsible for potent defense against inflammatory response. This study evaluated the inhibitory effects of HMG-CoA reductase inhibitors on the monosodium urate (MSU)-induced inflammatory response through the regulation of interleukin-37 (IL-37) expression. Methods: Serum was collected from patients with gout (n = 40) and from healthy controls (n = 30). The mRNA and protein expression of the target molecules IL-1β, IL-37, caspase-1, and Smad3 were measured in THP-1 macrophages stimulated with MSU, atorvastatin, or rosuvastatin using a real-time quantitative polymerase chain reaction and Western blot assay. Transfection with IL-1β or Smad3 siRNA in THP-1 macrophages was used to verify the pharmaceutical effect of statins in uric-acid-induced inflammation. Results: Serum IL-37 levels in gout patients were significantly higher than in controls (p < 0.001) and was associated with the serum uric acid level (r = 0.382, p = 0.008). THP-1 cells stimulated with MSU markedly induced IL-37 mRNA expression and the transition of IL-37 from the cytoplasm to the nucleus. Recombinant IL-37 treatment dose-dependently inhibited activation of caspase-1 and IL-1β in MSU-induced inflammation. Atorvastatin and rosuvastatin attenuated caspase-1 activation and mature IL-1β expression but augmented translocation of IL-37 from the cytoplasm to the nucleus. Atorvastatin and rosuvastatin induced phosphorylation of Smad3 in THP-1 cells treated with MSU crystals. Statins potently attenuated translocation of IL-37 from the cytoplasm to the nucleus in THP-1 macrophages transfected with Smad3 siRNA compared to cells with negative control siRNA. Conclusions: This study revealed that statins inhibit the MSU-induced inflammatory response through phosphorylated Smad3-mediated IL-37 expression in THP-1 macrophages.

Resveratrol as an Anti-inflammatory Agent in Coronary Artery Disease: A Systematic Review, Meta-Analysis and Meta-Regression.

Resveratrol is a non-flavonoid polyphenol that shows promise in reducing pro-inflammatory factors and maintaining endothelial function, which hints at its potential role in slowing atherosclerosis and preventing acute coronary events. To study the cardioprotective effects of resveratrol on inflammatory mediators and endothelial function in patients with coronary artery disease (CAD). A thorough search was conducted in databases (Cochrane Library, ProQuest, PubMed, LILACS, ScienceDirect, Springer, Taylor&Francis, CNKI, Wanfang, and Weipu) until September 24, 2023. The vasopro-inflammatory mediators, endothelial function and outcomes related to cardiovascular events were observed. Titles and abstracts were assessed, and bias was evaluated with Cochrane RoB 2.0. Heterogeneity of results was explored by meta-regression, certainty of evidence was assessed by the GRADE system, and conclusive evidence was enhanced by trial sequence analysis. Ten randomized controlled trials and 3 animal studies investigated resveratrol's impact on inflammatory mediators and endothelial function. In primary prevention studies, meta-analysis showed a significant reduction (95% CI: -0.73 to -0.20; P=0.0005) in tumor necrosis factor-α (TNF-α) expression with resveratrol, demonstrating a dose-dependent relationship. No significant difference was observed in interleukin-6 (IL-6) expression with P=0.58 for primary prevention and P=0.57 for secondary prevention. Vascular endothelial nitric oxide synthase (eNOS) expression was significantly increased after resveratrol pre-treatment following CAD events. Secondary prevention studies yielded no significant results; however, meta-regression identified associations between age, hypertension, and lower doses with the extent of TNF-α alterations. High certainty of evidence supported TNF-α reduction, while evidence for IL-6 reduction and eNOS elevation was deemed low. Resveratrol reduces TNF-α in individuals at risk for CAD, specifically 15 mg per day. However, its usefulness in patients with confirmed CAD is limited due to factors such as age, high blood pressure, and insufficient dosage. Due to the small sample size, the reduction of IL-6 is inconclusive. Animal studies suggest that resveratrol enhances endothelial function by increasing eNOS. (PROSPERO registration No. CRD42023465234).

Role of the IL-8/CXCR2 axis in promoting vasculogenic mimicry in triple-negative breast cancer through epithelial-mesenchymal transition

Vasculogenic mimicry (VM) &amp;mdash; a phenomenon where tumor cells form de novo vascular networks independent of endothelial cells &amp;mdash; supports the growth of highly aggressive tumors, including triple-negative breast cancer (TNBC). Evidence indicates that the interleukin 8 (IL-8)/CXCR2 axis and epithelial-mesenchymal transition (EMT) independently promote VM in TNBC. This study tested the hypothesis that the IL-8/CXCR2 axis promotes VM via EMT. Tissue samples from 71 female breast cancer cases (age range: 50 &amp;ndash; 55 years), comprising 37 TNBC and 34 non-TNBC cases, were retrieved from the Department of Pathology at the University of Ghana Medical School. Out of the 37 TNBC tissues, 10 expressed either IL-8, CXCR2, or vimentin exclusively; three expressed all three markers; and 14 did not express any of these markers. For the non-TNBC tissues, 31 expressed CXCR2 (alone or co-expression with IL-8 and/or vimentin), 27 co-expressed IL-8 with CXCR2 and/or vimentin, and two expressed all three markers. Notably, 24 of the 37 non-TNBC tissues co-expressed IL-8 and CXCR2. A phi coefficient analysis displayed an inverse relationship between CXCR2 or IL-8 expression and TNBC and a positive correlation between vimentin expression and TNBC. Inhibiting the IL-8/CXCR2 axis with the CXCR2 antagonist SB225002 suppressed VM in MDA-MB-231 breast cancer cells. In addition, inhibiting the IL-8/CXCR2 axis using SB225002 and siRNA-mediated CXCR2 knockdown suppressed EMT by upregulating E-cadherin expression and downregulating N-cadherin and vimentin expression. Our findings suggest that the IL-8/CXCR2 signaling axis promotes VM in TNBC by facilitating EMT. Therefore, therapies targeting IL-8/CXCR2 may be used to suppress EMT and VM in TNBC simultaneously.

Causal relationships between inflammatory cytokines and myopia: an analysis of genetic and observational studies.

This study aims to explore the causal relationship between inflammatory markers and myopia through the use of bidirectional Mendelian randomization (MR) and myopia animal models. The authors utilized data from a comprehensive and publicly accessible genome-wide association study (GWAS) for our analysis, which includes 460536 European ancestry control subjects and 37362 myopia patients. Utilizing a two-sample Mendelian randomization analysis framework, 27 inflammatory markers were investigated as exposure variables with myopia serving as the outcome variable. Nine MR analysis techniques were employed, with inverse-variance weighting (IVW) as the principal MR analysis method. Heterogeneity was assessed using Cochrane's Q test. The identification of single-nucleotide polymorphisms (SNPs) and outliers linked to myopia was achieved via MR-PRESSO. The expression of interleukin-2 (IL-2) in the vitreous of guinea pigs subjected to experimentally induced form-deprivation myopia (FDM) was examined. Elevated concentrations of IL-2 and IL-2ra were found to be associated [IVW estimate odds ratio (OR): 1.003, 95% CI: 1.001-1.005, P=0.001] and strongly associated (IVW estimate OR: 1.002, 95% CI: 1.000-1.003, P=0.049) with an increased risk of myopia, respectively. Conversely, lower levels of C-reactive protein (CRP) (IVW estimate OR: 0.996, 95% CI: 0.994-0.999, P=0.002) and tumour necrosis factor alpha (IVW estimate OR: 0.995, 95% CI: 0.994-0.996, P<0.001) were robustly linked to a heightened risk of myopia. IL-2 expression was notably upregulated in the vitreous of guinea pigs with experimentally induced FDM. Elevated levels of inflammatory factors, especially IL-2 and IL-2ra, have a potential causal relationship with myopia susceptibility, providing new insights into the pathogenesis of myopia.

Enviromental endocrine disruptor risks in the central nervous system: Neurotoxic effects of PFOS and glyphosate

Endocrine disruptors (EDs) pose significant risks to human and environmental health, with potential implications for neurotoxicity. This study investigates the synergistic neurotoxic effects of perfluorooctane sulfonate (PFOS) and glyphosate (GLY), two ubiquitous EDs, using SHSY5Y neuronal and C6 astrocytic cell lines. While individual exposures to PFOS and glyphosate at non-toxic concentrations did not induce significant changes, their combination resulted in a marked increase in oxidative stress and neuroinflammatory responses. Specifically, the co-exposure led to elevated levels of interleukin-6, tumor necrosis factor alpha, and interferon gamma, along with reduced interleukin-10 expression, indicative of heightened neuroinflammatory processes. These findings underscore the importance of considering the synergistic interactions of EDs in assessing neurotoxic risks and highlight the urgent need for further research to mitigate the adverse effects of these compounds on neurological health.

Effects of Luhong Yixin Granules on myocardial fibrosis in heart failure rats based on TGF-β1/Smads signaling pathway

To investigate the effects of Luhong Yixin Granules on myocardial fibrosis in rats with heart failure and its possible mechanism, a total of 60 male Wistar rats were randomly divided into the control group, model group, and low-, medium-and high-dose Luhong Yixin Granules groups, with 12 rats in each group. Except for those in the control group, rats in the other groups were induced by intraperitoneal injection of doxorubicin(DOX) into a rat model. After the Luhong Yixin Granules were dissolved in the same amount of normal saline, they were given by gavage at low, medium and high doses(2.8, 5.6, 11.2 g·kg~(-1)·d~(-1)), and the control group and the model group were given the same amount of normal saline by gavage for 40 days. After the end of dosing, echocardiography was used to measure left ventricular ejection fraction(LVEF) and left ventricular fractional shortening(LVFS). Rat body weight(BW) and heart weight(HW) were calculated as HW/BW. Enzyme-linked immunosorbent assay was used to measure the levels of interleukin-6(IL-6), interleukin-17(IL-17), tumor necrosis factor-α(TNF-α), transforming growth factor-β1(TGF-β1), growth stimulation expressed gene 2 protein(ST2), N-terminal pro-B-type natriuretic peptide(NT-proBNP), galectin-3(Gal-3) and creatine kinase isoenzyme(CK-MB) in serum. Hematoxylin-eosin(HE) staining and Masson staining were used to observe the pathological morphology of myocardial tissue. Western blot and quantitative real-time polymerase chain reaction were used to detect the protein and mRNA expression levels of IL-6, IL-17, TNF-α, TGF-β1, Smad3, Smad7, α-smooth muscle actin(α-SMA), and collagen Ⅰ(COL-Ⅰ), respectively. RESULTS:: showed that compared with those in the control group, LVEF, LVFS, and HW/BW in the model group were decreased(P&lt;0.05), and the levels of IL-6, IL-17, TNF-α, TGF-β1, ST2, NT-proBNP, Gal-3, and CK-MB were increased(P&lt;0.05). HE staining showed inflammatory changes in myocardial tissue; Masson staining showed decreases in the cross-sectional area and ventricular cavity area of the heart, and myocardial fibrosis of varying degrees(P&lt;0.05). The protein and mRNA expression of IL-6, IL-17, TNF-α, TGF-β1, Smad3, α-SMA, and COL-Ⅰ were increased(P&lt;0.05), and the protein and mRNA expression of Smad7 protein was decreased(P&lt;0.01). Compared with those in the model group, LVEF, LVFS and HW/BW of the low-, medium-and high-dose Luhong Yixin Granules groups were increased(P&lt;0.05), and the levels of IL-6, IL-17, TNF-α, TGF-β1, ST2, NT-proBNP, Gal-3 and CK-MB were decreased(P&lt;0.05). HE staining showed gradually reduced inflammatory changes of myocardial tissue, and Masson staining showed increased cross-sectional area and ventricular cavity area of the heart and decreased area of myocardial fibrosis(P&lt;0.05). The protein and mRNA expression levels of IL-6, IL-17, TNF-α, TGF-β1, Smad3, α-SMA, and COL-Ⅰ were decreased(P&lt;0.05), while the protein and mRNA expression levels of Smad7 were increased(P&lt;0.05). Luhong Yixin Granules may be of great value in the treatment of heart failure by regulating the TGF-β1/Smads signaling pathway, inhibiting the expression of inflammation-related proteins, reducing the deposition of extracellular matrix, and alleviating myocardial fibrosis.

Gastrodin combined with electroacupuncture prevents the development of cerebral ischemia via rebalance of brain-derived neurotrophic factor and interleukin-6 in stroke model rats.

Traditional Chinese medicine (TCM) has long been used to treat various diseases, including cerebral ischemia. The specific molecular mechanism of TCM in the treatment of cerebral ischemia, however, is still unclear. This study investigated the effects of gastrodin, electroacupuncture and their combination on cerebral ischemic rats. We used Nissl staining, immunohistochemical staining and immunoblotting to detect the expression changes of brain-derived neurotrophic factor (BDNF) and interleukin-6 (IL-6) in the frontal cortex. The results showed that the combination therapy of gastrodin and electroacupuncture significantly increased the number of Nissl-positive neurons and improved cell morphology compared with other groups. Mechanistically, we found that the combination of gastrodin and electroacupuncture treatment group can restore the abnormal morphology of neuronal cells caused by cerebral ischemia by rebalancing the expression levels of BDNF and IL-6. Our research indicates that gastrodin combined with electroacupuncture has a significant protective effect on cerebral ischemic injury in rats, possibly by regulating the expression of BDNF and IL-6. This combination therapy is superior to single-drug or electroacupuncture therapy.

Interleukin-5 alleviates cardiac remodelling via the STAT3 pathway in angiotensin II-infused mice.

Interleukin-5 (IL-5) has been reported to be involved in cardiovascular diseases, such as atherosclerosis and cardiac injury. This study aimed to investigate the effects of IL-5 on cardiac remodelling. Mice were infused with angiotensin II (Ang II), and the expression and source of cardiac IL-5 were analysed. The results showed that cardiac IL-5 expression was time- and dose-dependently decreased after Ang II infusion, and was mainly derived from cardiac macrophages. Additionally, IL-5-knockout (IL-5-/-) mice were used to observe the effects of IL-5 knockout on Ang II-induced cardiac remodelling. We found knockout of IL-5 significantly increased the expression of cardiac hypertrophy markers, elevated myocardial cell cross-sectional areas and worsened cardiac dysfunction in Ang II-infused mice. IL-5 deletion also promoted M2 macrophage differentiation and exacerbated cardiac fibrosis. Furthermore, the effects of IL-5 deletion on cardiac remodelling was detected after the STAT3 pathway was inhibited by S31-201. The effects of IL-5 on cardiac remodelling and M2 macrophage differentiation were reversed by S31-201. Finally, the effects of IL-5 on macrophage differentiation and macrophage-related cardiac hypertrophy and fibrosis were analysed invitro. IL-5 knockout significantly increased the Ang II-induced mRNA expression of cardiac hypertrophy markers in myocardial cells that were co-cultured with macrophages, and this effect was reversed by S31-201. Similar trends in the mRNA levels of fibrosis markers were observed when cardiac fibroblasts and macrophages were co-cultured. In conclusions, IL-5 deficiency promote the differentiation of M2 macrophages by activating the STAT3 pathway, thereby exacerbating cardiac remodelling in Ang II-infused mice. IL-5 may be a potential target for the clinical prevention of cardiac remodelling.

Estimation of Some Pro- and Anti-Inflammatory Interleukins in Rheumatoid Arthritis of Iraqi Patients

Abstract Background: Rheumatoid arthritis (RA) is an inflammatory condition that mostly affects synovial joints. It produces severe swelling and ongoing inflammation, and as it worsens, the cartilage and bone begin to erode, resulting in deformed joints and bone erosion. Objectives: The purpose of this study is to evaluate the levels of anti-cyclic citrullinated peptide (anti-CCP) antibodies and determine the role of interleukin-1 beta (IL-1β), interleukin-18 (IL-18), interleukin-38 (IL-38), and transforming growth factor-beta2 (TGF-β2) in studied groups (RA patients and apparently healthy control). Materials and Methods: The study included collecting blood samples from a group of patients infected with RA involving 60 patients (21 male and 39 female), and the healthy group included 50 individuals as control group (21 males and 29 females). Results: The outcomes showed of anti-CCP a highly significant difference for RA patients compared to the control group by 0.603 ± 0.02 and 0.274 ± 0.01, respectively, and some immunological parameters that involve inflammation-promoting interleukins (IL-1β and IL-18), the results showed the significant differences at the level (P &lt; 0.01) of patients was 126.79 ± 4.18 and 194.37 ± 12.71 compared with control 91.85 ± 2.11 and 92.27 ± 2.08, respectively. The identical results to measure anti-inflammatory interleukins (IL-38, TGF-β2) represented of patients were 190.43 ± 9.82 and 403.23 ± 21.20 compared with control group was 88.39 ± 1.56 and 115.59 ± 5.63, respectively. Conclusion: The immunological parameters represented high expression of pro-inflammatory interleukins (IL-1β and IL-18), so, elevation levels of anti-inflammatory interleukins (IL-38 and TGF-β2) of RA patients.

Interleukin-6 and Interleukin-8 Gene Expressions Differ Between Male and Female Patients at Time of Hip Arthroscopy for Femoroacetabular Impingement Syndrome

Interleukin-6 and Interleukin-8 Gene Expressions Differ Between Male and Female Patients at Time of Hip Arthroscopy for Femoroacetabular Impingement Syndrome

Relationship between the serum level, polymorphism and gene expression of IL-33 in samples of recurrent miscarriage Iraqi women infected with toxoplasmosis

One of the many warm-blooded hosts that toxoplasmosis-causing intracellular protozoan parasite Toxoplasma gondii can infect is humans. Cytokines are crucial to stimulate an effective immune response against T. gondii. Interleukin-33 (IL-33) is a unique anti-inflammatory cytokine that suppresses the immune response. The levels of cytokine gene expression are regulated by genetics, and the genetic polymorphisms of these cytokines play a functional role in this process. Single nucleotide polymorphisms (SNPs) are prognostic indicators of illnesses. This study aimed to determine whether toxoplasmosis interacts with serum levels of IL-33 and its SNP in miscarriage women as well as whether serum levels and IL-33 gene expression are related in toxoplasmosis-positive miscarriage women. Two hundred blood samples from patients and controls were collected from AL-Alawiya Maternity Teaching Hospital and AL-Yarmouk Teaching Hospital in Baghdad, Iraq from 2021 to 2022 in order to evaluate the serum level of IL-33 using ELISA test. For the SNP of IL-33, the allelic high-resolution approach was utilized, and real time-PCR was performed to assess gene expression. The results showed that compared to healthy and pregnant women, recurrent miscarriage with toxoplasmosis and recurrent miscarriage women had lower IL-33 concentrations. Additionally, there were significant differences among healthy women, pregnant women, and women with repeated miscarriage who experienced toxoplasmosis. Furthermore, no differences between patients and controls were revealed by gene expression data. The results revealed that recurrent miscarriage, pregnancy, and healthy women all had a slightly higher amount of the IL-33 gene fold. Additionally, the SNP of IL-33 data demonstrated that there was no significant genetic relationship between patients and controls. Recurrent miscarriage women with toxoplasmosis have showed significant differences from pregnant women in the genotypes GG and AA as well as the alleles A and G. There were notable variations between recurrent miscarriage with and without toxoplasmosis in terms of the genotypes AA and AC. The genotypes GG, AA, and allele A in recurrent miscarriage women with toxoplasmosis and recurrent miscarriage women is a protective factor. Taking together, there was a statistically significant negative correlation between toxoplasmosis and IL-33 gene expression, which calls for more quantitative investigation in order to fully comprehend the interaction of mRNA and protein.

Cantharidin overcomes IL-2Rα signaling-mediated vorinostat resistance in cutaneous T-cell lymphoma through reactive oxygen species

BackgroundVorinostat (SAHA) is a histone deacetylase inhibitor that has shown clinical efficacy against advanced cutaneous T-cell lymphoma (CTCL). However, only a subset of patients with CTCL (30–35%) respond to SAHA...

Clinical advantage staging and underlying mechanisms of Wangbi Tablets against knee osteoarthritis based on "disease-formula" interaction network

The clinical advantage staging and underlying mechanisms of Wangbi Tablets against knee osteoarthritis(KOA) were studied based on the &quot;disease-formula&quot; interaction network. Firstly, the clinical symptoms and related genes corresponding to Wangbi Tablets and KOA in the acute, remission, and recovery phases were collected from clinical guidelines/consensus and SoFDA database, and the putative targets of Wangbi Tablets were obtained from ETCM 2.0. Then, Jaccard similarity and cosine similarity were employed to assess the similarities of clinical symptoms, genes, and enriched pathways between Wangbi Tablets and KOA in different phases. The &quot;disease-formula&quot; interaction network of the drug targets and disease genes was constructed, and the key targets were screened by topological feature calculation. KEGG and Reactome database were used for the functional enrichment of the key targets, on the basis of which the functional characteristics of Wangbi Tablets against KOA in the acute, remission, and recovery phases were predicted. Finally, the SW1353 cells exposed to lipopolysaccharide were used to decipher the mechanism of Wangbi Tablets against KOA. The results showed that 92/3 921, 138/3 708, 139/3 800, and 196/3 946 clinical symptoms and the related genes corresponded to KOA in the acute, remission, and recovery phases and Wangbi Tablets were collected from SoFDA, and 260 putative targets of Wangbi Tablets were obtained from ETCM 2.0. Wangbi Tablets had highest similarity of clinical symptoms, genes, and enriched pathways with KOA in the remission phase and the secondary highest similarity with KOA in the recovery phase. The key targets of Wangbi Tablets mainly participated in the regulation of immunity-inflammation imbalance and exerted pain-relieving and bone-protecting effects to alleviate symptoms such as knee joint pain, joint swelling, soreness, fatigue, and dysfunction. Intriguingly, the key targets of Wangbi Tablets possessed antioxidant effects during KOA in the acute and remission phases, while they maintained material and energy metabolism homeostasis and protected vessels during KOA in the recovery phase. The cell experiment indicated that Wangbi Tablets down-regulated the expression of interleukin(IL)-6, IL-1β, tumor necrosis factor-α(TNF-α), and Bcl-2-associated X protein(Bax)/B-cell lymphoma 2(Bcl-2) via regulating the phosphatidylinositol 3-kinase(PI3K)-protein kinase B(Akt) signaling pathway. The findings lay a theoretical foundation for further clarifying the clinical advantage stage and precise clinical application of Wangbi Tablets in treating KOA.

Impact of Interleukin-6 on Oral Squamous Cell Carcinoma Among the South Indian Population.

Introduction Oral squamous cell carcinoma (OSCC) isassociated with high rates of morbidity and mortality. Despite advances in research and treatment, the survival rate of OSCC patients has not changed considerably in recent years. Interleukin-6 (IL-6) is a proinflammatory cytokinethat is involved in the development of various cancers including OSCC. The role of IL-6 is being studied in various cancers;however, its exact mechanism of action in OSCC among the South Indian population has not yet been studied. Thus, the current study aimsto evaluate and assess the impact of IL-6 on OSCC among the South Indian population. Materials and methods Twenty tissues fromOSCC patients and 20 normal tissues surrounding the same area from normal people were gathered from theDepartment of Oral and Maxillofacial Surgery, Saveetha Dental College and Hospital. The tissues were prepared for expression investigations and hematoxylin and eosin staining. The data was presented as mean ± standard deviation, with statistical significance at p<0.05. Results Our results indicate that, in comparison to normal tissues, OSCC samples had increased IL-6 expression levels (p<0.05). Conclusion We conclude that IL-6 has been identified as a key oncogene in the development of tumors and their spread in several types of cancers, including OSCC. Therefore, IL-6 can be used as a potential diagnostic or prognostic biomarker and the use of IL-6 inhibitors can be formulated as a potential treatment forOSCC.

A prognostic impact of interleukin 32 (IL-32) as an immune marker in patients with bladder cancer

Background. Urinary bladder cancer is a prevalent global health concern. IL-32 is a cytokine that promotes inflammation and has been shown in multiple studies to suppress the development of cancer cells and trigger cell death in different types of cancer cells. Materials and methods. Expression of 32 interleukins was determined using an immunohistochemistry technique, which uses analysis of the exact concentrations and locations of specific compounds in tissues. This is done by using antibodies (antibodies) that react with the target protein (in this case IL-32), then identifying the sites where the active protein is located. The study included 114 diagnosed bladder cancer samples and 10 healthy controls. Results. By analyzing the expression of IL-32 using IHC technology on both bladder tissue from cancer patients and healthy bladder tissue that was considered a control, the results of evaluating IL-32 levels in bladder tissue from cancer patients showed a high level. Conclusion. High levels of IL-32 indicate disease progression or a poor outcome, while low levels can indicate an improvement or a good outcome. This is consistent with the fundamental aim of this study: the possibility of using IL-32 as a diagnostic or prognostic marker for disease progression and outcome prediction in cancer patients.

Pilot study: Significance of I-FABP2 in the diagnosis of acute abdominal episodes in children

BackgroundPediatric abdominal conditions, including necrotizing gastrointestinal diseases, pose significant diagnostic challenges due to clinic symptoms and limited diagnostic tools. Intestinal fatty acid binding protein 2 (I-FABP2) has emerged as a potential biomarker for intestinal damage, but its efficacy in diagnosing pediatric intestinal necrosis remains under explored. MethodsA prospective study was conducted on 55 pediatric patients presenting with abdominal pain and suspected intestinal necrosis or intestinal perforation. Clinical, laboratory, and radiological data were collected, and intraoperative assessment of bowel necrosis was performed. Gene expression of I-FABP2 in peripheral blood was measured using Real-Time RT-PCR, and correlations with surgery and laboratory parameters were analyzed. ResultsIntraoperative assessment revealed a moderate sensitivity (61.1%) and specificity (73.7%) of I-FABP2 in identifying bowel necrosis. Positive predictive value (PPV) was high (81.5%), indicating a high likelihood of the condition when I-FABP2 is positive. However, the negative predictive value (NPV) was limited (50%), suggesting challenges in confidently excluding necrosis based on negative I-FABP2 results. Correlations were observed between I-FABP2 expression and elevated levels of C-reactive protein (CRP), interleukin-6 (IL-6), and white blood cell count (WBC), indicating its association with inflammatory processes. ConclusionsWhile I-FABP2 shows promise as a biomarker for pediatric intestinal necrosis, its diagnostic utility may be enhanced when considered alongside other clinical parameters. Further research and validation studies are warranted to refine its clinical application and improve diagnostic accuracy in pediatric gastrointestinal conditions.

Identification and Molecular Mechanism of Anti-inflammatory Peptides Isolated from Jack Bean Protein Hydrolysates: in vitro Studies with Human Intestinal Caco-2BBe Cells

Jack bean (JB), Canavalia ensiformis (L.) DC, is a commonly cultivated legume in Indonesia. It is rich in protein, which can be hydrolyzed, making it potentially a good source of bioactive peptides. Intestinal inflammation is associated with several diseases, and the production of interleukin-8 (IL-8) in intestinal epithelial cells induced by tumor necrosis factor (TNF)-α has an important role in inflammatory reaction. The present study investigated the anti-inflammatory effects of peptides generated from enzymatic hydrolysis of JB protein on human intestinal Caco-2BBe cells. Additionally, in silico approaches were used to identify potential bioactive peptides. JB protein hydrolysate (JBPH) prepared using pepsin and pancreatin reduced the IL-8 expression at protein and mRNA levels in Caco-2BBe cells stimulated with TNF-α. Immunoblot analysis showed that the JBPH reduced the TNF-α-induced phosphorylation of c-Jun-NH(2)-terminal kinase, nuclear factor kappa B (NF-κB), and p38 proteins. Anti-inflammatory activity was observed in the 30% acetonitrile fraction of JBPH separated on a Sep-Pak C18 column. An ultrafiltration method revealed that relatively small peptides (< 3 kDa) had a potent inhibitory effect on the IL-8 production. Purification of the peptides by reversed-phase and anion-exchange high performance chromatography produced three peptide fractions with anti-inflammatory activities. A combination of mass spectrometry analysis and in silico approaches identified the potential anti-inflammatory peptides. Peptides derived from JB protein reduces the TNF-α-induced inflammatory response in Caco-2BBe cells via NF-κB and mitogen-activated protein kinase signaling pathways. Our results may lead to a novel therapeutic approach to promote intestinal health.