Cytokines IL-6 Research Articles

A Novel Look at Mechanisms and Applications of Xanthohumol (XN) in Dermatology and Cosmetology

Xanthohumol (XN), representing the group of chalcones, is a hydroxyl and superoxide free radical scavenger. It also has antimicrobial properties, showing antibacterial activity against Staphylococcus aureus, Staphylococcus pyogenes, Staphylococcus epidermidis and Propionibacterium acnes. XN exerts an inhibitory effect on tyrosinase (it hinders the oxidation of l-tyrosine and l-DOPA). However, it also affects the transport of pigment (through a reduction in the number and length of dendrites) and its degradation (through damage to melanosomes). Additionally, it has been shown to inhibit the different activation pathways of the premeditated response in macrophages and reduce the secretion of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β. Xanthohumol also improves skin elasticity by reducing the activity of elastase and MMP 1, 2 and 9, and it increases the expression of type I, III and V collagen, as well as elastin and fibrillins in skin fibroblasts. It acts against the main factors contributing to the pathogenesis of acne by inhibiting pro-inflammatory mediators (e.g., COX-2, PGE2, IL-1β and TNF-α). Moreover, it shows antibacterial activity against P. acnes and S. aureus, as well as seboregulatory and antioxidant properties. It has also been recognized that XN intake could affect diabetic wound healing. XN shows antitumoral activity, e.g., in the case of skin melanoma, which is associated with the antioxidant, pro-apoptotic, anti-angiogenic and immunostimulating effects of this compound.

A Long-Term Follow-Up Study of Serum NFATc3 Levels in Pediatric Patients with Bronchial Asthma: A Prospective Observational Case-Control Investigation.

The early and precise diagnosis of asthma significantly impacts the long-term health outcomes of pediatric patients. The sensitivity and specificity of current biomarkers, however, are frequently limited. Our study aimed to evaluate the clinical significance of nuclear factor of activated T cells, cytoplasmic 3 (NFATc3), in pediatric bronchial asthma, focusing on its diagnostic and prognostic value for disease severity and recurrence. This observational, prospective case-control study involved 200 pediatric patients with bronchial asthma and 200 age- and sex-matched healthy controls, from January 2020 to January 2023. Follow-up varied from 1 to 3 years. We measured levels of NFATc3 and inflammatory cytokines interleukin-1β (IL-1β), IL-6, and TNF-α via enzyme-linked immunosorbent assay. NFATc3 and IL-1β levels at enrollment were markedly higher in patients with acute exacerbations and those classified as severe, compared with their less severe counterparts. Throughout the study, NFATc3, IL-1β, and IL-6 levels significantly increased in severe or acutely exacerbating cases. The diagnostic value of NFATc3 was assessed through receiver operating characteristic curve analysis, which showed its potential in diagnosing bronchial asthma and identifying severe cases. Spearman's analysis confirmed positive associations between peak NFATc3 and cytokine levels. Importantly, disease type, NFATc3 values at enrollment, as well as peak IL-6 levels were identified as independent risk factors for severe bronchial asthma. Elevated NFATc3 is linked with the severity of pediatric bronchial asthma and serves as a potential biomarker for diagnosis and severity prediction, emphasizing its role in guiding treatment strategies.

Amyloid beta-induced signalling in leptomeningeal cells and its impact on astrocyte response.

The pathological signature of Alzheimer's disease (AD) includes the accumulation of toxic protein aggregates, mainly consisting of amyloid beta (Aβ). Recent strides in fundamental research underscore the pivotal role of waste clearance mechanisms in the brain suggesting it may be an early indication of early onset AD. This study delves into the involvement of leptomeningeal cells (LMCs), crucial components forming integral barriers within the clearance system, in the context of AD. We examined the inflammatory cytokine responses of LMCs in the presence of Aβ, alongside assessments of LMC growth response, viability, oxidative stress, and changes in vimentin expression. The LMCs showed no changes in growth, viability, oxidative stress, or vimentin expression in the presence of Aβ, indicating that LMCs are less susceptible to Aβ damage compared to other CNS cells. However, LMCs exhibited a unique pro-inflammatory response to Aβ when compared to an LPS inflammatory control, showing an mRNA expression of pro-inflammatory cytokines such IL-6, IL-10 and IL-33 but no changes in IL-1α and IL-1β. Furthermore, LMCs influenced the astrocyte response to Aβ, as conditioned media from Aβ-treated LMCs was observed to downregulate somatic S100β in astrocytes. We also investigated whether the JAK/STAT3 pathway was involved in the Aβ response of the LMCs, as this pathway has been shown to be activated in astrocytes and neurons in the presence of Aβ. JAK/STAT3 activation was assessed through phosphorylated STAT3, revealing that JAK/STAT3 was not active in the cells when in the presence of Aβ. However, when JAK1 and JAK2 were inhibited, cytokine protein levels of IL7, IL10, IL15 and IL33 levels, which had shown alteration when LMCs were treated with Aβ, returned to base levels. This indicates that although JAK1/STAT3 and JAK2/STAT3 are not the direct pathway for Aβ response in LMCs, JAK1 and JAK2 may still play a role in regulating cytokine levels, potentially through indirect means or crosstalk. Overall, our findings reveal that LMCs are resilient to Aβ toxicity and suggest that JAK1/STAT3 and JAK2/STAT3 does not play a central role in the inflammatory response, providing new insights into the cellular mechanisms underlying AD.

Biochanin A Attenuates Psoriasiform Inflammation by Regulating Nrf2/HO-1 Pathway Activation and Attenuating Inflammatory Signalling.

Psoriasis is a long-term inflammatory skin condition marked by an overabundance of keratinocytes and the release of pro-inflammatory cytokines in the outer layer of skin. For the comprehensive management of intermediate to advanced psoriasis, innovative biological treatments have been developed. Products for the superficial therapy of mild to moderate psoriasis are still necessary, though. Trifolium pratense contains the isoflavone biochanin A (BCA), which exhibits antiviral, antioxidant, anti-carcinogenic, and anti-inflammatory properties, and helps protect the integrity and function of the endothelium. Although investigations have not shown that BCA is effective in treating psoriasis, it has been shown to slow down the breakdown of the skin barrier by regulating keratinocyte growth. We sought to clarify the basic mechanisms behind BCA's impact on psoriasis in vitro and in vivo using experimental research via regulating Nrf2/HO-1 signaling pathway. By subjecting human primary keratinocytes to psoriasis-related cytokines, psoriasis-like keratinocytes were produced. The CCK8 test was used in this investigation to assess cell viability. BCA reduced keratinocyte growth and inflammatory cascade stimulation produced by TNF-α and IL-6, according to in vitro investigations conducted on HaCaT cells. The in vivo findings showed that six days of BCA therapy significantly decreased the skin, hematological indicators, levels of NO, TBARS, histopathological, and pro-inflammatory factors of COX-2, iNOS, NF-κB pathway. It additionally influenced the protein content of pro-inflammatory cytokines such as IL-17, IL-23, IL-1β in the epidermis along with IL-6, TNF-α among the epidermis and serum. In addition, in contrast to the IMQ group, BCA improved the skin's level of Nrf2/HO-1 protein, anti-inflammatory cytokine IL-10, and antioxidant indicators like SOD, CAT, GST, GSH, GR, and Vit-C. Ultimately, our research shows that BCA was effective in treating psoriasis in pre-clinical animal models by activating the Nrf2/HO-1 pathway, leading to an increase in antioxidant and anti-inflammatory markers.

Association of the humoral immune response with the inflammatory profile in Plasmodium vivax infections in pregnant women.

Plasmodium vivax infection, when it occurs during pregnancy, has often been associated with serious adverse pregnancy outcomes. However, immunological alterations in pregnancy and their consequences have been little explored. We characterized the humoral immune response in pregnant women exposed to malaria by P. vivax antigens and its association with the maternal inflammatory profile and poor pregnancy outcomes. An observational cohort study in the Brazilian Amazon was conducted between 2013 and 2015. After applying exclusion criteria, 242 mother-child pairs were included in the analysis. Data on maternal infection, gestational outcomes, and inflammatory factors were evaluated in the maternal peripheral plasma. In samples from the first infection, the presence of total IgG and its subclasses in plasma against PvMSP119 protein were also quantified. Previous exposure to malaria, observed by anti-total IgG antibodies to the PvMSP119 antigen, increased the inflammatory response to infection when the pregnant woman had malaria during pregnancy. IL-6 and IL-10 levels were positively correlated with parasitemia and with total IgG levels; but they were negatively correlated with the gestational age at delivery from Pv-infected woman. In multivariate linear regression analyses, IgG 1, 2 and 4 was negatively and positively associated with cytokines IL-6 and IL-10, respectively, in P. vivax-infection. An association between the humoral immune response and the peripheral inflammatory cytokine profile with the adverse outcomes in malaria in pregnancy by P. vivax was observed. Previous exposure to the parasite can influence the IL-6 and IL-10 response, which is associated with increased parasitemia, reduced maternal weight gain and premature delivery.

Cardioprotective effects of liposomal resveratrol in diabetic rats: unveiling antioxidant and anti-inflammatory benefits

ABSTRACT As a consequence of chronic hyperglycemia, diabetes complications and tissue damage are exacerbated. There is evidence that natural phytochemicals, including resveratrol, a bioactive polyphenol, may be able to reduce oxidative stress and improve insulin sensitivity. However, resveratrol's limited bioavailability hampers its therapeutic effectiveness. By using liposomes, resveratrol may be better delivered into the body and be more bioavailable. The objective of this study was to assess the cardioprotective potential of liposome-encapsulated resveratrol (LR) in a streptozotocin-induced (STZ) diabetic rat model. Adult male Wistar rats were categorized into five groups: control, diabetic, resveratrol-treated (40 mg/kg), liposomal resveratrol (LR)-treated (20 mg/kg) and liposomal resveratrol (LR)-treated (40 mg/kg) for a five-week study period. We compared the effects of LR to those of resveratrol (40 mg/kg) on various parameters, including serum levels of cardiac markers, tissue levels of pro-inflammatory cytokines, nuclear transcription factor, oxidative stress markers, and apoptotic markers. LR treatment in STZ-diabetic rats resulted in notable physiological improvements, including blood glucose regulation, inflammation reduction, oxidative stress mitigation, and apoptosis inhibition. LR effectively lowered oxidative stress and enhanced cardiovascular function. It also demonstrated a remarkable ability to suppress NF-kB-mediated inflammation by inhibiting the pro-inflammatory cytokines TNF-α and IL-6. Additionally, LR restored the antioxidant enzymes, catalase and glutathione peroxidase, thereby effectively counteracting oxidative stress. Notably, LR modulated apoptotic regulators, including caspase, Bcl2, and Bax, suggesting a role in regulating programmed cell death. These biochemical alterations were consistent with improved structural integrity of cardiac tissue as revealed by histological examination. In comparison, resveratrol exhibited lower efficacy at an equivalent dosage. Liposomal resveratrol shows promise in alleviating hyperglycemia-induced cardiac damage in diabetes. Further research is warranted to explore its potential as a therapeutic agent for diabetic cardiovascular complications and possible cardioprotective effects.

Intestinal epithelial Gasdermin C is induced by IL-4R/STAT6 signaling but is dispensable for gut immune homeostasis

Gasdermin C is one of the least studied members of the gasdermin family of proteins, known for their critical involvement in pyroptosis and host defense. Furthermore, evidence for the role of Gasdermin C in the intestine is scarce and partly controversial. Here, we tested the functional role of Gasdermin C in intestinal homeostasis, inflammation and tumorigenesis. : We studied Gasdermin C in response to cytokines in intestinal organoids. We evaluated epithelial differentiation, cell death and immune infiltration under steady state conditions in a new mouse line deficient in Gasdermin C. The role of Gasdermin C was analyzed in acute colitis, infection and colitis-associated cancer. Gasdemin C is highly expressed in the intestinal epithelium and strongly induced by the type 2 cytokines IL-4 and IL-13 in a STAT6-dependent manner. Gasdermin C-deficient mice show no changes in tissue architecture and epithelial homeostasis. Epithelial organoids deficient in Gasdermin C develop normally and show no alterations in proliferation or cell death. No changes were found in models of acute colitis, type 2 intestinal infection and colitis-associated cancer. Gasdermin C genes are upregulated by type 2 immunity, yet appear dispensable for the development of intestinal inflammation, infection and colitis-associated cancer.

Keep neuroinflammation in mind when addressing Alzheimer's disease: A microglia perspective.

This commentary offers a detailed examination of a newly published paper on the effects of small molecule decoys of amyloid-β (Aβ) aggregation on microglial activation. It was discovered that the NSC16224 decoy peptide inhibited proinflammatory cytokines TNFα and IL6 release from microglia in response to Aβ40 and Aβ42 treatment. The research addresses the potential of blocking a sequence of events that lead to the progression of Alzheimer's disease (AD). Here, we discuss the significance of these results in neuroinflammation, highlighting the greater implications for how decoy peptides would be interesting for the research and development of new drugs for AD therapy.

In-Depth Analysis of Olea europaea L. Leaf Extract: Alleviating Pulmonary Histological Disturbances, Pro-Inflammatory Responses, and Oxidative Stress from Isolated or Combined Exposure to Inhaled Toluene and Noise in Rats

The primary objective of this study was to investigate the pulmonary damage resulting from isolated or combined exposure to inhaled toluene (300 ppm) and noise 85 dB (A), with a focus on evaluating the potential protective effects of Olea europaea L. leaf extract (OLE). Forty-eight male Wistar rats were divided into eight groups: control (C), OLE treatment (O), noise exposure (N), noise exposure with OLE treatment (N+OLE), toluene exposure (T), toluene exposure with OLE treatment (T + OLE), co-exposure to toluene and noise (NT), and co-exposure with OLE treatment (NT + OLE). OLE (40 mg/kg/day) was administered daily for six weeks via oral gavage. Exposure to toluene and noise resulted in significant disruption of the pulmonary tissue structure, accompanied by oxidative stress, as evidenced by increased lipid peroxidation, diminished catalase and superoxide dismutase activities, and elevated pro-inflammatory cytokines IL6, IL-β, and TNF-α. Notably, the administration of OLE effectively mitigated oxidative stress and inflammation and preserved pulmonary histology. In conclusion, exposure to toluene and its combination with noise significantly elevated oxidative stress, inflammatory responses, and histological disruptions in the lung tissue. In contrast, noise exposure alone is characterized by minimal effects, although it is still associated with an inflammatory response. Notably, Olea europaea L. leaf extract (OLE) exhibits a substantial protective role, effectively mitigating the adverse effects of combined exposure and highlighting its potential as a therapeutic agent for lung health.

Improvement of RBD-FC Immunogenicity by Using Alum-Sodium Alginate Adjuvant Against SARS-COV-2.

Adjuvants use several mechanisms to boost immunogenicity and to modulate immune response. The strength of adsorption of antigen by adjuvants can be a determinant factor for significant improvement of immunopotentiation. We expressed recombinant RBD-FC in PichiaPink Strain 4 and examined the vaccination of mice by vaccine formulation with different adjuvants (sodium alginate and aluminum hydroxide, alone and together). Sodium alginate significantly increased the immunogenicity and stability of RBD-FC antigen, so RBD-FC formulated with combined alginate and alum (AlSa) and sodium alginate alone showed higher antibody titer and stability. Immunogenicity of RBD-FC:AlSa was determined by serological assays including direct enzyme-linked immunosorbent assay (ELISA) and surrogate virus neutralization test (sVNT). High levels of IgGs and neutralizing antibodies were measured in serum of mice immunized with the RBD-FC:AlSa formulation. On the other hand, cytokines IL-10 and INF-γ were severely accumulated in response to RBD-FC:AlSa, and after 10 days, their accumulation was significantly declined, whereas IL-4 showed the highest and the lowest accumulation in response to alum and alginate, respectively. Our data may suggest that combination of alum and sodium alginate has a better compatibility with RBD-FC in vaccine formulation.

Characterization of interferon-stimulated gene 15 from Bostrychus sinensis: cloning, expression and functional analyses

In this study, the interferon-stimulated gene 15 (referred to as BsISG15) was sequenced and characterized in Bostrychus sinensis. BsISG15 encodes a 155-amino-acid protein weighing ∼17 kDa, featuring two conserved ubiquitin-like domains and an LRGG conjugation motif at the C-terminal. The real-time PCR assays revealed constitutive expression of the BsISG15 gene in all examined organs of healthy B. sinensis, with the peripheral blood showing the highest level of expression. The expression levels of the BsISG15 gene in the head kidney, liver, spleen, and peripheral blood of B. sinensis were significantly altered by both poly (I:C) stimulation and Vibrio parahaemolyticus infection. Western blot analyses showed that the expression of the BsISG15 protein was induced in both the liver and spleen of B. sinensis infected with either poly (I:C) or bacteria, with a concomitant increase in the levels of protein ISGylation, particularly evident in the bacterial-infected liver tissues. Besides, Western blot analyses have demonstrated that head kidney lymphocytes of B. sinensis are capable of secreting the free BsISG15 protein. The recombinant BsISG15 protein significantly increased the production of reactive oxygen species, synthesis of NO, and phagocytosis in macrophages from B. sinensis and also upregulated the expression of proinflammatory cytokine genes (IFNg, IL-1β, IL-6, and IL-8) in these cells. Knockdown of endogenous BsISG15 elevated the expression levels of proinflammatory cytokines IL-1β, IL-6, and IL-8, suggesting a negative regulation of BsISG15 on the inflammatory response in macrophages. The results indicate that BsISG15 plays a significant role in the innate antiviral and antibacterial immunity of B. sinensis.

Berberine attenuates ECM accumulation and the progression of acute liver failure through inhibition of NLRP3 inflammasome signalling

Acute liver failure (ALF) is a life-threatening disease, characterized by upregulated extracellular matrix deposition and inflammatory signalling, with no effective treatment options and targets. The present study was designed to investigate the preventive and therapeutic effects of berberine (BBR) and its underlying mechanism in thioacetamide (TAA)-induced ALF. Male SD rats were administered with TAA 300 mg/kg, i.p., thrice to induce ALF and pre- or post-treated with BBR. To decipher the effects of BBR LFT markers, histopathological analysis of key fibrotic and inflammatory proteins was performed. In addition, the levels of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α were assessed by ELISA. Our work showed TAA-induced ALF animals were associated with increased ALT, AST, bilirubin (LFT markers) and histopathological alterations with profuse infiltration of inflammatory cells in the liver tissue. Treatment with BBR has significantly inhibited LFT markers and histological alterations triggered by TAA. In addition, TAA animals demonstrated increased collagen accumulation and upregulated expression of TGF-β1, vimentin, and α-SMA compared to control. The excessive accumulation of collagen, TGF-β1, vimentin, and α-SMA were significantly modulated with BBR treatment. Further, the fluorescence intensity of ROS an activator of NLRP3 including the NLRP3 inflammasome, and its downstream signalling ASC, cleaved IL-1β, and other pro-inflammatory cytokines like TNF-α and IL-6 stimulated by TAA were attenuated by BBR treatment. The current work indicated that BBR significantly ameliorated TAA-induced ALF by inhibiting the extracellular matrix accumulation associated with the NLRP3/IL-1β signalling pathway and could be a viable therapeutic option to treat ALF and other fibroinflammatory diseases.

Transcriptomic evidence of black soybean ethanolic extract and 2-aminobutyric acid in suppressing neuroinflammation and enhancing synaptic transmission

IntroductionRecently, the awareness of the beneficial utilization of natural bioactive compounds in treating neuroinflammation has gained particular attention. We aimed to understand the anti-neuroinflammatory effect of black soybeans (Glycine max (L.) Merr) ethanolic extract (BBEE) and its bioactive compound, 2-aminobutyric acid (2-AB), against LPS-induced SH-SY5Y cells. MethodCell viability and the optimum therapeutic dose were confirmed by MTT assay. We conducted a whole-transcriptomic analysis of BBEE and 2-AB in LPS-induced SH-SY5Y cells using microarray normalized with SST-RMA. DEGs were selected based on p-value < 0.05 and fold change > 2, and validated by RT-qPCR and immunocytochemical analyses. ResultsWe found that both BBEE and 2-AB down-regulated the expression of inflammatory cytokines IL6 and TNFA under LPS-induced conditions. This was also observed in the microarray data, showing downregulation of several inflammatory pathways, such as NF-kB, and IL6-JAK/STAT3-signaling pathways. In contrast, it upregulated the expression of CALML3, GRIN2, and GRIA2 gene expressions, which influence the AMPK and CAMK2 signaling pathways, indicating the potential of BBEE in neurotransmission and synaptic function. Also, immunofluorescence analysis revealed that 2-AB treatment significantly increased PSD-95 and Ca2+ levels, suggesting its effect on synaptic transmission essential for brain function. ConclusionOur findings suggest the potential anti-neuroinflammatory effects of BBEE and 2-AB, which may offer therapeutic and preventive benefits in mitigating neurological disorders. Given that BB is widely consumed in many Asian countries, our study may encourage its incorporation into the daily diet to slow inflammation-induced neurodegenerative disorders, reduce age-related cognitive decline, and enhance overall brain function.

Jianghua Kucha black tea containing theacrine attenuates depression-like behavior in CUMS mice by regulating gut microbiota-brain neurochemicals and cytokines

Theacrine and theaflavins are known for their potential to mitigate depression and cognitive impairment. Jianghua Kucha black tea (JH) contains both compounds, yet its antidepressant properties are seldom documented. This study evaluated the effects of JH on depression in chronic unpredictable mild stress (CUMS) mice and explored the underlying mechanisms through integrative analyses of gut microbiota and fecal metabolomics. JH was found to significantly alleviate CUMS-induced depression-like behavior by improving body weight, food intake, 1% sucrose preference, immobility time, and numbers of crossings and standings compared to Zhuyeqi black tea (ZYQ), which contains theaflavins. JH notably altered the gut microbiota composition, enriching genera such as Turicibacter, Faecalibaculum, Akkermansia, and Desulfovibrio, while inhibiting genera norank_f__Muribaculaceae and Lactobacillus. Additionally, JH modified the fecal metabolite profile, characterized by increased levels of several secondary bile acids (BAs) and decreased levels of several purine intermediate metabolites. Furthermore, JH upregulated levels of monoamine neurotransmitters (5-HT and DA) and brain-derived neurotrophic factor (BDNF), while downregulating pro-inflammatory cytokines IL-6 and TNF-α in brain tissue. These findings suggested that JH could mitigate CUMS-induced depression-like behavior, potentially by modulating gut microbiota composition and function, as well as brain neurochemicals and cytokines.

Replacing Hydrolyzed Soybean Meal with Recombinant β-Glucosidase Enhances Resistance to Clostridium perfringens in Broilers Through Immune Modulation

Aglycone soy isoflavones have notable immune-regulatory bioactivity, while glycosidic forms in soybean meal pose challenges for absorption. β-Glucosidase (EC 3.2.1.21) catalyzes the non-reducing terminal β-d-glucosidic bonds, releasing β-d-glucan and aglycones. This study evaluated the impact of enzymatically hydrolyzed soybean meal (ESM) using recombinant β-glucosidase from Aspergillus niger on the growth performance and intestinal immune function of broilers under Clostridium perfringens infection. Prior to the feeding trial, soybean meal was enzymatically digested with recombinant β-glucosidase, ensuring almost complete conversion of glycosides to aglycones. After a week of pre-feeding, a total 180 healthy AA broilers were randomly assigned to three groups—control, semi-replacement of ESM (50% ESM), and full-replacement of ESM (100% ESM)—with 6 replicates of 10 chickens, and the trial lasted 28 days. On the 36th day, broilers were challenged with 1 mL of 1 × 1010 CFU/mL Clostridium perfringens (Cp) via gavage for 3 days. The results showed that the substitution of ESM had no effect on the body weight gain of broilers but significantly reduced the feed consumption and feed-to-gain ratio (p &lt; 0.01). The study revealed that Cp significantly disrupted jejunal morphology, while ESM significantly mitigated this damage (p &lt; 0.05). Real-time PCR results demonstrated that compared to the Cp group, ESM restored Cp-induced intestinal barrier impairments (e.g., Occludin, Claudin-1, Muc2), normalized aberrant cellular proliferation (PCNA) and apoptosis (Caspase-1 and Caspase-3), and upregulated the expression of anti-inflammatory factor Il-10 while suppressing pro-inflammatory cytokines (Il-1β, Il-6, and Il-8) (p &lt; 0.05). Moreover, flow cytometry analyses demonstrated that ESM promoted Treg cell-derived Il-10, which alleviated macrophage-derived inflammation. Substituting conventional soybean meal with β-glucosidase, enzymatically treated, significantly reduced feed consumption and alleviated the intestinal damage and immune dysfunctions induced by Clostridium perfringens infection in broilers.

Effect of Trichosanthis Radix Extract on Anti-allergy and Skin Inflammation

This study was conducted to study the effects of TR-W and TR-E on anti-allergy and skin inflammation inhibition. In order to check the concentration used in the experiment and its toxicity to cells, RBL-2H3 cells and HMC-1 cells were treated with TR-W and TR-E at different concentrations and tested at a concentration of 100 mg/ml or less, which does not affect the survival rate. proceeded. In order to determine the effect on the inflammatory response to mast cells, the inflammatory cytokines TNF-α, IL-8, and IL-6 were measured. As a result, TR-W and TR were found in TNF-α and IL-8, which promote the early inflammatory response. -E showed a significant effect at 100 mg/ml, and TR-E showed a significant effect at 50 mg/ml, showing the effect even at a lower concentration than TR-W. IL-6, which is involved in causing allergic dermatitis, showed a significant effect at 100 and 50 mg/ml in TR-W and TRE, indicating that it is effective in suppressing inflammation in TR-W and TR-E. In addition, histamine and β-hexosaminidase, which are inflammatory mediators involved in the initial allergic reaction, were significantly suppressed at 100 and 50 mg/ml in TR-W and TR-E, demonstrating anti-allergy effect. These research results are believed to have the highest utility value as a functional cosmetic material in the future, and additional research is considered necessary.

Evaluation of TNF-α Concentration Level in Al-Najaf Hospitals Patients Infected with Hydatid Cysts

Human echinococcosis is a zoonotic disease caused by a species of medical importance, the Echinococcus granulosus , an etiological agent of cystic echinococcosis (CE). A radiological examination will be performed for these patients to diagnose Echinococcus granulosus parasite by find echinococcal cysts. All of these patients were involved in this study and during the period starting from October 2023 to the end of January 2024, from all ages of patient from both sex (Males and Females At Al-Sader Medical City, AL-Hakeem General Hospital, AL-Haidarya general Hospital and Al-Hayat Hospital. The mean level of TNF-α in patients is 163.27 pg/ml, which is significantly higher than the mean level of 38.58 pg/ml in controls (p-value &lt; 0.001). The prevalence of hydatid disease in Al-Najaf Al-Ashraf in this study was 33%. Levels of the cytokines IL-6, TNF-α, IL-1ß, and IL-4 are more important in patients with Echinococcus granulosus under 40 years of age than in those over 40 years of age.

Cordycepin Alleviates Lipopolysaccharides-Induced Preeclampsia-Like Impairments in Rats

ABSTRACT Introduction Preeclampsia is a serious pregnancy complication that can lead to life-threatening conditions such as seizures, strokes, and even death. A dysregulated inflammatory response in the placenta plays a crucial role in the development of preeclampsia. Cordycepin, known for its anti-inflammatory and antioxidant properties, was the focus of this study, which aimed to investigate its effects on preeclampsia. Methods A preeclampsia-like rat model was established via tail vein injection of lipopolysaccharides (LPS) at a dose of 1 μg/kg in pregnant rats. These rats were then treated with cordycepin at doses of 5, 25, or 50 mg/kg from embryonic day 6 (E6) today 18 (E18). Systolic blood pressures and urinary protein levels were monitored, and pregnancy outcomes, such as fetal body length and weight, were measured. The expression of target genes or proteins was assessed by qPCR, ELISA, and Western blot. Results Our findings revealed that cordycepin significantly reduced systolic blood pressure and proteinuria in preeclampsia-like rats. Additionally, cordycepin improved pregnancy outcomes, as shown by increased fetal body length and weight. The treatment also lowered serum sFlt-1 levels, elevated PIGF levels, decreased placental pro-inflammatory cytokine levels (IL-1β, TNF-α, IL-6, MCP-1, and MIP-2), and raised levels of anti-inflammatory cytokine IL-10 level in preeclampsia-like rats. Furthermore, cordycepin helped restore macrophage population imbalances, increasing M1-type macrophage markers (iNOS, TNF-α, and IL-1β) and reducing M2-type macrophage markers (Arg 1, IL-10, and TGF-β). Conclusion This study suggests that cordycepin alleviates LPS-induced preeclampsia by reducing placental inflammation and correcting the M1/M2 macrophage imbalance, offering potential therapeutic benefits for managing preeclampsia.

Th17 and T Regulatory Cytokines in Serum, Lesional Skin, and Stimulated Peripheral Blood Mononuclear Cell Culture Supernatants from Type 1 Leprosy Reaction Patients

There are conflicting reports regarding the roles of T helper-17 (Th17) and T regulatory (Treg) cells in type 1 leprosy reactions (T1Rs). Also, literature on the correlation of immunological parameters with a validated scoring system and the effect of treatment on cytokines is lacking. Adult patients with untreated T1R and nonreactional spectrum–matched controls were included in the study for comparison of levels of Th17 and Treg pathway cytokines in serum, skin lesions (reactional), and peripheral blood mononuclear cells (PBMCs) culture supernatants. Venous blood samples were collected at baseline and after resolution of reaction (post treatment with nonsteroidal anti-inflammatory drugs [NSAIDs] or steroids) for serum cytokine estimation and PBMC stimulation assays, and lesional (reactional) skin biopsy for cytokine messenger RNA (mRNA) estimation. Thirty-two cases of T1R were recruited (23 patients completed follow-up). Serum levels of cytokines were not significantly different between cases and controls or between pre- and post-treatment samples. Tissue mRNA and Mycobacterium leprae (M. leprae) antigen–stimulated PBMC culture supernatant levels of Interleukin (IL)-17A, IL-17F, IL-6, and IL-23 were significantly higher in T1R than in controls. Levels of IL-10 and Transforming Growth Factor-beta (TGF-β) were comparable among the two groups. The levels of all cytokines were significantly reduced after treatment. There was no significant difference in magnitude of the fall between those treated with steroids versus NSAIDs. This study suggests heightened Th17 response in T1R, with a prominent inability of the regulatory cytokines IL-10 and TGF-β to control the associated inflammation. The dynamics of change after resolution of T1R were comparable between NSAID and oral steroid treatment groups.

Anti-inflammatory effects of para-quinone methide derivatives on ulcerative colitis

A series of para-quinone methide derivatives were evaluated their anti-inflammatory activity. Through the screening of the lipopolysaccharide (LPS)-induced inflammatory cell model in Raw264.7 cells, it was found that the inhibitory activity of meta-substituted derivatives on NO production was superior to that of ortho- and para-substituted derivatives. Among them, in the inflammatory cell model, the meta-trifluoromethyl substituted para-quinone methide derivative 1i had the best activity in inhibiting LPS-induced excess generation of NO. And 1i could effectively inhibit the increase of ROS in inflammatory cells, the expression of iNOS related to the production of NO, and the expressions of inflammation related initiating protein TLR4, pro-inflammatory cytokines IL-6 and TNF-α, inflammasome NLRP3 and Caspase1. In the dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) mouse model, the active derivative 1i could inhibit DSS-induced colon shortening, and reverse DSS-induced pathological changes in colon tissue, such as inflammatory infiltration, structural destruction and crypt disappearance. 1i could effectively inhibit oxidative stress, inflammation and apoptosis in UC mice. Moreover, through the determination of serum biochemical indicators, tissue pathologies and tissue organ indexes, 1i could effectively reverse the damage to mouse liver and kidney caused by DSS, playing a protective role in liver and kidney of mice. In summary, 1i was an effective anti-inflammatory reagent and could be developed as a potential drug for anti-UC.