Over expression of IL-32β- exaggerated myocardial injury after ischemia and reperfusion in mice model

2021 ◽  
Vol 9 (1) ◽  
pp. 110-122
Keyword(s):  
Inflammatory Response ◽  
Myocardial Injury ◽  
Sham Group ◽  
Rna Isolation ◽  
Ischemia And Reperfusion ◽  
Mice Model ◽  
Over Expression ◽  
Tnf Α ◽  
Polymerase Chain ◽  
Necrosis Factor

Interleukin-32 (IL-32) is discovered as proinflammatory cytokine by inducing IL-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α. However, there are unclear data regarding IL-32β associated with worsening of myocardial injury after cardiac ischemia and reperfusion (I/R). In this study, we investigate the prognostic value of IL-32β in inflammatory response after myocardial injury. Anesthetized mice subjected to the myocardial ischemia for 30 min and 2 hours reperfusion. Expression and Regulation of IL-32β were measured by RNA Isolation and Real-Time Polymerase Chain Reaction, inflammatory response in blood and myocardial tissue, were assayed accordingly by ELISA and Western blotting, while Echo for cardiac elements measurement. The I/R group had a significantly higher expression level of IL-32β (0.643±0.012, vs. sham group 0.121±0.013; P<0.05) and associated with worsen myocardial injury, and low cardiac function. In-conclusion, IL-32β might be a new marker associated with adverse event after myocardial injury and may contribute with cardiac remodeling.

scholarly journals Anti-Arthritis Effect through the Anti-Inflammatory Effect of Sargassum muticum Extract in Collagen-Induced Arthritic (CIA) Mice

Molecules ◽  
2019 ◽  
Vol 24 (2) ◽  
pp. 276 ◽  
Author(s):  
Hyelin Jeon ◽  
Weon-Jong Yoon ◽  
Young-Min Ham ◽  
Seon-A Yoon ◽  
Se Kang
Keyword(s):  
Inflammatory Response ◽  
Immunohistochemical Analysis ◽  
Cartilage Destruction ◽  
Sargassum Muticum ◽  
Mice Model ◽  
Articular Damage ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Chronic Autoimmune Disease ◽  
Necrosis Factor

(1) Background: Rheumatoid arthritis is a chronic autoimmune disease that causes progressive articular damage and functional loss. It is characterized by synovial inflammation that leads to progressive cartilage destruction. For this reason, research on functional foods that reduce the inflammatory response are under progress. (2) Methods: We focused on the anti-inflammatory effects of Sargassum muticum, and confirmed the effect of the extract on the collagen-induced arthritis (CIA) DBA/1J mice model. (3) Results: The extract was given at concentrations of 50, 100, and 200 mg/kg, and the arthritis score and edema volume of the experimental group were significantly different from the CIA group. The level of interleukin (IL)-6, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ were determined in serum and lymphocytes. The expression of these cytokines in the serum remarkably decreased from S. muticum extract (SME)100 mg/kg, and decreased from SME 200 mg/kg in lymphocytes. Also, immunohistochemical analysis of IL-6 and TNF-α in the joints revealed that the inflammatory response was noticeably lower when treated with S. muticum extract. (4) Conclusions: This study provides results of the experiment of S. muticum extract treatment in a mouse model. The treatment was found to contribute to the alleviation of edema and symptoms by reducing the expression of inflammatory cytokines. It was concluded that it may be a useful substance to help in the mitigation of arthritis symptoms.

scholarly journals DETEKSI GEN IL-6 DAN TNF-α DENGAN METODE PCR PADA PENDERITA HEPATITIS B DI LABORATORIUM KLINIK MAXIMA KOTA KENDARI

2021 ◽  
Vol 7 (1) ◽  
pp. 21-28
Author(s):  
Sanatang Abbas ◽  
Sri Anggarini Rasyid ◽  
Tiara Mayang Pratiwi Lio
Keyword(s):  
Tumor Necrosis Factor ◽  
Hepatitis B ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Virus Hepatitis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Polymerase Chain ◽  
Necrosis Factor

Penyakit Hepatitis B adalah inflamasi yang terjadi pada organ hati yang dapat disebabkan oleh virus hepatitis B. Pada saat terjadi inflamasi sitokin yang ada dalam tubuh akan merespon atau mengenali jenis patogen berupa virus yang masuk ke dalam tubuh. Tumor Necrosis Factor (TNF-α) adalah salah satu sitokin pro-inflamasi yang berperan dalam proses inflamasi hati, dan Interleukin-6 (IL-6) adalah sitokin yang disekresikan dari jaringan tubuh pada fase infeksi akut atau kronik. Tujuan dari penelitian ini adalah untuk mendeteksi gen TNF-α dan IL-6 pada penderita hepatitis B dengan metode polymerase chain reaction (PCR). Jenis penelitian yang digunakan dalam penelitian ini adalah semi kuantitatif, dengan desain penelitian eksperimental. Populasi pada penelitian adalah seluruh penderita suspek yang melakukan pemeriksaan rapid Hepatitis B (HbsAg) di Laboratorium Klinik Maxima Kota Kendari sebanyak 7 orang. Teknik penarikan sampel menggunakan total sampling dengan kriteria inklusi sampel yaitu pasien yang tidak memiliki riwayat penyakit lain selain hepatitis B. Berdasarkan hasil penelitian diketahui bahwa dari ketujuh sampel penderita hepatitis B yang diperiksa menggunakan metode PCR 3 sampel dengan hasil positif (45%) terhadap gen TNF-α dan 7 (100%) hasil negative terhadap gen Interleukin 6 (IL-6). Sehingga dapat di simpulkan bahwa jenis sitokin yang berperan saat terjadi inflamasi ketika seseorang terinfeksi Virus Hepatitis B adalah Tumor Necrosis Factor Alpha (TNF-α).

scholarly journals Andrographis paniculata and Its Bioactive Diterpenoids Against Inflammation and Oxidative Stress in Keratinocytes

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 530 ◽  
Author(s):  
Eugenie Mussard ◽  
Sundy Jousselin ◽  
Annabelle Cesaro ◽  
Brigitte Legrain ◽  
Eric Lespessailles ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Quantitative Polymerase Chain Reaction ◽  
Andrographis Paniculata ◽  
Ros Production ◽  
Inflammatory Conditions ◽  
Tnf Α ◽  
Dichlorofluorescein Diacetate ◽  
Polymerase Chain ◽  
Factor Α ◽  
Necrosis Factor

Andrographis paniculata was widely used in traditional herbal medicine to treat various diseases. This study explored the potential anti-aging activity of Andrographis paniculata in cutaneous cells. Human, adult, low calcium, high temperature (HaCaT) cells were treated with methanolic extract (ME), andrographolide (ANDRO), neoandrographolide (NEO), 14-deoxyandrographolide (14DAP) and 14-deoxy-11,12-didehydroandrographolide (14DAP11-12). Oxidative stress and inflammation were induced by hydrogen peroxide and lipopolysaccharide/TNF-α, respectively. Reactive oxygen species (ROS) production was measured by fluorescence using a 2′,7′-dichlorofluorescein diacetate (DCFH-DA) probe and cytokines were quantified by ELISA for interleukin-8 (IL-8) or reverse transcription-quantitative polymerase chain reaction (RT-qPCR) for tumor necrosis factor-α (TNF-α). Hyaluronic acid (HA) secretion was determined by an ELISA. Our results show a decrease in ROS production and TNF-α expression by ME (5 µg/mL) in HaCaT under pro-oxidant and pro-inflammatory conditions, respectively. ME protected HaCaT against oxidative stress and inflammation. Our findings confirm that ME can be used for the development of bioactive compounds against epidermal damage.

scholarly journals Shiga Toxin 1-Induced Inflammatory Response in Lipopolysaccharide-Sensitized Astrocytes Is Mediated by Endogenous Tumor Necrosis Factor Alpha

2009 ◽  
Vol 78 (3) ◽  
pp. 1193-1201 ◽  
Author(s):  
Verónica I. Landoni ◽  
Marcelo de Campos-Nebel ◽  
Pablo Schierloh ◽  
Cecilia Calatayud ◽  
Gabriela C. Fernandez ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Tumor Necrosis Factor Alpha ◽  
Shiga Toxin ◽  
Tumor Necrosis ◽  
Brain Inflammation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Hemolytic-uremic syndrome (HUS) is generally caused by Shiga toxin (Stx)-producing Escherichia coli. Endothelial dysfunction mediated by Stx is a central aspect in HUS development. However, inflammatory mediators such as bacterial lipopolysaccharide (LPS) and polymorphonuclear neutrophils (PMN) contribute to HUS pathophysiology by potentiating Stx effects. Acute renal failure is the main feature of HUS, but in severe cases, patients can develop neurological complications, which are usually associated with death. Although the mechanisms of neurological damage remain uncertain, alterations of the blood-brain barrier associated with brain endothelial injury is clear. Astrocytes (ASTs) are the most abundant inflammatory cells of the brain that modulate the normal function of brain endothelium and neurons. The aim of this study was to evaluate the effects of Stx type 1 (Stx1) alone or in combination with LPS in ASTs. Although Stx1 induced a weak inflammatory response, pretreatment with LPS sensitized ASTs to Stx1-mediated effects. Moreover, LPS increased the level of expression of the Stx receptor and its internalization. An early inflammatory response, characterized by the release of tumor necrosis factor alpha (TNF-α) and nitric oxide and PMN-chemoattractant activity, was induced by Stx1 in LPS-sensitized ASTs, whereas activation, evidenced by higher levels of glial fibrillary acid protein and cell death, was induced later. Furthermore, increased adhesion and PMN-mediated cytotoxicity were observed after Stx1 treatment in LPS-sensitized ASTs. These effects were dependent on NF-κB activation or AST-derived TNF-α. Our results suggest that TNF-α is a pivotal effector molecule that amplifies Stx1 effects on LPS-sensitized ASTs, contributing to brain inflammation and leading to endothelial and neuronal injury.

Interleukin-27 attenuates myocardial injury after ischemia-reperfusion through down-regulation of inflammatory response

2021 ◽  
Vol 9 (1) ◽  
pp. 62-75
Author(s):  
Mai HN ◽  
Lee YS
Keyword(s):  
Inflammatory Response ◽  
Ventricular Function ◽  
Myocardial Injury ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Left Ventricular ◽  
Mice Model ◽  
Down Regulation ◽  
Stat Pathway

The proinflammatory cytokines may mediate myocardial dysfunction associated with myocardial injury and inflammatory response is an important process during the pathogenesis of myocardial I/R injury. IL-27, this cytokine is mainly produced by cells of myeloid origin such as monocytes, macrophages, dendritic cells, and microglial cells, in response to stimuli acting through Toll-like receptors. The objective of present study is to assess whether IL-27 can improve ventricular function after myocardial ischemia by down-regulation of inflammatory response. The results demonstrated that the IL-27 markedly attenuated Left Ventricular Function (LVF) in mice model, and reduced plasma level of cTn-I as marker of cardiac injury. Moreover, the IL-27 was associated with up-regulation in both chemokine and cytokines expression following I/R, through down-regulation of activation of JAK/STAT pathway.

scholarly journals Expression of LOXs and MMP-1, 2, 3 by ACL Fibroblasts and Synoviocytes Impact of Coculture and TNF-α

2018 ◽  
Vol 32 (04) ◽  
pp. 352-360 ◽  
Author(s):  
Chunli Wang ◽  
Qingjia Chi ◽  
Chunming Xu ◽  
Kang Xu ◽  
Yanjun Zhang ◽  
...  
Keyword(s):  
Cruciate Ligament ◽  
Cartilage Degradation ◽  
Ligament Injury ◽  
Tnf Α ◽  
Gene And Protein Expression ◽  
Polymerase Chain ◽  
Anterior Cruciate ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor

AbstractThis study aims to confirm the effects of synoviocytes (SCs) on regulating lysyl oxidases (LOXs) and matrix metalloproteinase (MMP)-1, 2, 3 in the normal and injured anterior cruciate ligament (ACL) fibroblasts response to tumor necrosis factor-α(TNF-α). The gene and protein expression levels of LOXs and MMP-1, 2, 3 in SCs cocultured ACL fibroblasts (ACLfs) induced by TNF-α and mechanical injury were analyzed by real-time polymerase chain reaction (PCR) and western bolting; the MMP-2 activity were analyzed by zymography. The results exhibited that TNF-α alone slightly downregulated the expressions of LOXs and upregulated the expression of MMP-1, 2, 3 in both normal and injured ACL fibroblasts. The decrease of LOXs and increase of MMP-1, 2, 3 in ACLfs response to TNF-α were further promoted by coculture. Taken together, these results show for the first time that the crosstalk between ACLfs and SCs could modulate the LOXs and MMP-1, 2, 3 synthesis in ACLfs in the presence of TNF-α. Accumulation of MMPs in the isolated fluid-containing space not only disrupts the balance of ACL healing, but also increases cartilage degradation and accelerates osteoarthritis (OA) in injured joint. Based on this mechanism, targeting inhibition of MMPs could provide a promising therapeutic strategy for acute ligament injury.

TNF-α and intPLA2 genes' polymorphism in anorexia nervosa

2004 ◽  
Vol 16 (6) ◽  
pp. 290-294 ◽  
Author(s):  
Agnieszka Slopien ◽  
Filip Rybakowski ◽  
Monika Dmitrzak-Weglarz ◽  
Piotr Czerski ◽  
Joanna Hauser ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Gene Polymorphism ◽  
Control Group ◽  
Study Group ◽  
Intron 1 ◽  
Tnf Α ◽  
The Mean ◽  
Polymerase Chain ◽  
And Control ◽  
Necrosis Factor

Objective:The aim of this study was the assessment of −308G/A tumor necrosis factor (TNF)-α gene polymorphism and intPLA2 gene polymorphism in patients with anorexia nervosa (AN) and healthy controls.Subjects:We studied 91 non-related patients with AN and 144 healthy women (blood donors and students). The mean age of women from study group was 18.22 years (SD ± 3.13 years) and from control group was 31.71 years (SD ± 8.22).Methods:Gene polymorphisms were studied with the use of polymerase chain reaction-restriction fragment length polymorphism method. TNF-α gene polymorphism consists of G/A substitution in −308 promoter region. IntPLA2 gene polymorphism is related to intron 1, in which restrictive region is found and recognized by BanI enzyme.Results:We did not obtain statistically significant differences in the frequency of genotypes and alleles of −308G/A TNF-α polymorphism between the study and control groups (genotypes: P = 0.106, alleles: P = 0.076). We did analogous analysis in the restrictive and bulimic subgroups. We did not observe statistically relevant differences in the frequency of genotypes (P = 0.700) and alleles (P = 0.305). We did not obtain statistically relevant difference in the frequency of genotypes and alleles of intPLA2 gene between the study group and controls (genotypes: P = 0.300, alleles: P = 0.331). We did analogous analysis in both subgroups of AN. We did not observe statistically relevant differences in the frequency of genotypes (P = 0.344) and alleles (P = 0.230).Conclusions:There was no statistically relevant trend for the association between TNF-α polymorphism and AN. We did not find association between studied polymorphism of intPLA2 gene and risk of AN.

scholarly journals Induction of various cytokines and development of severe mucosal inflammation by cagA gene positive Helicobacter pylori strains

Gut ◽  
1997 ◽  
Vol 41 (4) ◽  
pp. 442-451 ◽  
Author(s):  
Y Yamaoka ◽  
M Kita ◽  
T Kodama ◽  
N Sawai ◽  
K Kashima ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Expression Patterns ◽  
Mucosal Inflammation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Biopsy Specimens ◽  
Tnf Α ◽  
Polymerase Chain ◽  
H Pylori ◽  
Factor Α ◽  
Necrosis Factor

Background—Helicobacter pyloristrains possessing the cagA gene are thought to induce interleukin 8 (IL-8) in gastric mucosa. However, it is still unclear whether a relation exists between the cagA gene and the expression patterns of cytokines other than IL-8.Aims—To investigate the relation between the cagA gene and the production of various cytokine proteins using an enzyme linked immunosorbent assay (ELISA).Patients and methods—In 184 patients, the cagA gene was detected by polymerase chain reaction (PCR), and levels of production of IL-1β, IL-6, IL-7, IL-8, IL-10, and tumour necrosis factor α (TNF-α) in antral biopsy specimens were measured by ELISA.Results—Mucosal levels of IL-1β, IL-6, IL-8, and TNF-α were significantly higher in H pyloripositive than in H pylori negative patients. Furthermore, the mucosal levels of IL-1β and IL-8 were significantly higher in specimens infected with cagApositive strains than in those infected with cagAnegative strains. In H pylori positive patients, the mucosal level of IL-8 was closely correlated with that of IL-1β (p<0.0001), and the mucosal level of IL-6 was closely correlated with that of TNF-α (p<0.0001).Conclusion—These findings suggest that the ability to induce cytokines differs among the strains;cagA+ strains induce various kinds of cytokines and may cause severe inflammation, whereascagA− strains induce IL-8 and IL-1β only weakly and may cause only mild inflammation. However, as most patients infected with the cagA+ strains have gastritis, these strains may not be equivalent to ulcerogenic strains.

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