Mediterranean meal favorably effects postrandial oxidative stress response compared with a western meal in healthy women

2021 ◽  
Author(s):  
Tuğçe Bulmuş Tüccar ◽  
Gamze Akbulut
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Low Grade ◽  
Necrosis Factor Alpha ◽  
Total Thiol ◽  
Healthy Women ◽  
Meal Intake ◽  
Tnf Α ◽  
Hs Crp ◽  
The Impact

Abstract. Oxidative stress and inflammation are underlying factors in the pathogenesis of chronic diseases. The postprandial state is characterized by low-grade oxidative and inflammatory responses, but the impact of different dietary patterns on these responses is unclear. The objective of this study was to investigate postprandial oxidative and inflammatory responses to Mediterranean diet (MED) and Western diet (WD) meals. In a randomised crossover design, eleven healthy women, aged between 19–45 years with a body mass index of 20.0–24.9 kg/m2, consumed two different isocaloric meals: MED and WD. Blood samples were collected at fasting and 2, 3, 4 h postprandially and analyzed for oxidative [total antioxidant status (TAS), total oxidant status (TOS), total thiol, native thiol, malondialdehyde (MDA)] and inflammatory [high sensitivity C-reactive protein (hs-CRP), interleukin (IL)-6, IL-17, IL-23, tumor necrosis factor alpha (TNF-α) and nuclear factor kappa B (NF-κB)] markers. MED meal intake resulted in increases in TAS (0.05±0.02 mmol/L; p=0.017), total thiol (23.00±7.69 μmol/L; p=0.013) and native thiol (12.82±4.94 μmol/L; p=0.027), while a decrease in MDA (−0.17±0.06 nmol/L; p=0.022) at 2 h. On the other hand, TAS reduced significantly overall (p=0.005) after WD meal intake. There was a significant increase after WD meal intake for IL-6 (1.39±0.49 pg/mL; p=0.017), IL-17 (4.30±1.50 pg/mL; p=0.017), IL-23 (8.38±3.51 pg/mL; p=0.038) at 4 h. However, serum hs-CRP, TNF-α and NF-κB levels were not changed significantly by meal intake. The results indicate that MED meal induces favorable effects on oxidative stress, while WD meal partially increases inflammation in daily life.

Effects of Olive Oil on TNF-α and IL-6 in Humans: Implication in Obesity and Frailty

2017 ◽  
Vol 18 (1) ◽  
pp. 63-74 ◽  
Author(s):  
Nagendra S. Yarla ◽  
Angela Polito ◽  
Ilaria Peluso
Keyword(s):  
Olive Oil ◽  
Inflammatory Responses ◽  
Synergistic Effects ◽  
Mediterranean Area ◽  
Dietary Advice ◽  
Low Grade ◽  
Necrosis Factor Alpha ◽  
Potential Implication ◽  
Healthy Behaviors ◽  
Tnf Α

Background and Objective: Tumor necrosis factor-alpha (TNF)-α and interleukin (IL)-6 are important mediators of chronic low-grade systemic inflammation. The latter plays a central role in several obesity-related pathologies, such as diabetes, metabolic syndrome and cardiovascular diseases. Besides, these cytokines have been also implicated in geriatric and cancer-induced anorexia, cachexia, sarcopenia and frailty. Potential interventions for both obesity and frailty include dietary advice and nutraceuticals. In this context, the consumption of olive oil (OO) has been associated with the health effects of the Mediterranean diet (Med-diet). This review is aimed to discuss the OO-mediated modulation of TNF- α and IL-6 in human studies and the potential implication in obesity and frailty. Results: The reviewed studies suggest that the improvement of postprandial TNF-α and IL-6 observed with OO consumption is affected by body mass index (BMI). The effects on TNF-α and IL-6 after medium and long-term consumptions involved many factors and the cross-talk between adipose tissue, liver, skeletal muscle and brain. Major anti-inflammatory effects were observed when OO was consumed with Med-diet, which is associated with healthy behaviors. In this context, the role of microbioma- polyphenols, diet-gene and exercise-gene interactions in the effects of OO on immune-mediated inflammatory responses involved in obesity and frailty deserves further investigation. Conclusion: Further studies are needed to clarify the effect of OO net of possible synergistic effects with other dietary and lifestyle factors of Mediterranean area.

scholarly journals Oxidative Stress Is Increased in Combined Oral Contraceptives Users and Is Positively Associated with High-Sensitivity C-Reactive Protein

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1070
Author(s):  
Sabina Cauci ◽  
Serena Xodo ◽  
Cinzia Buligan ◽  
Chiara Colaninno ◽  
Mattia Barbina ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Sensitivity ◽  
Low Grade ◽  
Strong Positive Correlation ◽  
Obese Women ◽  
C Reactive Protein ◽  
Oxidative Stress Biomarkers ◽  
Free Oxygen Radical ◽  
Reactive Protein ◽  
Healthy Women

Information concerning the mechanisms underlying oxidative stress and low-grade inflammation in young healthy women predisposing eventually to future diseases is scarce. We investigated the relationship of oxidative stress and high-sensitivity C-reactive protein (hsCRP) in fertile-age women by oral combined contraceptive (OC) use. Caucasian Italian healthy non-obese women (n = 290; 100 OC-users; 190 non-OC-users; mean age 23.2 ± 4.7 years) were analyzed. Blood hydroperoxides, as oxidative stress biomarkers, were assessed by Free Oxygen Radical Test (FORT). Serum hsCRP was determined by an ultra-sensitive method (hsCRP). Markedly elevated oxidative stress (≥400 FORT Units) was found in 77.0% of OC-users and 1.6% of non-OC-users, odds ratio (OR) = 209, 95% CI = 60.9–715.4, p < 0.001. Elevated hsCRP levels ≥ 2.0 mg/L, considered risky for cardiovascular diseases (CVDs), were found in 41.0% of OC-users and 9.5% of non-OC-users, OR = 6.6, 95%CI 3.5–12.4, p < 0.001. Hydroperoxides were strongly positively correlated to hsCRP in all women (rs = 0.622, p < 0.001), in OC-users (rs = 0.442, p < 0.001), and in non-OC-users (rs = 0.426, p < 0.001). Women with hydroperoxides ≥ 400 FORT Units were eight times as likely to have hsCRP ≥ 2 mg/L. In non-OC-users only, hydroperoxides values were positively correlated with weight and body mass index, but negatively correlated with red meat, fish and chocolate consumption. Our research is the first finding a strong positive correlation of serum hydroperoxides with hsCRP, a marker of low-grade chronic inflammation, in young healthy women. Further research is needed to elucidate the potential role of these two biomarkers in OC-use associated side-effects, like thromboembolism and other CVDs.

scholarly journals The Role of TNF-α and Anti-TNF-α Agents during Preconception, Pregnancy, and Breastfeeding

2021 ◽  
Vol 22 (6) ◽  
pp. 2922
Author(s):  
Katarzyna Romanowska-Próchnicka ◽  
Anna Felis-Giemza ◽  
Marzena Olesińska ◽  
Piotr Wojdasiewicz ◽  
Agnieszka Paradowska-Gorycka ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
First Trimester ◽  
Endocrine Function ◽  
Necrosis Factor Alpha ◽  
Hormone Synthesis ◽  
Migratory Activity ◽  
Immune System Diseases ◽  
Tnf Α ◽  
The Impact ◽  
In Pregnancy

Tumor necrosis factor-alpha (TNF-α) is a multifunctional Th1 cytokine and one of the most important inflammatory cytokines. In pregnancy, TNF-α influences hormone synthesis, placental architecture, and embryonic development. It was also shown that increased levels of TNF-α are associated with pregnancy loss and preeclampsia. Increased TNF-α levels in complicated pregnancy draw attention to trophoblast biology, especially migratory activity, syncytialisation, and endocrine function. Additionally, elevated TNF-α levels may affect the maternal-fetal relationship by altering the secretory profile of placental immunomodulatory factors, which in turn affects maternal immune cells. There is growing evidence that metabolic/pro-inflammatory cytokines can program early placental functions and growth in the first trimester of pregnancy. Furthermore, early pregnancy placenta has a direct impact on fetal development and maternal immune system diseases that release inflammatory (e.g., TNF-α) and immunomodulatory factors, such as chronic inflammatory rheumatic, gastroenterological, or dermatological diseases, and may result in an abnormal release of cytokines and chemokines in syncytiotrophoblasts. Pregnancy poses a challenge in the treatment of chronic disease in patients who plan to have children. The activity of the disease, the impact of pregnancy on the course of the disease, and the safety of pharmacotherapy, including anti-rheumatic agents, in pregnancy should be considered.

scholarly journals Fourteen days of smoking cessation improves muscle fatigue resistance and reverses markers of systemic inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mohammad Z. Darabseh ◽  
Thomas M. Maden-Wilkinson ◽  
George Welbourne ◽  
Rob C. I. Wüst ◽  
Nessar Ahmed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Smoking Cessation ◽  
Muscle Fatigue ◽  
Fatigue Resistance ◽  
Systemic Inflammation ◽  
Muscle Function ◽  
Low Grade ◽  
Skeletal Muscle Function ◽  
Tnf Α

AbstractCigarette smoking has a negative effect on respiratory and skeletal muscle function and is a risk factor for various chronic diseases. To assess the effects of 14 days of smoking cessation on respiratory and skeletal muscle function, markers of inflammation and oxidative stress in humans. Spirometry, skeletal muscle function, circulating carboxyhaemoglobin levels, advanced glycation end products (AGEs), markers of oxidative stress and serum cytokines were measured in 38 non-smokers, and in 48 cigarette smokers at baseline and after 14 days of smoking cessation. Peak expiratory flow (p = 0.004) and forced expiratory volume in 1 s/forced vital capacity (p = 0.037) were lower in smokers compared to non-smokers but did not change significantly after smoking cessation. Smoking cessation increased skeletal muscle fatigue resistance (p < 0.001). Haemoglobin content, haematocrit, carboxyhaemoglobin, total AGEs, malondialdehyde, TNF-α, IL-2, IL-4, IL-6 and IL-10 (p < 0.05) levels were higher, and total antioxidant status (TAS), IL-12p70 and eosinophil numbers were lower (p < 0.05) in smokers. IL-4, IL-6, IL-10 and IL-12p70 had returned towards levels seen in non-smokers after 14 days smoking cessation (p < 0.05), and IL-2 and TNF-α showed a similar pattern but had not yet fully returned to levels seen in non-smokers. Haemoglobin, haematocrit, eosinophil count, AGEs, MDA and TAS did not significantly change with smoking cessation. Two weeks of smoking cessation was accompanied with an improved muscle fatigue resistance and a reduction in low-grade systemic inflammation in smokers.

Abstract 14849: Gender Differences in Impact of CYP2C19 Polymorphism and Low Grade Inflammation on Coronary Spasm in Patients with Vasospastic Angina (VSA)

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tomonori Akasaka ◽  
Seiji Hokimoto ◽  
Noriaki Tabata ◽  
Kenji Sakamoto ◽  
Kenichi Tsujita ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Coronary Artery Spasm ◽  
Coronary Spasm ◽  
Control Group ◽  
Low Grade ◽  
Cyp2c19 Genotype ◽  
Loss Of Function ◽  
Hs Crp ◽  
The Impact ◽  
Low Grade Inflammation

Background: Several cytochrome P450 (CYP) enzyme families have been identified in extra hepatic tissues such as heart, vasculature, kidney, and lung. CYP2C19 localized in vascular smooth muscle and endothelium contributes to the regulation of vascular tone and homeostasis. However, it is unknown whether CYP2C19 genotype is associated with the vascular tonus in patients with VSA. The aim of this study was to examine the impact of CYP2C19 genotype on coronary artery spasm in patients with VSA. Methods: We examined the distribution of CYP2C19 genotype in patients with VSA (n=129) who were diagnosed by intra-coronary acetylcholine infusion test and healthy subjects (n=455) as control group. CYP2C19 genotypes were divided into 3 groups; (1) CYP2C19*1/*1: EM, (2) one loss-of-function allele (*1/*2, *1/*3: IM), and (3) two loss-of-function alleles (*2/*2, *2/*3, *3/*3: PM). Moreover, we measured the level of high-sensitive CRP (hs-CRP) as a degree of low glade inflammation in each group. Results: The ratios of CYP2C19 genotype (EM, IM, and PM) were 30, 42, and 28% in VSA group, and 32, 49, and 19% in control group. In short, PM frequency was significantly higher in VSA than in control (28% vs 19%, P=0.026). In VSA group, the ratios of CYP2C19 genotype were 36, 44, and 20% in male, and 20, 39, and 41% in female, respectively. Briefly, the PM frequency was significantly higher in female than in male (41% vs 20%, P<0.001). Moreover, the level of hs-CRP was significantly higher in VSA group than in control group (0.17±0.367 vs 0.10.±0.240, P=0.02). When patients were stratified by gender, the level of hs-CRP was significantly higher in VSA group in female (0.11±0.198 vs 0.06±0.105, P=0.031) and male (0.20±0.438 vs 0.12±0.277, P=0.044). Multivariate analysis for coronary spasm indicated high age, hypertension, and high level of hs-CRP as predictive factors among all subjects. PM is a predictive factor for coronary spasm in female group only (OR3.1, 95%RI 1.525-6.317, P=0.002), but not in male (OR0.829, 95%RI 0.453-1.518, P=0.543). Conclusion: The CYP2C19 two loss-of-function alleles (PM) and low grade inflammation may be associated with pathophysiology of coronary artery spasm and the regulation of coronary tonus, especially in female.

Oxydative stress markers and cytokine levels in rosuvastatin-medicated hypercholesterolemia patients

2018 ◽  
Vol 44 (4) ◽  
pp. 530-538
Author(s):  
Aysun Çetin ◽  
İhsan Çetin ◽  
Semih Yılmaz ◽  
Ahmet Şen ◽  
Göktuğ Savaş ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Interleukin 1 ◽  
Paraoxonase 1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Phenotypic Effect ◽  
Necrosis Factor Alpha ◽  
Stress Markers ◽  
Tnf Α ◽  
Before And After

Abstract Background Limited research is available concerning the relationship between oxidative stress and inflammation parameters, and simultaneously the effects of rosuvastatin on these markers in patients with hypercholesterolemia. We aimed to investigate the connection between cytokines and oxidative stress markers in patients with hypercholesterolemia before and after rosuvastatin treatment. Methods The study consisted of 30 hypercholesterolemic patients diagnosed with routine laboratory tests and 30 healthy participants. The lipid parameters, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), paraoxonase-1 (PON1) and malondialdehyde (MDA) levels in controls and patients with hypercholesterolemia before and after 12-week treatment with rosuvastatin (10 mg/kg/day), were analyzed by means of enzyme-linked immunosorbent assay. Results It was found that a 12-week cure with rosuvastatin resulted in substantial reductions in IL-1β, IL-6 and TNF-α and MDA levels as in rising activities of PON1 in patients with hypercholesterolemia. Before treatment, the PON1 levels were significantly negatively correlated with TNF-α and IL-6 in control group, while it was positively correlated with TNF-α in patients. Conclusion Our outcomes provide evidence of protected effect of rosuvastatin for inflammation and oxidative damage. It will be of great interest to determine whether the correlation between PON1 and cytokines has any phenotypic effect on PON1.

scholarly journals Oral Mucosal Endotoxin Tolerance Induction in Chronic Periodontitis

2005 ◽  
Vol 73 (2) ◽  
pp. 687-694 ◽  
Author(s):  
Manoj Muthukuru ◽  
Ravi Jotwani ◽  
Christopher W. Cutler
Keyword(s):  
Immune Response ◽  
Oral Mucosa ◽  
Chronic Periodontitis ◽  
Intracellular Signaling ◽  
Inflammatory Responses ◽  
Endotoxin Tolerance ◽  
Necrosis Factor Alpha ◽  
Initial Stimulus ◽  
Tlr4 Mrna ◽  
Tnf Α

ABSTRACT The oral mucosa is exposed to a high density and diversity of gram-positive and gram-negative bacteria, but very little is known about how immune homeostasis is maintained in this environment, particularly in the inflammatory disease chronic periodontitis (CP). The cells of the innate immune response recognize bacterial structures via the Toll-like receptors (TLR). This activates intracellular signaling and transcription of proteins essential for the induction of an adaptive immune response; however, if unregulated, it can lead to destructive inflammatory responses. Using single-immunoenzyme labeling, we show that the human oral mucosa (gingiva) is infiltrated by large numbers of TLR2+ and TLR4+ cells and that their numbers increase significantly in CP, relative to health (P < 0.05, Student's t test). We also show that the numbers of TLR2+ but not TLR4+ cells increase linearly with inflammation (r 2 = 0.33, P < 0.05). Double-immunofluorescence analysis confirms that TLR2 is coexpressed by monocytes (MC)/macrophages (mφ) in situ. Further analysis of gingival tissues by quantitative real-time PCR, however, indicates that despite a threefold increase in the expression of interleukin-1β (IL-1β) mRNA during CP, there is significant (30-fold) downregulation of TLR2 mRNA (P < 0.05, Student's t test). Also showing similar trends are the levels of TLR4 (ninefold reduction), TLR5 (twofold reduction), and MD-2 (sevenfold reduction) mRNA in CP patients compared to healthy persons, while the level of CD14 was unchanged. In vitro studies with human MC indicate that MC respond to an initial stimulus of lipopolysaccharide (LPS) from Porphyromonas gingivalis (PgLPS) or Escherichia coli (EcLPS) by upregulation of TLR2 and TLR4 mRNA and protein; moreover, IL-1β mRNA is induced and tumor necrosis factor alpha (TNF-α), IL-10, IL-6, and IL-8 proteins are secreted. However, restimulation of MC with either PgLPS or EcLPS downregulates TLR2 and TLR4 mRNA and protein and IL-1β mRNA and induces a ca. 10-fold reduction in TNF-α secretion, suggesting the induction of endotoxin tolerance by either LPS. Less susceptible to tolerance than TNF-α were IL-6, IL-10, and IL-8. These studies suggest that certain components of the innate oral mucosal immune response, most notably TLRs and inflammatory cytokines, may become tolerized during sustained exposure to bacterial structures such as LPS and that this may be one mechanism used in the oral mucosa to attempt to regulate local immune responses.

scholarly journals The Impact of Oxidative Stress on Dental Implants

2021 ◽  
Vol 2 (1) ◽  
pp. 1-8
Author(s):  
César Esquivel-Chirino ◽  
Juan Carlos Gómez-Landeros ◽  
Erika Patricia Carabantes-Campos ◽  
Daniela Carmona-Ruiz ◽  
Yolanda Valero-Princet ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dental Implants ◽  
Alveolar Bone ◽  
Inflammatory Responses ◽  
Cell Damage ◽  
Pathological Condition ◽  
Periodontal Diseases ◽  
Tissue Destruction ◽  
Waste Products ◽  
The Impact

Periodontal disease is an inflammatory condition that alters the periodontium, resulting in destruction of the alveolar bone; without treatment the condition may lead to tooth loss. Dental implants are an alternative for substitution of naturally lost teeth as they have high success rates; however, some factors are related to its failure. Peri-implantitis (PI) is a pathological condition that affects the tissues surrounding dental implants and has been reported as the major cause of implant failure; PI and periodontal diseases are characterized by tissue inflammation and bone damage. In homeostasis conditions, reactive oxygen species (ROS) have been shown to be involved in cell maintenance, signal transduction, and repair of all tissues, but ROS overaccumulation leads to oxidative stress, which generates cell damage and tissue destruction; likewise, antioxidants protect against the destructive effects of ROS by turning free radicals into waste products. The main purpose of this review was to determine some aspects of inflammatory responses and oxidative stress and analyze their relationship with the lack of osseointegration and PI.

scholarly journals KORELASI KADAR HIGH SENSITIVITY C-REACTIVE PROTEIN DENGAN KADAR LOW DENSITY LIPOPROTEIN PADA PENYANDANG OBES

2020 ◽  
Vol 5 (3) ◽  
pp. 676
Author(s):  
Rama Dhanivita Djamin
Keyword(s):  
Interleukin 1 ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Sensitivity ◽  
Low Grade ◽  
Low Density ◽  
C Reactive Protein ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Hs Crp

<p><em>Obesitas terjadi karena akumulasi lemak berlebih di dalam tubuh. Akumulasi lemak menimbulkan low grade inflammation pada jaringan adiposa, menyebabkan peningkatan sitokin inflamasi seperti tumor necrosis factor-alpha, interleukin-1 beta, dan interleukin-6 (IL-6). Peningkatan sekresi IL-6 merangsang hepar meningkatkan produksi protein fase akut. High sensitivity C-reactive protein (hs-CRP) sebagai penanda inflamasi merupakan protein fase akut. Low density lipoprotein (LDL-kolesterol) adalah lipoprotein yang paling banyak mengandung kolesterol. Peningkatan kadar hs-CRP dan kadar LDL-kolesterol pada obesitas diidentifikasi sebagai faktor risiko aterosklerosis. Penelitian ini bertujuan menganalisis hubungan hs-CRP dengan LDL-kolesterol pada penyandang obes, merupakan penelitian analitik rancangan potong lintang dilakukan  September 2018 sampai Agustus 2019. Kadar hs-CRP diperiksa dengan metode enzyme linked immunoassay (ELISA), sedangkan kadar LDL-kolesterol dengan metode kalkulasi (rumus Friedewald). Uji korelasi Spearman digunakan untuk menganalisi data, jika didapatkan nilai p&lt;0,05 korelasi dinyatakan bermakna. Subjek penelitian berjumlah 26 penyandang obes terdiri dari 6 laki-laki (23,1%) dan 20 perempuan (76,9%). Rerata umur subjek penelitian adalah 36,46(7,68) tahun. Rerata kadar hs-CRP dan kadar LDL-kolesterol adalah 5,08(1,28) mg/L dan  154,69(45,8) mg/dL. Analisis korelasi menunjukkan korelasi positif lemah dan tidak bermakna secara statistik antara kadar hs-CRP dengan kadar LDL-kolesterol (r= 0,333, p=0,096). Simpulan: Terdapat korelasi positif lemah antara kadar hs-CRP dengan kadar LDL-kolesterol pada penyandang obes.</em></p><p><strong><em>Kata kunci</em></strong><em>: </em><em>Obesitas, High Sensitivity C-Reactive, Low Density Lipoprotein</em><em></em></p>

scholarly journals IL-23 Promotes Myocardial I/R Injury by Increasing the Inflammatory Responses and Oxidative Stress Reactions

2016 ◽  
Vol 38 (6) ◽  
pp. 2163-2172 ◽  
Author(s):  
Xiaorong Hu ◽  
Ruisong Ma ◽  
Jiajia Lu ◽  
Kai Zhang ◽  
Weipan Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Tunel Staining ◽  
Ischemia And Reperfusion ◽  
Stress Reactions ◽  
Sprague Dawley ◽  
Sod Activity ◽  
Myocardial Ischemia And Reperfusion ◽  
Tnf Α ◽  
And Oxidative Stress

Background/Aims: Inflammation and oxidative stress play an important role in myocardial ischemia and reperfusion (I/R) injury. We hypothesized that IL-23, a pro-inflammatory cytokine, could promote myocardial I/R injury by increasing the inflammatory response and oxidative stress. Methods: Male Sprague-Dawley rats were randomly assigned into sham operated control (SO) group, ischemia and reperfusion (I/R) group, (IL-23 + I/R) group and (anti-IL-23 + I/R) group. At 4 h after reperfusion, the serum concentration of lactate dehydrogenase (LDH), creatine kinase (CK) and the tissue MDA concentration and SOD activity were measured. The infarcte size was measured by TTC staining. Apoptosis in heart sections were measured by TUNEL staining. The expression of HMGB1 and IL-17A were detected by Western Blotting and the expression of TNF-α and IL-6 were detected by Elisa. Results: After 4 h reperfusion, compared with the I/R group, IL-23 significantly increased the infarct size, the apoptosis of cardiomyocytes and the levels of LDH and CK (all P < 0.05). Meanwhile, IL-23 significantly increased the expression of eIL-17A, TNF-α and IL-6 and enhanced both the increase of the MDA level and the decrease of the SOD level induced by I/R (all P<0.05). IL-23 had no effect on the expression of HMGB1 (p > 0.05). All these effects were abolished by anti-IL-23 administration. Conclusion: The present study suggested that IL-23 may promote myocardial I/R injury by increasing the inflammatory responses and oxidative stress reaction.

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