scholarly journals Malvidin Protects against and Repairs Peptic Ulcers in Mice by Alleviating Oxidative Stress and Inflammation

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3312
Author(s):  
Felipe Leonardo Fagundes ◽  
Quélita Cristina Pereira ◽  
Melina Luzzi Zarricueta ◽  
Raquel de Cássia dos Santos
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Acetic Acid ◽  
Peptic Ulcer ◽  
Gastric Ulcer ◽  
Defense Mechanisms ◽  
Ischemia Reperfusion ◽  
Peptic Ulcers ◽  
Anti Inflammatory ◽  
And Oxidative Stress

Peptic ulcer episodes cause damage to the stomach and intestine, with inflammatory cell infiltration and oxidative stress as the main players. In this study, we investigated the potential of anthocyanidin malvidin for preventive and curative peptic ulcer treatment. The anthocyanidin effects were examined in gastric ulcer mouse models induced by ethanol, non-steroidal anti-inflammatory drugs (NSAIDs), ischemia-reperfusion (IR), acetic acid and duodenal ulcer induced by polypharmacy. Expression levels of oxidative and inflammatory genes were measured to investigate the mechanism of anthocyanin activity. At a dose of 5 mg·kg−1, Malvidin prevented gastric ulcer induction by ethanol, NSAID and repaired the tissue after 6 days of IR. Moreover, the anthocyanidin accelerated the healing of acetic acid-induced ulcer, increased the gene expression of EGF and COX-1, and downregulated MMP-9. Anthocyanin treatment mitigated the effect of polypharmacy on inflammation and oxidative stress observed in the intestine. Additionally, the compound downregulated cytokine expression and TLR4 and upregulated HMOX-1 and IL-10, exhibiting protective activity in the mouse gut. Malvidin thus prevented gastric and duodenal ulcers due to prominent anti-inflammatory and antioxidative effects on the gastrointestinal tract that were related to gene expression modulation and an increase in endogenous defense mechanisms.

Naringenin attenuates cerebral Ischemia-Reperfusion injury through Inhibiting oxidative stress and Inflammation in Diabetic Rats

2021 ◽  
pp. 3751-3756
Author(s):  
Orsu Prabhakar
Keyword(s):  
Oxidative Stress ◽  
Cerebral Infarction ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
Factor Α ◽  
And Oxidative Stress ◽  
Necrosis Factor

Aim: Ischemic stroke is one of the important complications of diabetes. Diabetes exacerbate cerebral injury after ischemia and reperfusion. This study was designed to investigate whether the naringenin has a cerebroprotective action against the ischemic reperfusion injury via anti-oxidant and anti-inflammatory mechanisms in diabetic rats. Diabetes was induced by Streptozocine (50mg/kg) intraperitoneal injection at once. Medial carotid artery occlusion (30 min) and reperfusion (3 hr) was employed to induce cerebral infarction in diabetic rats. The animals were divided in to groups as: normal, sham, ischemia-reperfusion and naringenin treated (50, 100, 150 and 200mg/kg). These were used for evaluation of percentage of cerebral infarction. Further, 200mg/kg dose was selected for the estimation of inflammatory biomarkers such as Tumor necrosis factor-α, Interlukin-6, Interlukin-10 and oxidative stress biomarkers such as malondialdehyde, superoxide dismutase, and catalase were estimated and histopathological changes were studied. Dose dependent reduction in percentage of cerebral infarction was observed in narigenin treated groups. With Naringenin 200mg/kg dose, inflammatory and oxidative stress markers like Tumor necrosis factor-α, Interlukin-6, myeloperoxidase and malondialdehyde levels were distinctively reduced and there was a remarkable increased levels of anti-inflammatory and anti-oxidant markers like Interlukin-10, catalase, and superoxide dismutase. Conclusion: Collectively, these findings demonstrate that the mechanism (s) responsible for a cerebroprotective effect of naringenin against the ischemic reperfusion injury in the diabetic rats involves anti-oxidant and anti-inflammatory actions.

scholarly journals Study on the Influence of Free Radicals and Oxidative Stress on Peptic Ulcers

2019 ◽  
Vol 70 (9) ◽  
pp. 3254-3257
Author(s):  
Germaine Savoiu Balint ◽  
Emeric Toth ◽  
Mihaiela Andoni ◽  
Ioan Demeter ◽  
Claudia Borza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastric Ulcer ◽  
Gastric Carcinoma ◽  
Organ Bath ◽  
Vascular Endothelial ◽  
Peptic Ulcers ◽  
Antioxidant Treatment ◽  
And Oxidative Stress

It can be observed that oxidative stress initiates and aggravates many diseases, including peptic ulcers and gastric carcinoma. An increase in rat mucosal glandular lipid peroxidation (LPO) and superoxide dismutase (SOD) and a decrease in catalase (CAT) levels in gastric ulceration induced by cold retention stress were observed, whereas in patients with ulcerated clinical peptic and gastric carcinoma LPO serum is associated with a decrease in SOD and CAT. It was intended to determine the parameters of oxidative stress in the blood and brain in rats after induction of gastric ulcer, the effect of antioxidant treatment on these parameters and on the appearance of gastric ulcer, determination of correlation between oxidative stress and severity of gastric ulcer in rats and also evaluation of vascular endothelial function by in vitro studies in the organ bath, from rat aortic rings with gastric ulcer vs. normal and others under treatment vs. untreated.

Effects of Off-Pump Versus On-Pump Coronary Artery Bypass Grafting: Apoptosis, Inflammation, and Oxidative Stress

2014 ◽  
Vol 17 (5) ◽  
pp. 271 ◽  
Author(s):  
Murat Bicer ◽  
Tunay Senturk ◽  
Murat Yanar ◽  
Ahmet Tutuncu ◽  
Arzu Yilmaztepe Oral ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion ◽  
Artery Bypass ◽  
Bypass Grafting ◽  
Artery Bypass Grafting ◽  
Cabg Surgery ◽  
Off Pump ◽  
Pump Cabg ◽  
Hs Crp ◽  
And Oxidative Stress

<strong>Background</strong>: It has been suggested that off-pump coronary<br />artery bypass grafting (CABG) surgery reduces myocardial<br />ischemia-reperfusion injury, postoperative systemic<br />inflammatory response, and oxidative stress. The aim of this<br />study was to measure serum malondialdehyde (MDA), highsensitivity<br />C-reactive protein (hs-CRP), M30, and M65 levels<br />and to investigate the relationship between M30 levels and<br />oxidative stress and inflammation in patients undergoing onand<br />off-pump CABG surgery.<br /><strong>Methods</strong>: Fifty patients were randomly assigned to onpump<br />or off-pump CABG surgery (25 patients off-pump and<br />25 on-pump CABG surgery), and blood samples were collected<br />prior to surgery, and 30 minutes, 60 minutes, 6 hours,<br />and 24 hours after CABG surgery.<br /><strong>Results</strong>: Compared to the on-pump group, serum MDA<br />levels at 30 minutes, 60 minutes, 6 hours, and 24 hours after<br />the CABG surgery were significantly lower in the off-pump<br />group (P = .001, P = .001, P = .001, and P = .001, respectively).<br />Serum M30 levels were found to be elevated in both groups,<br />returning to baseline at 24 hours. When compared to baseline,<br />the hs-CRP level reached its peak at 24 hours at 13.28 ±<br />5.32 mg/dL in the on-pump group, and 15.44 ± 4.02 mg/dL<br />in the off-pump group.<br /><strong>Conclusion</strong>: CABG surgery is associated with an increase<br />in inflammatory markers and serum M30 levels, indicating<br />epithelial/endothelial apoptosis in the early period.

LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

2020 ◽  
Vol 17 (4) ◽  
pp. 394-401
Author(s):  
Yuanhua Wu ◽  
Yuan Huang ◽  
Jing Cai ◽  
Donglan Zhang ◽  
Shixi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cell Activity ◽  
Ht22 Cells ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

Neuroprotection of chromobox 7 knockout in the mouse after cerebral ischemia-reperfusion injury via nuclear factor E2-related factor 2/hemeoxygenase-1 signaling pathway

2021 ◽  
pp. 096032712110361
Author(s):  
Hai-Tao Zhang ◽  
Xi-Zeng Wang ◽  
Qing-Mei Zhang ◽  
Han Zhao
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Infarct Size ◽  
Water Content ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion ◽  
Related Factor ◽  
Nuclear Factor ◽  
Cerebral Ischemia Reperfusion ◽  
And Oxidative Stress

Objective To explore the mechanism of chromobox 7 (CBX7)-mediated nuclear factor E2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) signaling pathway in the cerebral ischemia/reperfusion (I/R) injury. Methods The experimental wild-type (WT) and CBX7-/- mice were used to establish cerebral I/R models using the middle cerebral artery occlusion (MCAO) surgery to determine CBX7 levels at different time points after MCAO injury. For all mice, neurological behavior, infarct size, water content, and oxidative stress–related indicators were determined, and transferase (TdT)-mediated dUTP-biotin nick-end labeling (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL)) staining method was employed to observe cell apoptosis, while Western blot to measure the expression of CBX7 and Nrf/HO-1 pathway-related proteins. Results At 6 h, 12 h, 24 h, 3 days, and 7 days after mice with MCAO, CBX7 expression was gradually up-regulated and the peak level was reached at 24 h. Mice in the WT + MCAO group had increased infarct size, with significant increases in the modified neurological severity scores and water content in the brain, as well as the quantity of TUNEL-positive cells. For the oxidative stress-indicators, an increase was seen in the content of MDA (malondial dehyde), but the activity of SOD (superoxide dismutase) and content of GSH-PX (glutathione peroxidase) and CAT (catalase) were decreased; meanwhile, the protein expression of CBX7, HO-1, and nuclear Nrf2 was up-regulated, while the cytoplasmic Nrf2 was down-regulated. Moreover, CBX7 knockout attenuated I/R injury in mice. Conclusion Knockout of CBX7 may protect mice from cerebral I/R injury by reducing cell apoptosis and oxidative stress, possibly via activating the Nrf2/HO-1 pathway.

scholarly journals GLP-1 Analog Liraglutide Improves Vascular Function in Polymicrobial Sepsis by Reduction of Oxidative Stress and Inflammation

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1175
Author(s):  
Johanna Helmstädter ◽  
Karin Keppeler ◽  
Franziska Aust ◽  
Leonie Küster ◽  
Katie Frenis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vascular Function ◽  
Vascular Inflammation ◽  
Cecal Ligation ◽  
Isometric Tension ◽  
Polymicrobial Sepsis ◽  
Dot Blot ◽  
Markers Of Inflammation ◽  
Anti Inflammatory ◽  
And Oxidative Stress

Sepsis causes high mortality in the setting of septic shock. LEADER and other trials revealed cardioprotective and anti-inflammatory properties of glucagon-like peptide-1 (GLP-1) analogs like liraglutide (Lira). We previously demonstrated improved survival in lipopolysaccharide (LPS)-induced endotoxemia by inhibition of GLP-1 degradation. Here we investigate the effects of Lira in the polymicrobial sepsis model of cecal ligation and puncture (CLP). C57BL/6J mice were intraperitoneally injected with Lira (200 µg/kg/d; 3 days) and sepsis induced by CLP after one day of GLP-1 analog treatment. Survival and body temperature were monitored. Aortic vascular function (isometric tension recording), protein expression (immunohistochemistry and dot blot) and gene expression (qRT-PCR) were determined. Endothelium-dependent relaxation in the aorta was impaired by CLP and correlated with markers of inflammation (e.g., interleukin 6 and inducible nitric oxide synthase) and oxidative stress (e.g., 3-nitrotyrosine) was higher in septic mice, all of which was almost completely normalized by Lira therapy. We demonstrate that the GLP-1 analog Lira ameliorates sepsis-induced endothelial dysfunction by the reduction of vascular inflammation and oxidative stress. Accordingly, the findings suggest that the antioxidant and anti-inflammatory effects of GLP-1 analogs may be a valuable tool to protect the cardiovascular system from dysbalanced inflammation in polymicrobial sepsis.

Fetuin-A exerts a protective effect against experimentally induced intestinal ischemia/reperfusion by suppressing autophagic cell death

2021 ◽  
pp. 153537022199520
Author(s):  
Nanees F El-Malkey ◽  
Amira E Alsemeh ◽  
Wesam MR Ashour ◽  
Nancy H Hassan ◽  
Husam M Edrees
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Beclin 1 ◽  
Male Rats ◽  
Fetuin A ◽  
Intestinal Ischemia Reperfusion ◽  
And Oxidative Stress

Intestinal tissue is highly susceptible to ischemia/reperfusion injury in many hazardous health conditions. The anti-inflammatory and antioxidant glycoprotein fetuin-A showed efficacy in cerebral ischemic injury; however, its protective role against intestinal ischemia/reperfusion remains elusive. Therefore, this study investigated the protective role of fetuin-A supplementation against intestinal structural changes and dysfunction in a rat model of intestinal ischemia/reperfusion. We equally divided 72 male rats into control, sham, ischemia/reperfusion, and fetuin-A-pretreated ischemia/reperfusion (100 mg/kg/day fetuin-A intraperitoneally for three days prior to surgery and a third dose 1 h prior to the experiment) groups. After 2 h of reperfusion, the jejunum was dissected and examined for spontaneous contractility. A jejunal homogenate was used to assess inflammatory and oxidative stress enzymes. Staining of histological sections was carried out with hematoxylin, eosin and Masson’s trichrome stain for evaluation. Immunohistochemistry was performed to detect autophagy proteins beclin-1, LC3, and p62. This study found that fetuin-A significantly improved ischemia/reperfusion-induced mucosal injury by reducing the percentage of areas of collagen deposition, increasing the amplitude of spontaneous contraction, decreasing inflammation and oxidative stress, and upregulating p62 expression, which was accompanied by beclin-1 and LC3 downregulation. Our findings suggest that fetuin-A treatment can prevent ischemia/reperfusion-induced jejunal structural and functional changes by increasing antioxidant activity and regulating autophagy disturbances observed in the ischemia/reperfusion rat model. Furthermore, fetuin-A may provide a protective influence against intestinal ischemia/reperfusion complications.

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