scholarly journals Eff ects of hemin, a heme oxygenase-1 inducer in L-arginine-induced acute pancreatitis and associated lung injury in adult male albino rats

2017 ◽  
Vol 51 (1) ◽  
pp. 20-30 ◽  
Author(s):  
N. M. Aziz ◽  
M. Y. Kamel ◽  
R. A. Rifaai
Keyword(s):  
Acute Pancreatitis ◽  
Heme Oxygenase ◽  
Adult Male ◽  
Antioxidant Properties ◽  
Pulmonary Complications ◽  
Control Group ◽  
Albino Rats ◽  
Heme Oxygenase 1 ◽  
Inflammatory Disorder ◽  
Pre Treatment

AbstractObjective. The aim of the current study was to assess the protective outcome of hemin, a heme oxygenase-1 (HO-1) inducer on L-arginine-induced acute pancreatitis in rats. Acute pancreatitis (AP) is considered to be a critical inflammatory disorder with a major impact on the patient health. Various theories have been recommended regarding the pathophysiology of AP and associated pulmonary complications.Methods. Twenty-four adult male albino rats were randomly divided into four groups: control group, acute pancreatitis (AP), hemin pre-treated AP group, and hemin post-treated AP group.Results. Administration of hemin before induction of AP significantly attenuated the L-arginine- induced pancreatitis and associated pulmonary complications characterized by the increasing serum levels of amylase, lipase, tumor necrosis factor-α, nitric oxide, and histo-architectural changes in pancreas and lungs as compared to control group. Additionally, pre-treatment with hemin significantly compensated the deficits in total antioxidant capacities and lowered the elevated malondialdehyde levels observed with AP. On the other hand, post-hemin administration did not show any protection against L-arginine-induced AP.Conclusions. The current study indicates that the induction of HO-1 by hemin pre-treatment significantly ameliorated the L-arginine-induced pancreatitis and associated pulmonary complications may be due to its anti-inflammatory and antioxidant properties.

scholarly journals The Potential Role of Hemopexin and Heme Oxygenase-1 Inducer in a Model of Sepsis

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Passainte S. Hassaan ◽  
Radwa A. Mehanna ◽  
Abeer E. Dief
Keyword(s):  
Severe Sepsis ◽  
Heme Oxygenase ◽  
Histopathological Examination ◽  
Survival Rates ◽  
Cecal Ligation ◽  
Lung Parenchyma ◽  
Control Group ◽  
Albino Rats ◽  
Heme Oxygenase 1 ◽  
Sepsis Induction

Background and Aims. Sepsis can evoke disseminated intravascular coagulation, resulting in multiple organ failure and death. Heme oxygenase-1 (HO-1) and hemopexin (HPx) can mediate cytoprotective mechanisms against these deleterious effects. This study aims to determine a role for HO-1 and HPx in coagulopathy induced by septic inflammation and define whether they can enhance the production of anti-inflammatory cytokine IL-10. Materials and Methods. 48 healthy male albino rats were divided equally into 4 groups: control group: animals subjected to laparotomy and bowel manipulation; CLP group: severe sepsis induced by cecal ligation puncture (CLP); CLP + hemin group: animals received single intraperitoneal injection of hemin (50 µmol/kg) 12 h before sepsis induction; CLP + HPx group: animals received single HPx dose (150 µg/rat, i.v.) 30 min before sepsis induction. Survival rates were calculated. Prothrombin time (PT), activated partial thromboplastin time (APTT), and activated protein C (APC), liver HO-1, serum, and liver IL-10 levels were measured, 48 hrs after sepsis induction. Liver and lung were excised for histopathological examination. Results. Hemin and HPx administration upregulated liver HO-1 and IL-10. They prolonged PT, PTT and increased APC. They reduced the inflammatory infiltrate and thrombosis in liver and lung parenchyma. However, hemin was superior in controlling coagulopathy and HO-1 production, while HPx was more potent stimulant of IL-10 expression. Conclusions. Hemin and HPx have a potential beneficial effect in severe sepsis regarding coagulopathy and inflammation.

scholarly journals Evaluation of the role of captopril on clozapine-induced cardiotoxicity and hematotoxicity in adult male albino rats

2017 ◽  
Vol 1 ◽  
pp. 239784731769653
Author(s):  
Omaima I Abdel Hamid ◽  
Marwa G Ahmed ◽  
Hanan MA Hassaneine ◽  
Hayam E Rashed
Keyword(s):  
Bone Marrow ◽  
Adult Male ◽  
Troponin I ◽  
Complete Blood Count ◽  
Enzyme Inhibitor ◽  
Protective Action ◽  
Antioxidant Properties ◽  
Control Group ◽  
Albino Rats ◽  
Group I

Clozapine (CLZ) is considered the most effective drug in treatment of resistant schizophrenia. However, its cardiotoxic effect has raised concerns about its safety. Captopril is a well-known angiotensin-converting enzyme inhibitor with unique antioxidant properties. The aim of this study was to investigate the protective effect of captopril against CLZ-induced myocarditis, and since both drugs have hematotoxic effects, this study aimed to clarify the effect of their combined use on the bone marrow. The study was conducted for 4 weeks on 50 adult male albino rats divided into five groups: group I (negative control), group II (positive control), group III treated with captopril 5 mg/kg/day, group IV treated with CLZ 25 mg/kg/day, and group V treated with captopril (5 mg/kg) 1 hour before CLZ (25 mg/kg/day). CLZ group showed a significant increase in serum troponin I, marked histopathological changes, and immunohistochemical staining of DNA degradation product 8-hydroxy-2-deoxy guanosine (8-OHdG). It significantly increased malondialdehyde level and decreased glutathione peroxidase. Captopril coadministration decreased the histopathological hallmarks and biochemical marker of myocarditis and attenuated CLZ effects on the oxidative stress parameters and 8-OHdG, suggesting its protective action against CLZ-induced myocarditis. Complete blood count and bone marrow evaluation was normal indicating that captopril, in the protective dose given, didn’t increase the risk of CLZ-induced hematotoxicity

scholarly journals Evaluation of the heme oxygenase-1 expression in esophagitis and esophageal cancer induced by different reflux experimental models and diethylnitrosamine

2010 ◽  
Vol 25 (3) ◽  
pp. 304-310 ◽  
Author(s):  
Cleber Rosito Pinto Kruel ◽  
Luis Felipe Ribeiro Pinto ◽  
Tania Cristina Moita Blanco ◽  
Theresa Christina Barja-Fidalgo ◽  
Levi Lourenzo Melo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Experimental Model ◽  
Heme Oxygenase ◽  
Inflammatory Cells ◽  
Acid Reflux ◽  
Experimental Models ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Duodenal Reflux ◽  
Esophageal Carcinogenesis

PURPOSE: To study the expression of heme-oxygenase-1 (HO-1), an enzyme induced by oxidative stress, in specimens obtained from an experimental model in rats that evaluated the role of gastric and duodenal reflux in esophageal carcinogenesis. METHODS: Esophageal specimens embedded in paraffin obtained from different experimental groups of rats were used for immunohistochemistry analysis of HO-1 expression. The rats had been divided into the following groups and were killed after 22 weeks: (1) cardioplasty to induce acid reflux; (2) esophagoduodenal anastomosis to induce duodenal reflux; (3) no treatment; (4) cardioplasty + diethylnitrosamine (DEN); (5) esophagoduodenal anastomosis + DEN; and (6) DEN. The study sample comprised 3 specimens from each group with the most severe histopathological lesions found on each study branch. RESULTS: The expression of HO-1 was seen only in rat specimens submitted to esophagoduodenal anastomosis (Groups 2 and 5), and the analysis of mean fluorescence intensity revealed a significant increase of HO-1 expression (4.8 and 4.6 fold, respectively) when compared with the control group (Group 3) (p<0.05). The main target for HO-1 induction was the inflammatory cells inside the tumor or in subepithelial areas. Rats exposed to gastric reflux had no HO-1 expression. CONCLUSION: Reflux esophagitis induced by reflux of duodenal contents, which provoked considerable oxidative stress, may play an important role in esophageal carcinogenesis. Acid reflux did not induce oxidative stress in this experimental model.

scholarly journals Heme oxygenase-1 is induced in peripheral blood mononuclear cells of patients with acute pancreatitis: a potential therapeutic target

2011 ◽  
Vol 300 (1) ◽  
pp. G12-G20 ◽  
Author(s):  
Aida Habtezion ◽  
Raymond Kwan ◽  
Alice L. Yang ◽  
Maureen E. Morgan ◽  
Ehsaan Akhtar ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Heme Oxygenase ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Ex Vivo ◽  
Therapeutic Benefit ◽  
Heme Oxygenase 1 ◽  
Potential Therapeutic Target ◽  
Peripheral Blood Mononuclear ◽  
Mouse Splenocytes

Heme oxygenase-1 (HO-1) induction by hemin or Panhematin protects against experimental pancreatitis. As a preclinical first step toward determining whether HO-1 upregulation is a viable target in acute pancreatitis (AP) patients, we tested the hypothesis that HO-1 expression in peripheral blood mononuclear cell (PBMC) subsets of hospitalized patients with mild AP is upregulated then normalizes upon recovery and that cells from AP patients have the potential to upregulate their HO-1 ex vivo if exposed to Panhematin. PBMCs were isolated on days 1 and 3 of hospitalization from the blood of 18 AP patients, and PMBC HO-1 levels were compared with PMBCs of 15 hospitalized controls (HC) and 7 volunteer healthy controls (VC). On day 1 of hospitalization, AP patients compared with VCs had higher HO-1 expression in monocytes and neutrophils. Notably, AP monocyte HO-1 levels decreased significantly upon recovery. Panhematin induced HO-1 in ex vivo cultured AP PBMCs more readily than in HC or VC PBMCs. Furthermore, PBMCs from acutely ill AP patients on day 1 were more responsive to HO-1 induction compared with day 3 upon recovery. Similarly, mouse splenocytes had enhanced HO-1 inducibility as their pancreatitis progressed from mild to severe. In conclusion, AP leads to reversible PBMC HO-1 upregulation that is associated with clinical improvement and involves primarily monocytes. Leukocytes from AP patients or mice with AP are primed for HO-1 induction by Panhematin, which suggests that Panhematin could offer a therapeutic benefit.

scholarly journals Shenmai Injection Upregulates Heme Oxygenase-1 to Confer Protection Against Severe Acute Pancreatitis

2020 ◽  
Vol 256 ◽  
pp. 295-302
Author(s):  
Fei-hu Zhang ◽  
Yang Liu ◽  
Xiao-bin Dong ◽  
Hao Hao ◽  
Kai-liang Fan ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Shenmai Injection

Heme oxygenase-1 induced by desoxo-narchinol-A attenuated the severity of acute pancreatitis via blockade of neutrophil infiltration

2019 ◽  
Vol 69 ◽  
pp. 225-234 ◽  
Author(s):  
Gi-Sang Bae ◽  
Dong-Goo Kim ◽  
Il-Joo Jo ◽  
Sun-Bok Choi ◽  
Myoung-Jin Kim ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Heme Oxygenase ◽  
Neutrophil Infiltration ◽  
Heme Oxygenase 1

scholarly journals Differential Expression of CD3, TNF-α, and VEGF Induced by Olanzapine on the Spleen of Adult Male Albino Rats and the Possible Protective Role of Vitamin C

Biomedicines ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 39
Author(s):  
Sahar Youssef ◽  
Marwa Salah
Keyword(s):  
Body Weight ◽  
Vitamin C ◽  
Adult Male ◽  
Control Group ◽  
Albino Rats ◽  
White Pulp ◽  
Group Iii ◽  
Group I ◽  
Tnf Α ◽  
Group Ii

Olanzapine is an antipsychotic drug effective in the treatment of stress-associated psychiatric illnesses, but its effect on the spleen remains unclear. Vitamin C is essential for the optimum function of the immune system. We aim to investigate the effect of Olanzapine on spleen structures and to assess the protective effect of vitamin C. Forty adult male albino rats were divided into four groups: group (I), a control; group (II), rats were given vitamin C at 40 mg/kg body weight; group (III), rats were given Olanzapine at 2 mg/kg body weight; and group (IV), rats were given vitamin C and Olanzapine at the same dose of group (II) and group (III) for one month. The hematoxylin and eosin (H&E) of the olanzapine treated group showed focal areas of cellular depletion and a decrease in the size of the white pulp. The red pulp was expanded and showed marked congestion and dilatation of blood sinusoids. Cluster of differentiation 3 (CD3) was significantly reduced, however both tumor necrosis factor alpha (TNF-α), and vascular endothelial growth factor (VEGF) were significantly higher. The administration of vitamin C repaired structural and immunohistochemical changes via increased CD3 and decreased TNF-α and VEGF. Therefore, the oxidative and the inflammatory pathways may be the possible mechanisms underlying olanzapine immunotoxicity. Vitamin C exerted immune modulator and antioxidant effects against olanzapine.

Amelioration of estrogen-induced endometrial hyperplasia in female rats by hemin via heme-oxygenase-1 expression, suppression of iNOS, p38 MAPK, and Ki67

2019 ◽  
Vol 97 (12) ◽  
pp. 1159-1168
Author(s):  
Fatma F. Ali ◽  
Walaa Yehia Abdelzaher ◽  
Randa Ahmed Ibrahim ◽  
Doaa Mohamed Elroby Ali
Keyword(s):  
Protein Kinase ◽  
Heme Oxygenase ◽  
Endometrial Hyperplasia ◽  
Mitogen Activated Protein Kinase ◽  
Female Rats ◽  
Interleukin 1Β ◽  
Estradiol Valerate ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Mitogen Activated Protein

Although heme oxygenase-1 (HO-1) is part of an endogenous defense system implicated in the homeostatic response, its role in cell proliferation and tumor progression is still controversial. Endometrial hyperplasia (EH) is associated with high risk of endometrial cancer (EC). Therefore, we aimed to evaluate the effect of hemin, a HO-1 inducer, against EH. Thirty-two female rats (60–70 days old) were divided into 4 groups treated for 1 week: vehicle control group, hemin group (25 mg/kg; i.p. 3 times/week), estradiol valerate (EV) group (2 mg/kg per day, p.o.), and hemin plus EV group. Sera were obtained for reduced glutathione level. Uterine malondialdehyde, superoxide dismutase, total nitrite/nitrate, and interleukin-1β levels were estimated. HO-1 and p38 mitogen-activated protein kinase expressions were obtained in uterine tissue. Uterine histological and immunohistochemical assessment of iNOS and Ki67 were also done. Results demonstrated that upregulation of HO-1 expression in hemin plus EV rats led to amelioration of EH which was confirmed with histological examination. This was associated with significant decrease in oxidative stress parameters, p38 mitogen-activated protein kinase expression, and interleukin-1β level. Also, uterine iNOS and Ki67 expressions were markedly suppressed. In conclusion, upregulation of HO-1 expression via hemin has ameliorative effect against EH through its antioxidant, anti-inflammatory, and antiproliferative actions.

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