scholarly journals Metallothionein Induction Reduces Caspase-3 Activity and Tnfα Levels with Preservation of Cognitive Function and Intact Hippocampal Neurons in Carmustine-Treated Rats

2009 ◽  
Vol 2 (1) ◽  
pp. 26-35 ◽  
Author(s):  
Gouda K. Helal ◽  
Abdulaziz M. Aleisa ◽  
Omayma K. Helal ◽  
Salim S. Al-Rejaie ◽  
Abdulaziz A. Al-Yahya ◽  
...  
Keyword(s):  
Normal Saline ◽  
Hippocampal Neurons ◽  
Caspase 3 ◽  
Short Term Memory ◽  
Control Group ◽  
Albino Rats ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Wistar Albino Rats ◽  
Necrosis Factor

Hippocampal integrity is essential for cognitive functions. On the other hand, induction of metallothionein (MT) by ZnSO4and its role in neuroprotection has been documented. The present study aimed to explore the effect of MT induction on carmustine (BCNU)-induced hippocampal cognitive dysfunction in rats. A total of 60 male Wistar albino rats were randomly divided into four groups (15/group): The control group injected with single doses of normal saline (i.c.v) followed 24 h later by BCNU solvent (i.v). The second group administered ZnSO4(0.1 µmol/10 µl normal saline, i.c.v, once) then BCNU solvent (i.v) after 24 h. Third group received BCNU (20 mg/kg, i.v, once) 24 h after injection with normal saline (i.c.v). Fourth group received a single dose of ZnSO4(0.1 µmol/10 µl normal saline, i.c.v) then BCNU (20 mg/kg, i.v, once) after 24 h. The obtained data revealed that BCNU administration resulted in deterioration of learning and short-term memory (STM), as measured by using radial arm water maze, accompanied with decreased hippocampal glutathione reductase (GR) activity and reduced glutathione (GSH) content. Also, BCNU administration increased serum tumor necrosis factor-alpha (TNFα), hippocampal MT and malondialdehyde (MDA) contents as well as caspase-3 activity in addition to histological alterations. ZnSO4pretreatment counteracted BCNU-induced inhibition of GR and depletion of GSH and resulted in significant reduction in the levels of MDA and TNFα as well as the activity of caspase-3. The histological features were improved in hippocampus of rats treated with ZnSO4+ BCNU compared to only BCNU-treated animals. In conclusion, MT induction halts BCNU-induced hippocampal toxicity as it prevented GR inhibition and GSH depletion and counteracted the increased levels of TNFα, MDA and caspase-3 activity with subsequent preservation of cognition.

scholarly journals Investigation of the Effects of L-carnitine and magnesium on Oxidative Stress and Cytokines in the Tissue of Experimental diabetic rats

2021 ◽  
Vol 71 (4) ◽  
pp. 477-489
Author(s):  
Meryem Senturk ◽  
Meryem Eren ◽  
Zeynep Soyer Sarica
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Control Group ◽  
Albino Rats ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Group 2 ◽  
Necrosis Factor

Abstract The aim of this study was to determine the effects of L-carnitine and magnesium on the levels of tissue malondialdehyde, 8-hydroxy-2’-deoxyguanosine, and cytokines (tumor necrosis factor alpha, interleukin-6) in streptozotocin-induced experimental diabetes in rats. Eighty male Wistar albino rats (200-250 g) were divided into 8 groups with 10 rats in each group. The groups received the following treatments: Control group; 2 ml distilled water (by gavage); Group 2: 50 mg/kg (b.w.) i.p. streptozotocin; Group 3: 125 mg/kg (b.w.) magnesium; Group 4: 300 mg/kg (b.w.) L-carnitine; Group 5: 125 mg/kg (b.w.) magnesium +300 mg/kg (b.w.) L-carnitine; Group 6: 50 mg/kg (b.w.) streptozotocin +125 mg/kg (b.w.) magnesium; Group 7: 50 mg/kg (b.w.) streptozotocin +300 mg/kg (b.w.) L-carnitine and Group 8: 50 mg/kg (b.w.) streptozotocin +125 mg/ kg (b.w.) magnesium+300 mg/kg (b.w.) L-carnitine administered for 4 weeks. Liver and kidney malondialdehyde, 8-hydroxy-2’-deoxyguanosine, tumor necrosis factor alpha and interleukin-6 levels did not change in the magnesium, L-carnitine, and magnesium + L-carnitine groups compared to the control. The highest levels of malondialdehyde, 8-hydroxy-2’-deoxyguanosine, tumor necrosis factor alpha and interleukin-6 were determined only in the group with diabetes (Group 2). Lipid peroxidation, DNA damage, and cytokine levels were significantly reduced in diabetic animals with the administration of magnesium and L-carnitine separately or in combination. Based on the obtained results it can be concluded that magnesium and L-carnitine may have antidiabetic effects, especially in combination.

Leukogram and cortisol parameters in Swiss mice experimentally infected with Angiostrongylus costaricensis

2021 ◽  
Vol 95 ◽  
Author(s):  
E. Benvegnú ◽  
C.C. Hermes ◽  
J.A. Guizzo ◽  
S.M. Soares ◽  
M.M. Costa ◽  
...  
Keyword(s):  
Cytokine Profile ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Swiss Mice ◽  
Hypochromic Anaemia ◽  
Third Stage ◽  
Factor Alpha ◽  
Cortisol Levels ◽  
Necrosis Factor

Abstract This study describes changes in haematological parameters, cytokine profile, histopathology and cortisol levels in Swiss mice experimentally infected with Angiostrongylus costaricensis. Twenty-eight Swiss mice were divided into two groups (G1 and G2) of 14 animals each. In each group, eight animals were infected orally with ten third-stage larvae of A. costaricensis and six were used as a control group. The mice of groups G1 and G2 were sacrificed 14 and 24 days after infection, respectively. Samples were collected for histopathological and haematological analyses and determination of the cytokine profile and cortisol levels. Granulomatous reaction, eosinophilic infiltrate and vasculitis in the intestinal tract, pancreas, liver and spleen were observed with varying intensity in infected animals. Our results showed that the mice developed normocytic and hypochromic anaemia, and that the histopathological lesions caused by the experimental infection influenced increases in cortisol, neutrophil and monocyte levels. In addition to this, we detected increased interleukin-6 and tumour necrosis factor alpha levels in the infected animals.

scholarly journals EKSPRESI Tumor Necrosis Factor alpha (TNF-α) DAN Transforming growth factors beta (TGF-β) PADA PERIODONTITIS APIKALIS KRONIS AKIBAT INDUKSI Enterococcus faecalis PADA TIKUS WISTAR

2019 ◽  
Vol 7 (2) ◽  
pp. 66
Author(s):  
Richard Fritzgerald ◽  
Cecilia Lunardhi ◽  
Ruslan Effendy ◽  
Tamara Yuanita
Keyword(s):  
Tissue Damage ◽  
Treated Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Transforming Growth Factors ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background. Root canal treatment is a main role in decreasing infection from root canal and pulp. The main cause of periapical damage mostly are bacteries. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation then lead to bone destruction. LTA stimulates immunology reaction that produce Tumor Necrosis Factor alpha (TNF-α) and Transforming growth factors beta (TGF-ß). TNF-α is a main mediator and also have an important role in inflamation response otherwise TGF-ß is working as a multifunction  regulator of cell growth and differentiation during reforming and remodelling.  Purpose. The aim of this study is to know about the expression of TNF-α and TGF-ß during the periapical tissue damage due to induction of E.faecalis. Method. This study used laboratory experimental with the post test only control group design. A total of 30 male rats were randomly divided into 3 main groups, Group A (control negative) : normal tooth. Group B (control positive) : every tooth was induced only by sterile BHI-b. Group C (treated group) : every tooth  was induced by 10 μl BHI-b E.faecalis ATCC212(106 CFU). The animals were sacrificed 21 days later and prepared for histological examination of tissue damage, then we did the immunohistochemistry  followed by calculation on the light microscope. Result. The analysis revealed that the expression of TNF-α at treated group are higher than negative control and positive control but the expression of  TGF-ß at treated group are higher than the negative control group but lower than positive control. Conclusion. From this study we know that the expression of TNF-α and TGF-ß are changing during the periapical tissue damage that induced by E.faecalis.

scholarly journals Assessment Of Tumour Necrosis Factor-Alpha (Tnf- Α) And Creatinine Levels In Echis Ocellatus Bite Victims In Jos Metropolis, Nigeria

2016 ◽  
Vol 12 (21) ◽  
pp. 70
Author(s):  
Manafa P.O. ◽  
Osmond E.O. ◽  
Onyenekwe C.C. ◽  
Okeke C.O. ◽  
Chukwuma G.O. ◽  
...  
Keyword(s):  
Serum Level ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Alpha ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Significant Difference ◽  
Factor Alpha ◽  
The Mean ◽  
Necrosis Factor

This study was designed to assess tumour necrosis factor-alpha and creatinine levels in Echis ocellatus bite victims. A total of 50 subjects were recruited. Out of this number, 40 were victims of E. ocellatus bite and the remaining 10 were non-victims of snake bite who served as the control group. Blood samples were collected from the victims within 24 hours of the snake bite and EchiTAb-G antivenom administered within the same period. Another batch of blood sample was collected 48 hours post-administration of the anti-venom. Tumour necrosis factor-alpha (TNF-alpha) levels were estimated by the Enzyme Linked Immunosorbent Assay technique while creatinine levels were determined using kinetic-spectrophotometric procedure. The mean serum levels of tumour necrosis factor-alpha and creatinine were significantly increased in E. ocellatus bite victims compared with the control group (P<0.05). Furthermore, the mean serum level of TNFalpha was significantly lower in E. ocellatus bite victims, post-administration of anti-venom, compared with the pre-administration of anti-venom (P<0.05). In contrast, no significant difference was observed in the mean serum level of creatinine in E. ocellatus bite victims, post-administration of anti-venom, compared with the pre-administration of anti-venom (P>0.05). Moreover, the mean serum level of creatinine was found to be significantly increased in E. ocellatus bite victims, post-administration of anti-venom, compared with the control group (P<0.05), while no significant difference was observed in the mean serum level of tumour necrosis factor-alpha in E. ocellatus bite victims, post-administration of anti-venom, compared with the control group(P>0.05). A positive correlation existed between tumour necrosis factor-alpha and creatinine levels in E. ocellatus bite subjects (r= 0.782). Echis ocellatus bite is a risk factor for renal damage indicated by an elevated serum creatinine, thus health authorities should make EchiTAb-G anti-venom freely available in health facilities and administered as quickly as possible to reduce the risk of renal damage in Echis ocellatus bite-prone areas.

scholarly journals Possible Protective Effect of Diacerein on Doxorubicin-Induced Nephrotoxicity in Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Marwa M. M. Refaie ◽  
Entesar F. Amin ◽  
Nashwa F. El-Tahawy ◽  
Aly M. Abdelrahman
Keyword(s):  
Protective Effect ◽  
Low Dose ◽  
Caspase 3 ◽  
Interleukin 1 ◽  
Treated Group ◽  
Limiting Factors ◽  
High Dose ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Nephrotoxicity is one of the limiting factors for using doxorubicin (DOX). Interleukin 1 has major role in DOX-induced nephrotoxicity, so we investigated the effect of interleukin 1 receptor antagonist diacerein (DIA) on DOX-induced nephrotoxicity. DIA (25 and 50 mg/kg/day) was administered orally to rats for 15 days, in the presence or absence of nephrotoxicity induced by a single intraperitoneal injection of DOX (15 mg/kg) at the 11th day. We measured levels of serum urea, creatinine, renal reduced glutathione (GSH), malondialdehyde (MDA), total nitrites (NOx), catalase, and superoxide dismutase (SOD). In addition, caspase-3, tumor necrosis factor alpha (TNFα), nuclear factor kappa B (NFκB) expressions, and renal histopathology were assessed. Our results showed that DOX-induced nephrotoxicity was ameliorated or reduced by both doses of DIA, but diacerein high dose (DHD) showed more improvement than diacerein low dose (DLD). This protective effect was manifested by significant improvement in all measured parameters compared to DOX treated group by using DHD. DLD showed significant improvement of creatinine, MDA, NOx, GSH, histopathology, and immunohistochemical parameters compared to DOX treated group.

Serum tumor necrosis factor-alpha does not mediate endotoxin-induced myocardial depression in rabbits

1996 ◽  
Vol 270 (2) ◽  
pp. H485-H491 ◽  
Author(s):  
Y. Nishikawa ◽  
J. Mathison ◽  
W. Y. Lew
Keyword(s):  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Control Group ◽  
Lv Function ◽  
Necrosis Factor Alpha ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor-alpha (TNF-alpha) is an endogenous mediator for several effects of endotoxin. To evaluate whether TNF-alpha mediates endotoxin-induced left ventricular (LV) dysfunction, we measured LV function (sonomicrometers) and serum TNF-alpha (cytolytic assay) in anesthetized rabbits given endotoxin (100 micrograms/kg iv). In the control group (n = 8), systolic depression (defined by a > 10% increase in end-systolic volume at a matched end-systolic pressure) developed in four rabbits and diastolic dilation (> 10% increase in end-diastolic volume at a matched end-diastolic pressure) developed in three rabbits. Neither the increase in end-systolic volume nor the increase in end-diastolic volume correlated with the increase in TNF-alpha, which reached a peak of 2,875 +/- 762 U/ml. In a second group of rabbits (n = 7), a goat polyclonal anti-rabbit antibody to TNF-alpha was given 30-60 min before endotoxin. Anti-TNF-alpha antibody alone did not alter LV function. Although the TNF-alpha response to endotoxin was effectively blunted (peak TNF-alpha remained < 100 U/ml), all seven rabbits developed systolic depression (P = 0.08 compared with control group) and diastolic dilation (P = 0.03). We conclude that serum TNF-alpha does not mediate endotoxin-induced LV systolic depression or diastolic dilation in this model.

scholarly journals The Mitochondrial Permeability Transition Is Required for Tumor Necrosis Factor Alpha-Mediated Apoptosis and Cytochrome c Release

1998 ◽  
Vol 18 (11) ◽  
pp. 6353-6364 ◽  
Author(s):  
Cynthia A. Bradham ◽  
Ting Qian ◽  
Konrad Streetz ◽  
Christian Trautwein ◽  
David A. Brenner ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Necrosis ◽  
Caspase 3 ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition ◽  
Necrosis Factor Alpha ◽  
Mitochondrial Permeability ◽  
Factor Alpha ◽  
Induced Apoptosis ◽  
Necrosis Factor

ABSTRACT This study assesses the controversial role of the mitochondrial permeability transition (MPT) in apoptosis. In primary rat hepatocytes expressing an IκB superrepressor, tumor necrosis factor alpha (TNFα) induced apoptosis as shown by nuclear morphology, DNA ladder formation, and caspase 3 activation. Confocal microscopy showed that TNFα induced onset of the MPT and mitochondrial depolarization beginning 9 h after TNFα treatment. Initially, depolarization and the MPT occurred in only a subset of mitochondria; however, by 12 h after TNFα treatment, virtually all mitochondria were affected. Cyclosporin A (CsA), an inhibitor of the MPT, blocked TNFα-mediated apoptosis and cytochrome c release. Caspase 3 activation, cytochrome c release, and apoptotic nuclear morphological changes were induced after onset of the MPT and were prevented by CsA. Depolarization and onset of the MPT were blocked in hepatocytes expressing ΔFADD, a dominant negative mutant of Fas-associated protein with death domain (FADD), or crmA, a natural serpin inhibitor of caspases. In contrast, Asp-Glu-Val-Asp-cho, an inhibitor of caspase 3, did not block depolarization or onset of the MPT induced by TNFα, although it inhibited cell death completely. In conclusion, the MPT is an essential component in the signaling pathway for TNFα-induced apoptosis in hepatocytes which is required for both cytochrome c release and cell death and functions downstream of FADD and crmA but upstream of caspase 3.

scholarly journals Tumor Necrosis Factor-Alpha in Peripical Tissue Exudates of Teeth with Apical Periodontitis

2007 ◽  
Vol 2007 ◽  
pp. 1-4 ◽  
Author(s):  
Sonja Pezelj-Ribaric ◽  
Karolina Magašic ◽  
Jelena Prpic ◽  
Ivana Miletic ◽  
Zoran Karlovic
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Control Group ◽  
Radiological Findings ◽  
Necrosis Factor Alpha ◽  
Root Canals ◽  
Factor Alpha ◽  
Radiological Changes ◽  
Necrosis Factor

Aim.The aim of this study was to determine tumor necrosis factor-alpha (TNF-α) levels in periapical exudates and to evaluate their relationship with radiological findings.Methodology.Periapical exudates were collected from root canals of 60 single-rooted teeth using absorbent paper points. TNF-αlevels were determined by enzyme-linked immunosorbent assays. The samples were divided into three groups according to the periapical radiolucent area.Results.Nonparametric Kruskal-Wallis test revealed significant differences between TNF-αconcentrations in control group (40,57±28, 15 pg/mL) and group with larger radiolucent areas (2365,79±582, 95 pg/mL), as well as between control and canals with small radiolucent areas (507,66±278, 97) (P<.05).Conclusions.The levels of TNF-αincrease significantly in teeth with periapical pathosis, from smaller to bigger lesions. This research and its results have shown that objective analysis of the TNF-αlevels enables establishment of a relationship between different concentrations of TNF-αand different radiological changes.

scholarly journals Tula hantavirus infection of Vero E6 cells induces apoptosis involving caspase 8 activation

2004 ◽  
Vol 85 (11) ◽  
pp. 3261-3268 ◽  
Author(s):  
Xiao-Dong Li ◽  
Sami Kukkonen ◽  
Olli Vapalahti ◽  
Alexander Plyusnin ◽  
Hilkka Lankinen ◽  
...  
Keyword(s):  
Influenza A ◽  
Time Course ◽  
Caspase 3 ◽  
Hantavirus Infection ◽  
Caspase 8 ◽  
Type I ◽  
Tnf Receptor ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Hantaviruses are known to cause two severe human diseases: haemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome. The mechanisms of pathogenesis of these two diseases are progressively becoming understood. Recently, two hantaviruses, Hantaan and Prospect Hill were reported to cause programmed cell death of Vero E6 cells. This study shows that Tula hantavirus (TULV) infection efficiently triggers an apoptotic programme in infected Vero E6 cells, and that the replication of TULV is required for the activation of caspase 3 and the cleavage of poly (ADP-ribose) polymerase, two molecular hallmarks of apoptosis. The enforced treatment of infected Vero E6 cells with tumour necrosis factor alpha (TNF-α), but not interferon alpha (IFN-α), advanced the time course of apoptosis. Furthermore, caspase 8 was activated on day 4 post-infection, the same day when caspase 3 was activated. TNF receptor 1 was induced during a late stage of TULV infection. These data suggest that, unlike during influenza A virus infection, TNF-α, but not type I IFN-α/β, may contribute significantly to apoptosis in a synergistic manner with TULV propagation. Interestingly, pretreatment with a broad-spectrum caspase inhibitor, z-VAD-fmk, efficiently inhibited apoptosis of TULV-infected Vero E6 cells. Taken together, these results suggest that TULV replication initiates a typical apoptotic programme involving caspase 8 activation.

scholarly journals Role of an acidic compartment in tumor-necrosis-factor-alpha-induced production of ceramide, activation of caspase-3 and apoptosis

1998 ◽  
Vol 251 (1-2) ◽  
pp. 295-303 ◽  
Author(s):  
Laurent Monney ◽  
Reynald Olivier ◽  
Isabelle Otter ◽  
Burkhard Jansen ◽  
Guy G. Poirier ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Caspase 3 ◽  
Necrosis Factor Alpha ◽  
Acidic Compartment ◽  
Factor Alpha ◽  
Necrosis Factor
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