Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
1.
Annals of Surgical Treatment and Research ; : 34-40, 2019.
Article in English | WPRIM | ID: wpr-719657

ABSTRACT

PURPOSE: To research the effects of iloprost (IL) and hyperbaric oxygen (HBO) combination treatment on lung injury and on tumor necrosis factor alpha (TNF-α), myeloperoxidase (MPO), malondialdehyde (MDA), and soluble intercellular adhesion molecule-1 (sICAM-1) levels after tissue or organ ischemia-reperfusion, and on ischemia-reperfusion induced lung neutrophil sequestration. METHODS: Forty white New Zealand rabbits were assigned randomly into 5 groups: HBO, IL, HBO+IL, control, and sham groups. TNF-α values were checked before ischemia, in the 1st hour of ischemia and in the 1st and 4th hours of reperfusion, also at the end of reperfusion period, plasma and tissue MPO values, MDA values, and sICAM-1 levels were detected. After sacrifice, the degree of lung injury was determined by histopathological examination. RESULTS: Compared to the control group all therapy groups showed a drastically meaningful reduction in TNF-α increase in 1, 2, and 4 hours. Plasma and lung MDA, MPO, and sICAM-1 levels were significantly lower in IL, HBO, HBO+IL, and sham groups compared with the control group. IL and/or HBO suppressed MDA and MPO increase in the lung tissue and in plasma. Additionally, histopathological score was significantly lower in HBO, IL, HBO+IL, and sham groups than that of the control group. CONCLUSION: Both HBO and IL therapy have a beneficial effect by causing a meaningful reduction in TNF-α production, MPO, MDA, sICAM-1 levels and pulmonary neutrophil sequestration; which play a role, especially, in ischemia reperfusion induced lung damage.


Subject(s)
Rabbits , Acute Lung Injury , Hyperbaric Oxygenation , Iloprost , Intercellular Adhesion Molecule-1 , Ischemia , Lung , Lung Injury , Malondialdehyde , Neutrophils , Oxygen , Peroxidase , Plasma , Reperfusion , Reperfusion Injury , Tumor Necrosis Factor-alpha
2.
Medical Principles and Practice. 2016; 25 (2): 181-186
in English | IMEMR | ID: emr-178543

ABSTRACT

Objective: The aim of this study was to assess the impact of resveratrol [RST] on oxidative stress induced by methotrexate in rat ileum tissue


Materials and Methods: Twenty-four rats were divided into 4 groups with 6 in each group. Each rat was orally administered the following every day for 30 days: group 1 [MTXG], methotrexate [MTX; 5 mg/kg]; group 2 [RMTXG], MTX [5 mg/kg] plus RST [25 mg/kg/day]; group 3 [RSTG], RST alone [25 mg/kg/day], and group 4 [controls], distilled water. After the rats had been sacrified, the ilea were removed for the assessment of malondialdehyde [MDA], total glutathione [tGSH] and glutathione peroxidase [GSH-Px]. Gene expression analyses for interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha] and myeloperoxidase [MPO] were also performed. Hematoxylin and eosin-stained paraffinembedded sections of the ileum were analyzed under a light microscope and the findings were recorded. Statistical analyses of the data were performed using one-way ANOVA


Results: The administration of MTX in group 1 yielded a higher level of MDA [8.33 +/- 2.5 micro mol/g protein, p < 0.001] and lower levels of tGSH [0.97 +/- 0.29 nmol/g protein] and GSH-Px [5.22 +/- 0.35 U/g protein, p < 0.001] compared to the other groups. MTX also increased IL-1beta [40.33 +/- 5.43 gene expression levels], TNF-alpha [6.08 +/- 0.59] and MPO gene expression [9 +/- 1.41] in group 1 compared to the controls [11.33 +/- 2.07, 2.15 +/- 0.33 and 3.43 +/- 0.48, respectively, p < 0.001]. The impact of RST on IL-1beta, TNF-alpha and MPO gene expression induced by MTX was observed as a reversal of these findings [p < 0.05]. Severe inflammation, damage to the villus epithelium and crypt necrosis was observed histopathologically in the MTXG group, whereas only mild inflammation was seen in the RMTXG group


Conclusion: In this study, ileal damage caused by MTX was inhibited by RST

3.
Saudi Medical Journal. 2014; 35 (9): 953-958
in English | IMEMR | ID: emr-154771

ABSTRACT

To investigate whether infliximab [Ib], an inhibitor of tumor necrosis factor alpha [TNF-alpja], prevents cisplatin [Cis] -induced nephrotoxicity. The study was performed in the Department of Internal Medicine, RecepTayyip Erdogan University, Rize, Turkey, between November 2012 and May 2013. Thirty male Wistar albino rats were divided into 3 groups, a control group, a Cis group, and a Cis+Ib group. The animals of the Cis group were injected with a single dose [7 mg/kg] of Cis intraperitoneally. The animals of the Cis+Ib group were injected with a single dose [7 mg/kg] of Ib 72 hours prior to Cis injection. The TNF-a, interleukin-1 beta [IL-1J3], nitric oxide [NO] and adenosine deaminase [ADA] levels of the Cis group were higher than both the control group TNF-alpha [p<0.001], IL-la [p<0.001], NO [p<0.001] and ADA [p<0.001], and the Cis+Ib group TNF-alpha [p<0.001], IL-1[3 [p<0.001], NO [p<0.001], and ADA [f=0.003]. Histopathological examination revealed extensive damage in the Cis group, while the damage in the Cis+Ib group was lower. While the carbonic anhydrase II [CA-II] level of the Cis group was lower than both groups, it was similar in the Cis+Ib and the control groups. Infliximab acts against Cis-induced nephrotoxicity by a strong inhibition of TNF-alpha. Additionally, the combination of these 2 drugs does not obviously change the level of CA-II

SELECTION OF CITATIONS
SEARCH DETAIL