Correction of oxidative stress in patients with chronic cerebral ischemia

2016 ◽  
Vol 94 (7) ◽  
pp. 549-553
Author(s):  
Olga A. Goroshko ◽  
K. N. Novikov ◽  
V. G. Kukes ◽  
V. L. Voeikov ◽  
V. V. Arkhipov ◽  
...  

A pilot study ofthe effect ofthe antioxidant drug ethylmethylhydroxypyridine malate on indicators of oxidative stress in patients with chronic cerebral ischemia. At 6 day course administration investigated the antioxidant in these patients significantly accelerates the process of generation of superoxide anion radical, established by lucigenin-depended chemiluminescence that probably regulate a feedback mechanism oxidase systems. This increases the activity of superoxide dismutase, and reduced the concentration of secondary peroxidation product - malondialdehyde, making reasonable use of antioxidants in the treatment of this pathology.

1988 ◽  
Vol 255 (2) ◽  
pp. H401-H403 ◽  
Author(s):  
W. M. Armstead ◽  
R. Mirro ◽  
D. W. Busija ◽  
C. W. Leffler

Cerebral superoxide anion generation during reperfusion after total cerebral ischemia was measured in newborn pigs. Superoxide dismutase (SOD)-inhibitable nitroblue tetrazolium (NBT) reduction was determined using two closed cranial windows inserted over the parietal cortices. Twenty minutes of total cerebral ischemia was produced by increasing intracranial pressure, and SOD-inhibitable NBT reduction was determined during 20 min of reperfusion. SOD-inhibitable NBT reduction (8.7 +/- 1.5 pmol.mm-2.20 min-1) was greater in piglets subjected to cerebral ischemia followed by reperfusion than in control piglets not exposed to ischemia (1.6 +/- 1.3 pmol.mm-2.20 min-1). Pretreatment with indomethacin (5 mg/kg iv) markedly reduced postischemia SOD-inhibitable NBT reduction (2.8 +/- 1.1 pmol.mm-2.20 min-1). We conclude that superoxide anion radical is produced by newborn pig brain during postischemic reperfusion. Furthermore, cyclooxygenase metabolism of arachidonic acid appears to be a major source of this activated oxygen during reperfusion of ischemic piglet brain.


Author(s):  
Fangfang Zhao ◽  
Yumin Luo

: Chronic cerebral ischemia is one of the common ischemic cerebrovascular diseases. Chronic cerebral ischemia can lead to brain dysfunction, and its pathophysiological mechanism involves inflammation, blood-brain barrier destruction, oxidative stress, and other factors. Due to it being difficult to detect, it is easily overlooked, and it is often only observed following onset of cognitive dysfunction. At present, there are few drugs for this treatment. DL-3-N-BUTYLPHTHALIDE (NBP), a compound extracted from celery seed, may play an important role in protecting against brain damage caused by chronic cerebral ischemia. Therefore, we pay more attention to the prevention and treatment of NBP on chronic cerebral ischemia.


Author(s):  
Shahida Perveen ◽  
Syed Muhammad Saad ◽  
Khalid Mohammed Khan ◽  
Muhammad Iqbal Choudhary

Background: Antioxidants are small molecules that prevent or delay the process of oxidations caused by highly reactive free radicals. These molecules are known for their ability to protect various cellular architecture and other biomolecules from oxidative stress and free radicals. Thus, antioxidants play a key role in the prevention of oxidative damages caused by highly reactive free radicals. Method: In the present study, a series of previously synthesized heterocyclic 2-aryl-4(3H)-quinazolinone derivatives 1-25 was screened for antioxidant activity by employing in vitro DPPH and superoxide anion radical scavenging activities. ROS inhibitory activities were also evaluated by serum-opsonized zymosan activated whole blood phagocytes and isolated neutrophils. Cytotoxicity studies were carried out by employing an MTT assay against the 3T3 cell line. Results: Most of the 2-aryl-4(3H)-quinazolinone derivatives showed potent antioxidant activities in superoxide anion radical scavenging assay with IC50 value ranging between 0.57 µM – 48.93 µM, as compared to positive control quercetin dihydrate (IC50 = 94.1± 1.1 µM ). Compounds 5, 6, and 14 showed excellent activity in DPPH assay. Compounds 5-8, 12-15, 17, and 20 showed promising activities in the ROS inhibition assay. All compounds were found to be non-cytotoxic against the 3T3 cell line. Structure antioxidant activity has been established. Conclusion: It can be concluded that most of the heterocyclic 2-aryl-4(3H)-quinazolinone derivatives 1-25 are identified as promising antioxidant agents that are capable of fighting against free radicals and oxidative stress. Thus, they can serve as a lead towards treating oxidative stress and related pathologies.


Author(s):  
A.M. Yelins’ka ◽  
V.O. Kostenko

This study is aimed at investigating the effect of imatinib mesylate, an inhibitor of the transcription factor STAT-3, on the oxidative and nitrosative stress indicators in rat periodontal tissues during the experimental systemic inflammatory response (SIR) induced by the introduction of the Salmonella typhi lipopolysaccharide (LPS) (in a dose of 0.4 μg/kg body wt, 3 times for the 1 week and once a week through the next 7 weeks). Imatinib mesylate introduction in a dose of 15 mg/kg 3 times a week, starting from the 30th day of the SIR modeling, was accompanied by a significant decrease in the rate of production of superoxide anion radical by the mitochondrial respiratory chain (by 13.4%) compared with the data from the SIR modeled group. The production rate of this radical by NADPH-dependent electron transport chains and phagocytes did not change significantly. At the same time, in the periodontal tissues, the total activity of NO synthase decreased (by 27.4%) without significant changes in the concentration of peroxynitrite ions. As a result, lipid peroxidation (LPO) in periodontal soft tissues was limited: the concentration of secondary peroxidation products before and after the incubation in a prooxidant buffer solution when imatinib mesylate was added was inferior to the results of the SIR modeled group by 37.5 and 33.8%, respectively. The activity of superoxide dismutase and catalase exceeded the data of the comparison group by 40.0 and 60.0%, respectively. It was concluded that the use of the inhibitor of STAT-3 activation, imatinib mesylate, under LPS-induced SIR, limits the formation of reactive oxygen and nitrogen species in rat periodontal tissues: it decreases the production rate of superoxide anion-radical by the mitochondrial electron transport chain, reduces the total activity of NO synthase. This results in the reduced formation of secondary LPO products in periodontal tissues and the reduced activity of antioxidant enzymes in them (superoxide dismutase, catalase).


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