Protective effect of ellagic acid against cyclosporine A-induced histopathological, ultrastructural changes, oxidative stress, and cytogenotoxicity in albino rats

2016 ◽  
Vol 40 (4) ◽  
pp. 205-221 ◽  
Author(s):  
Manal Abdul-Hamid ◽  
Ehab M. Abdella ◽  
Sanaa R. Galaly ◽  
Rania H. Ahmed
2017 ◽  
Vol 44 (3) ◽  
pp. 1174-1187 ◽  
Author(s):  
Artur Rozentsvit ◽  
Kevin Vinokur ◽  
Sherin Samuel ◽  
Ying Li ◽  
A. Martin Gerdes ◽  
...  

Background/Aims: Elevated production of reactive oxygen species (ROS) is linked to endothelial dysfunction and is one of the key contributors to the pathogenesis of diabetic vascular complications. Emerging evidence has indicated that ellagic acid (EA), a polyphenol found in fruits and nuts, possesses numerous biological activities including radical scavenging. However, whether EA exerts a vasculo-protective effect via antioxidant mechanisms in blood vessels exposed to diabetic conditions remains unknown. Accordingly, the goal of this current study was to determine whether EA decreases vascular ROS production and thus ameliorates endothelial dysfunction in the diabetic milieu. Methods: Intact rat aortas and human aortic endothelial cells (HAEC) were stimulated with 30mM high glucose (HG) with and without EA co-treatment. Endothelium-dependent vasodilation was measured using a wire myograph. Gene and protein expression of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases 4 (NOX4) were detected using RT-PCR and western blotting, respectively. Oxidative stress was determined by measuring ROS levels using dihydroethidium (DHE) staining. Results: Intact aortas exposed to HG condition displayed exacerbated ROS production and impairment of endothelium-dependent vasodilation, characterizing endothelial dysfunction. These effects were markedly reduced with EA treatment. HG enhanced ROS production in HAEC, paralleled by increased ERK1/2 activation and NOX4 expression. EA treatment blunted the increase of ROS generation, ERK1/2 activation and decreased NOX4. Conclusions: EA significantly decreases endothelial ROS levels and ameliorates the impairment of vascular relaxation induced by HG. Our results suggest that EA exerts a vasculo-protective effect under diabetic conditions via an antioxidant effect that involves inhibition of ERK1/2 and downregulation of NOX4.


2020 ◽  
Vol 71 (1) ◽  
pp. 1997
Author(s):  
M. DÜZ ◽  
A. F. FIDAN

The present study was carried out to determine the effects of sub-chronic thinner addiction on the oxidant-antioxidant balance and oxidative stress on certain tissues and the possible protective effect of safranal against thinner toxication in rats. Adult male Wistar albino rats were randomly divided into four groups of 10 animals each as follows: control (C), safranal (S), thinner (T) and thinner+safranal (T+S). The control group received 1cc saline by gastric gavage. Safranal was administered to S and T+S groups by using gastric gavage at a dose of 100 mg/kg/day and volume of 0.1 mL/kg/day. Thinner inhalation was applied to T and T+S groups in a container with NaOH tablets twice a day. Levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NOx) metabolites, total antioxidant capacity (TAS) and total oxidant capacity (TOS) were determined in liver, lung, brain, kidney and testis tissues of the rats. In the T+S group, it was observed that the MDA levels significantly decreased in all tissues, except the kidney, in comparison to the thinner inhalation group (p = 0.000). When the NOx levels of the T+S group were compared with the levels of the T group, it was concluded that there existed a statistically significant decrease in the NOx levels in alltissues (p = 0.000). In T+S group, it was observed that safranal either eliminated or mitigated oxidative stress that developed in tissues through decreasing MDA and TOS levels and increasing GSH and TAS levels and caused significant decreases in NOX levels in all tissues. As a result, it was determined that safranal, although not uniform for all tissue types, had a protective potential against the damaging effects of oxidative stress caused by sub-chronic thinner inhalation.


2014 ◽  
Vol 153 (3) ◽  
pp. 744-752 ◽  
Author(s):  
Manjunath Manubolu ◽  
Lavanya Goodla ◽  
Sivajyothi Ravilla ◽  
Jayakumar Thanasekaran ◽  
Paresh Dutta ◽  
...  

2018 ◽  
Vol 102 (9-10) ◽  
pp. 473-478 ◽  
Author(s):  
Cigdem Aliosmanoglu ◽  
Halil Erbiş ◽  
Ibrahim Aliosmanoglu ◽  
Mehmet Akif Türkoglu ◽  
Burak Veli Ulger ◽  
...  

Isoniazid and rifampicin are drugs primarily used in antituberculosis treatment. Our aim in this study is to evaluate the effect of caffeic acid phenethyl ester's protective effect on liver function tests and to trace elements in hepatic damage caused by isoniazid and rifampicin on rats. Forty Wistar albino rats were divided into 4 groups. Group 1: Sham, Group 2: caffeic acid phenethyl ester application, Group 3: isoniazid and rifampicin given, Group 4: isoniazid + rifampicin and caffeic acid phenethyl ester application. After 30 days, the rats were sacrificed by taking blood from the heart. Alanine aminotransferase, aspartate aminotransferase, zinc, copper, total antioxidant capacity, total oxidative status, and oxidative stress index levels were evaluated. The rats to which isoniazid + rifampicin+ caffeic acid phenethyl ester were given had less oxidative stress and copper levels (P < 0.001, P = 0.019) but have higher zinc levels (P = 0.001) compared to the isoniazid + rifampicin group. Liver enzyme levels were also lower in rats that were given isoniazid + rifampicin + caffeic acid phenethyl ester (P < 0.001). The results of this study suggested that caffeic acid phenethyl ester influences the levels of trace elements (copper and zinc) that are important for the physiologic mechanisms of organisms, reducing liver damage.


2012 ◽  
Vol 2 (3) ◽  
pp. 94-98
Author(s):  
Dugganaboyana Guru Kumar ◽  
Purandekkattil Deepa ◽  
Muthaiyan Ahalliya Rathi ◽  
Periasamy Meenakshi ◽  
Velliyur Kanniappan Gopalakrishnan

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