scholarly journals Ginkgo Biloba Ameliorates Subfertility Induced by Testicular Ischemia/Reperfusion Injury in Adult Wistar Rats: A Possible New Mitochondrial Mechanism

2016 ◽  
Vol 2016 ◽  
pp. 1-19 ◽  
Author(s):  
Asmaa Ibrahim Ahmed ◽  
Noha N. Lasheen ◽  
Khaled Mohamed El-Zawahry
Keyword(s):  
Ginkgo Biloba ◽  
Wistar Rats ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Free Testosterone ◽  
Control Group ◽  
Protective Effects ◽  
Gingko Biloba ◽  
Group I ◽  
Testicular Ischemia

Testicular torsion, a surgical emergency, could affect the endocrine and exocrine testicular functions. This study demonstrates histopathological and physiological effects of testicular ischemia/perfusion (I/R) injury and the possible protective effects of Ginkgo biloba treatment. Fifty adult male Wistar rats, 180–200 gm, were randomly divided into sham-operated, Gingko biloba supplemented, ischemia only, I/R, and Gingko biloba treated I/R groups. Overnight fasted rats were anaesthetized by Pentobarbital; I/R was performed by left testis 720° rotation in I/R and treated I/R groups. Orchiectomy was performed for histopathological studies and detection of mitochondrial NAD+. Determination of free testosterone, FSH, TNF-α, and IL1-βin plasma was performed. Plasma-free testosterone was significantly decreased, while plasma FSH, TNF-α, IL-1β, and testicular mitochondrial NAD+were significantly increased in I/R group compared to control group. These parameters were reversed in Gingko biloba treated I/R group compared to I/R group. I/R caused marked testicular damage and increased APAF-1 in the apoptotic cells which were reversed by Ginkgo biloba treatment. It could be concluded that I/R caused subfertility induced by apoptosis and oxidative stress manifested by the elevated testicular mitochondrial NAD+, which is considered a new possible mechanism. Also, testicular injury could be reduced by Gingko biloba administration alone.

scholarly journals Effects of Thyroid Hormone Analogue and a Leukotrienes Pathway-Blocker on Reperfusion Injury Attenuation after Heart Transplantation

2013 ◽  
Vol 2013 ◽  
pp. 1-8
Author(s):  
Fadhil G. Al-Amran ◽  
Najah R. Hadi ◽  
Haider S. H. Al-Qassam
Keyword(s):  
Myocardial Ischemia ◽  
Heart Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Control Group ◽  
Group I ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Background. Global myocardial ischemia reperfusion injury after heart transplantation is believed to impair graft function and aggravate both acute and chronic rejection episodes. Objectives. To assess the possible protective potential of MK-886 and 3,5-diiodothyropropionic acid DITPA against global myocardial ischemia reperfusion injury after heart transplantation. Materials and Methods. Adult albino rats were randomized into 6 groups as follows: group I sham group; group II, control group; groups III and IV, control vehicles (1,2); group V, MK-886 treated group. Donor rats received MK-886 30 min before transplantation, and the same dose was repeated for recipients upon reperfusion; in group VI, DITPA treated group, donors and recipients rats were pretreated with DITPA for 7 days before transplantation. Results. Both MK-886 and DITPA significantly counteract the increase in the levels of cardiac TNF-α, IL-1β, and ICAM-1 and plasma level of cTnI (). Morphologic analysis showed that both MK-886 and DITPA markedly improved () the severity of cardiac injury in the heterotopically transplanted rats. Conclusions. The results of our study reveal that both MK-886 and DITPA may ameliorate global myocardial ischemia reperfusion injury after heart transplantation via interfering with inflammatory pathway.

EFFECTS OF MELATONIN AND CURCUMIN TREATMENTS ON THE OVARIUM IN KIDNEY ISCHEMIA-REPERFUSION INJURY: A HISTOPATHOLOGICAL INVESTIGATION

2021 ◽  
Vol 6 (15) ◽  
pp. 45-51
Author(s):  
Ayşe Köse Vuruşkan ◽  
Nur ELAGÜL ◽  
Tansel SAPMAZ ◽  
Sude TOPKARAOĞLU
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Periodic Acid ◽  
Control Group ◽  
Histological Structure ◽  
Periodic Acid Schiff ◽  
Group I ◽  
Vascular Congestion ◽  
Reperfusion Period ◽  
Female Wistar Rats

Aim: We aimed to investigate how bilateral renal ischemia-reperfusion (I/R) damage affects the ovaries as a distant organ and the effects of melatonin (MEL), curcumin (CUR) and melatonin+curcumin (MEL+CUR) treatments on I/R damage. Material and Method: 42 female Wistar rats were used in the study. Rats were divided into 6 groups and study was designed as follows: Control group (G1) – opening and closing the abdomen only (sham surgery group) –, I/R group (G2) – 45 min ischemia followed by 2 h reperfusion –, I/R+MEL group (G3) – 45 min ischemia, intraperitoneal (i.p) 20 mg/kg MEL injection 5 min before reperfusion, followed by 2 h reperfusion –, I/R+CUR group (G4) – 45 min ischemia, 5 min before reperfusion i.p 200 mg/kg CUR injection and then 2 hours reperfusion –, I/R+MEL+CUR group (G5) – 45 min ischemia, 5 min before reperfusion i.p 20 mg/kg MEL and 200 mg/kg CUR injection, followed by 2 hours reperfusion –. At the end of the reperfusion period, the rats were sacrificed. Right ovaries were removed from the peritoneum and fixed. After fixation and follow-up, tissue sections were stained with hematoxylin&eosin (H&E), Periodic acid-Schiff (PAS)+Hematoxylin (PAS+H) and Masson’s trichrome stains. Pathological changes were scored and statistically evaluated. Results: Compared to the control group, there was a decrease in hemorrhage, vascular congestion, follicular degeneration, inflammation, interstitial edema, vasodilation and growing follicle numbers in all groups; these changes were severe in the G2 group; Mild to moderate severity was observed in the G3, G4 and G5 groups. Conclusion: Renal I/R damage significantly affects the ovaries histopathologically. MEL, CUR, and MEL+CUR partially preserve the histological structure, but MEL treatment seems to be more effective than CUR treatment.

scholarly journals Urinary N-Acetyl-Beta-D-Glucosaminidase Activity in Rat Experimental Ischemic and Toxic Models of Acute Kidney Injury

2017 ◽  
Vol 74 (1) ◽  
pp. 105
Author(s):  
Razvan Andrei CODEA ◽  
Mircea MIRCEAN ◽  
Sidonia Alina BOGDAN ◽  
Andras Laszlo NAGY ◽  
Alexandra BIRIS ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Experimental Model ◽  
Wistar Rats ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Control Group ◽  
Tubular Injury ◽  
Group 2 ◽  
Group 1

The identification of a suitable prevention method which facilitates limiting the deleterious effects of acute kidney injuries is highly required. In order to identify a proper treatment for acute kidney injuries, a suitable experimental model that replicates the structural, metabolic and inflammatory lesions that occur in the natural acute injured kidney is highly necessary. Intense urinary NAG activity can be found in a variety of renal disease such as toxic nephropathies, ischemic renal injury following cardiac surgery or renal transplantation but also in glomerular disease especially in diabetic nephropathy. Rises in urinary NAG enzyme activity strongly suggests tubular cell damage and support NAG enzyme as a biomarker of renal tubular injury. The aim of this paper is to obtain a stable in vivo acute kidney injury experimental model, in Wistar, rats and to evaluate the urinary activity of N-acetyl-β-D-glucosaminidase (NAG) enzyme, blood levels of urea and creatinine and microstructural renal alterations induced by ischemia/reperfusion injury respectively gentamicin nephrotoxicity. For this purpose we have used a rat experimental model. Adult male Wistar rats weighing 250-300 g were randomly divided into 3 groups with 8 rats in each group. Group 1 served as a model for the renal ischemia/reperfusion injury experiment, group 2 served for toxic kidney injury experimental model and group 3 served as control group. All individuals in both groups 1 and 2 presented marked elevations in blood urea and creatinine at the moment of euthanasia (day 3 for group 1 and day 9 for group 2) compared to the control group where biochemical values remained within normal limits. Urine analysis of both group 1 and 2 showed marked urinary NAG index activity which suggests acute tubular injury, suggestion confirmed by histological evaluation of the renal parenchyma sampled from this subjects

Ischemic preconditioning and morphine attenuate myocardial apoptosis and infarction after ischemia-reperfusion in rabbits: role of δ-opioid receptor

2004 ◽  
Vol 287 (4) ◽  
pp. H1786-H1791 ◽  
Author(s):  
Shinji Okubo ◽  
Yujirou Tanabe ◽  
Kenji Takeda ◽  
Michihiko Kitayama ◽  
Seiyu Kanemitsu ◽  
...  
Keyword(s):  
Infarct Size ◽  
Opioid Receptor ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Apoptotic Cells ◽  
Protective Effects ◽  
Δ Opioid Receptor

We examined whether ischemic preconditioning (IPC) attenuates ischemia-reperfusion injury, in part, by decreasing apoptosis and whether the δ-opioid receptor (DOR) plays a pivotal role in the regulation of apoptosis. Rabbits were subjected to 30-min coronary artery occlusion (CAO) and 180 min of reperfusion. IPC was elicited with four cycles of 5-min ischemia and 10-min reperfusion before CAO. Morphine (0.3 mg/kg iv) was given 15 min before CAO. Naloxone (Nal; 10 mg/kg iv) and naltrindole (Nti; 10 mg/kg iv), the respective nonselective and selective DOR antagonists were given 10 min before either morphine or IPC. Infarct size (%risk area) was reduced from 46 ± 3.8 in control to 11.6 ± 1.0 in IPC and 19.5 ± 3.8 in the morphine group (means ± SE; P < 0.001 vs. control). Nal blocked the protective effects of IPC and morphine, as shown by the increase in infarct size to 38.6 ± 7.2 and 44.5 ± 1.8, respectively. Similarly, Nti blocked IPC and morphine-induced protection. The percentage of apoptotic cells (revealed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) decreased in IPC (3.6 ± 1.9) and morphine groups (5.2 ± 1.2) compared with control group (12.4 ± 1.6; P < 0.001). Nti pretreatment increased apoptotic cells 11.2 ± 2.2% in IPC and 12.1 ± 0.8% in morphine groups. Nal failed to block inhibition of apoptosis in the IPC group (% of cells: 5.7 ± 1.3 vs. 3.6 ± 1.9 in IPC alone; P > 0.05). These results were also confirmed by nucleosomal DNA laddering pattern. We conclude that IPC reduces lethal injury, in part, by decreasing apoptosis after ischemia-reperfusion and activation of the DOR may play a crucial role in IPC or morphine-induced myocardial protection.

scholarly journals Protective effects of tempol in an experimental ovarian ischemia–reperfusion injury model in female Wistar albino rats

2017 ◽  
Vol 95 (7) ◽  
pp. 861-865 ◽  
Author(s):  
Neslihan Pınar ◽  
Oya Soylu Karapınar ◽  
Oğuzhan Özcan ◽  
Esin Atik Doğan ◽  
Suphi Bayraktar
Keyword(s):  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Stress Index ◽  
Albino Rats ◽  
Protective Effects ◽  
Group V ◽  
Group Iii ◽  
Group I ◽  
Wistar Albino Rats

The aim of this study was to investigate the antioxidant effects of tempol on ovarian ischemia–reperfusion (I/R) injury in rats. Forty female Wistar albino rats were randomly divided into 5 groups: Group I, sham; Group II, ischemia (I); Group III, I/R; Group IV, I/R + tempol 30 mg/kg i.p; Group V, I/R + tempol 50 mg/kg i.p. Oxidative stress index (OSI) was significantly higher in the ischemia group and the I/R group than in the sham group. Catalase levels were significantly lower in the I/R group than in the I/R + tempol 30 mg/kg i.p. and the I/R + tempol 50 mg/kg i.p. groups. Glutathione peroxidase levels were lower in the I/R group than in the I/R + tempol 30 mg/kg i.p. and the I/R + tempol 50 mg/kg i.p. groups. MDA levels were significantly lower in the I/R + tempol 30 mg/kg i.p. group and the I/R + tempol 50 mg/kg i.p. group than in the I/R group. The levels of the histopathological parameters were significantly decreased in the I/R + tempol 50 mg/kg i.p. group compared with the I/R group. Tempol can be used for reducing ovarian I/R injury.

scholarly journals Protective Effects of Selenium Against Sodium Fluoride Induced Behavioral, Anti-Oxidant and Neurohistological Alterations in Wistar Rats

2018 ◽  
Vol 15 (2) ◽  
pp. 475-484 ◽  
Author(s):  
Gorantla Sri Charitha ◽  
Kurmeti Sudhakar ◽  
K. Pratap Reddy
Keyword(s):  
Sodium Fluoride ◽  
Wistar Rats ◽  
Motor Coordination ◽  
Soft Tissues ◽  
Tap Water ◽  
Control Group ◽  
Protective Effects ◽  
Sod Activity ◽  
Group I ◽  
Anti Oxidant

Fluoride naturally occurs in the earth’s crust and ground water and it causes fluorosis when it is consumed in high levels. The fluorosis also affects soft tissues like liver, kidney, heart, brain etc., in addition to skeletal and dental systems. The present study reports the protective effects of selenium against sodium fluoride induced neurotoxic effects. Three months old (around 250 – 280 g weight) wistar rats were randomly categorized into four groups viz. Group I (control) which received normal tap water, Group II (sodium fluoride, NaF) treated with 20 ppm of fluoride through IP, Group III treated with (NaF 20 ppm) + Selenium (5 mgkg-1 body wt./day/rat) and Group IV treated with Selenium (5 mgkg-1 body wt./day/rat) alone. The doses were continued for a period of 15 days and after that they were used for recording behavioral (rota rod, hot plate), anti-oxidant (LPO, SOD, CAT and GSH-Px) and histological (Golgi cox staining) observations. The rats treated with NaF showed the decreased motor coordination, thermal pain response, decreased CAT and SOD activity and increased LPO levels and GSH-Px activity with compared to control group. Moreover, NaF received rats also showed the decreased number of dendrites, synaptic connections and neural networks. These all alterations were reversed on administration of selenium towards fluoride toxicity and the results were significant (p<0.01). The results of selenium alone treated group of rats is comparable to control group. Based on these observed results, the present study evidenced the protective role of selenium against fluoride induced neurotoxicity.

scholarly journals Effects of Cilostazol and Diltiazem Hydrochloride on Ischemia-Reperfusion Injury in a Rat Hindlimb Model

2017 ◽  
Vol 20 (2) ◽  
pp. 058 ◽  
Author(s):  
Bekir İNAN ◽  
Selma SÖNMEZ ERGÜN ◽  
Asiye NURTEN ◽  
Canan KÜÇÜKGERGİN ◽  
Aslı ZENGİN TÜRKMEN ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Saline Group ◽  
Dimethyl Sulphoxide ◽  
Control Group ◽  
Albino Rats ◽  
Diltiazem Hydrochloride ◽  
Beneficial Effects ◽  
Group I

Objective: Free radicals and neutrophils are potent sources of ischemia-reperfusion injury (I/R) and they can be limited by the use of exogenous application of some therapeutic agents. The objective of this study was to compare the effects of cilostazol and diltiazem hydrochloride in a rat hind limb model of I/R injury. Methods: Skeletal muscles submitted to 2 hours of ischemia by placing an aneurysm clip to femoral artery and reperfused after 1, 2 and 4 hours. Seventy-two Wistar-Albino rats were randomly divided into mainly four groups according to treatment agents:  Group I (control group) was treated with saline; Group II was treated with diltiazem hydrochloride; Group III was treated with cilostazol in 30% dimethyl sulphoxide; and Group IV was treated with 30% dimethyl sulphoxide intraperitoneally. These four main groups also subdivided into three subgroups according to duration of the reperfusion times.  Blood samples were taken and all rats were sacrificed. Results: Cilostazol-treated groups demonstrated a significant decrease in tissue and serum malondialdehyde (MDA) levels, and tissue myeloperoxidase (MPO ) activity compared with other groups. Increase in serum nitric oxide (NOx) level was significantly higher in all subgroups of cilastazol, diltiazem hydrochloride, and dimethyl sulphoxide groups versus the control group.Conclusion: Although these results suggest the beneficial effects of cilostazol and diltiazem hydrochloride on I/R injury, the effect of cilostazol on I/R injury seems to be more efficient than diltiazem hydrochloride.

scholarly journals Protective Effect of BMSCs-derived Exosomes on Testicular Ischemia-reperfusion Injury in Rats

2021 ◽  
Author(s):  
Hu Tian ◽  
Wan-song Zhang ◽  
Cheng Yang ◽  
Jun-hao Zhou ◽  
Ran-ran Zhou ◽  
...  
Keyword(s):  
Treatment Group ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Testicular Tissue ◽  
Sd Rats ◽  
Group I ◽  
Group A ◽  
Testicular Ischemia ◽  
Group B

Abstract Background: Testicular Ischemia reperfusion injury(IRI) is a major pathophysiological process of surgical reduction after testicular torsion, and oxidative stress is the main injury factor. However, the role of BMSCs-derived exosomes in testicular IRI and its mechanism have not been reported. In this study, we investigated the protective effect of bone marrow mesenchymal stem cell-derived exosomes against testicular ischemia-reperfusion injury.Methods: BMSCs were isolated, cultured and identified by primary culture method. Exosomes derived from BMSCs were extracted by ultra-high speed centrifugation method. A testicular IRI model was established in male SD rats. Thirty healthy male SD rats were randomly divided into three groups. Group A: Sham group, group B: normal saline treatment group (I/R+NS), group C: BMSCs-derived exosomes (100 ug/mL) treatment group (I/R+ BMSCs-EXO). Finally take each side (left) of rat torsion by using optical microscope to detect testicular tissue pathology grade and fine structure of organization structure, adopt the method of biochemical determination of groups of testicular tissue MDA and NOS, SOD and CAT activity and T - AOC level.Results: BMSCs were successfully isolated and cultured from rat bone marrow, and exosomes secreted by BMSCs were successfully extracted. In animal model, Compared with the normal spermatogenic structure of testis in group A (Sham), the spermatogenic structure of testis in group B (I/R+NS) was obviously damaged to varying degrees, while the spermatogenic structure of testis in group C (I/R+ BMSCs-EXO) was improved to A certain extent (P<0.05). In the biochemical indexes of testis tissue, the contents of MDA and NOS in group B (I/R+NS) were significantly increased compared with group A (Sham), while the activities of SOD and CAT and T-AOC were decreased compared with group A (Sham) (P<0.05). In the exosome-treated group C (I/R+ BMSCs-EXO), compared with the normal saline treatment group B, The contents of MDA and NOS were decreased to a certain extent, while the activities of SOD and CAT and the level of T-AOC were increased (P<0.05).Conclusion: BMSCs-derived exosomes can be absorbed by rat spermatogonia and have antioxidant and anti-inflammatory protective effects against testicular ischemia-reperfusion injury。

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