scholarly journals The Neuroprotective Effect of Atorvastatin on Apoptosis of Hippocampus Following Transient Global Ischemia/ Reperfusion

2016 ◽  
Vol 5 (2) ◽  
pp. 82-89
Author(s):  
Masoumeh Faghani ◽  
Farhang Ejlali ◽  
Zahra Nadia Sharifi ◽  
Hassan Molladoost ◽  
Shabnam Movassaghi
Keyword(s):  
Treatment Group ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Pyramidal Cells ◽  
Male Rats ◽  
Intact Cells ◽  
Ischemic Reperfusion ◽  
Ca1 Region ◽  
Significant Difference ◽  
Ca1 Cells

Background: Hippocampus CA1 cells are highly sensitive to ischemia. Because of anti-oxida­tive property, atorvastatin by eliminating free radicals and other constituent due to cell lesions prevents damages or death of intact cells. The aim of this study is to determine neuroprotective effect of atorvastatin on apoptosis of hippocampus CA1 cells in male rats. Material and Meth­ods: In an experimental study 24 male rats –Wistar adult race- were divided into four groups: Ischemic, vehicle, treatment and control. In order to make an ischemic- reperfusion model, common carotid artery was clamped bilaterally for 20 minutes. In treatment group, the first dose of Atorvastatin (10mg/kg) was injected six hours after ischemic- reperfusion and 24, 48 and 72 later intraperitoneally. Four days after ischemic- reperfusion tissue section were obtained and stained using Nissl method. Then intact healthy pyramidal CA1 hippocampus cells were counted. TUKEY and One Way ANOVA were used for analyzing the obtained results. Results: No significant difference was found in numbers of healthy intake pyramidal and apoptotic cells of CA1 hippocampus region between treatment group (10mg/kg Atorvastatin) and controls, whereas a significant reduction of these cells was observed in ischemia and vehicle groups in comparison to controls (P<0.05). Conclusion: Using 10mg/kg atorvastatin following cerebral ischemia- reperfusion has a protective effect on pyramidal cells of CA1 region in hippocampus in male rats leading to reduction of degeneration and apoptosis.[GMJ.2016;5(2):82-89]

scholarly journals Neuroprotective Effect Of Musk On Rat Brain Ischemic Model

2020 ◽  
Author(s):  
Radnaa Gochoo ◽  
Oyuntsetseg Namsrai ◽  
Dagvatseren Begzsuren ◽  
Bat-Erdene Jargalsaikhan ◽  
Chimedragchaa Chimedtseren
Keyword(s):  
Cerebral Ischemia ◽  
Rat Brain ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Neuronal Cell ◽  
Neurological Deficits ◽  
Control Group ◽  
Ischemic Reperfusion ◽  
Cerebral Ischemia Reperfusion ◽  
Significant Difference

Abstract Background Stroke is leading cause of morbidity and mortality in worldwide. Despite valuable progresses in understanding neurological deficits after stroke, its therapeutic options are remaining limited. We aimed to study the neuroprotective effect of musk on cerebral ischemia/reperfusion injury model rats.Methods:In our experiment, we used 180 whore meal breed Wistar rats which weigh 180-220 g and divided these rats into 50 mg/kg of musk, 100 mg/kg of musk, 10 mg/kg of nimodipine, the ischemic-reperfusion groups by filling the midriff of the brain and take the drugs for 7 days in each group. Cerebral ischemia/reperfusion was induced in rats by temporary middle cerebral artery occlusion-reperfusion (MCAO/R) followed by treatment with musk at 50 mg/kg and 100 mg/kg doses. On days 1, 3 and 7 after MCAO/R, TGF-β, BDNF, TrkB and NGF mRNA expressions in the rat brain tissue were quantitatively analyzed using RT-PCR.Results:Musk 50 and 100 mg/kg treated groups brain stroke size were significantly decreased compared with the experimental group at 1, 3 and 7 days. Moreover, brain BDNF, TrkB, NGF and TGF-β mRNA express were not significant difference between experimental and control group. Also 3rd and 7th day, the data indicate that Musk 50 and 100 mg/kg were significantly (p<0,05) effective increasing rats brain BDNF, TrkB, NGF and TGF- β mRNA express in rats with ischemic stroke induced by MCAO/R. Conclusions: The 50 and 100 mg/kg doses of musk lead to increase neuro-protective factors BDNF, TRkB, NGF and TGF- β expression of mRNA in ischemic-reperfusion rat model. It implies that the Mongolian musk supports the neurogenesis of neuronal cell.

scholarly journals Catalase activity as signal of antioxydant system affection under influence of limb ischemia-reperfusion

2021 ◽  
pp. 24-30
Author(s):  
Nataliya Volotovska
Keyword(s):  
Risk Factors ◽  
Blood Loss ◽  
Catalase Activity ◽  
Ischemia Reperfusion ◽  
Limb Ischemia ◽  
Mechanical Injury ◽  
Male Rats ◽  
Mechanical Trauma ◽  
Control Group ◽  
Ischemic Reperfusion

The use of hemostatic tourniquet is a proved means of primary care. However, systemic disorders, as well as ultrastructural, in the area of compression can significantly worsen the condition of the injured organism. The aim. Estimation of catalase level in rats’ liver on the background of modifications of ischemic-reperfusion syndrome to know the severest pathogenic combination for organism. Materials and methods. 260 white adult male rats were divided into 5 groups: control (KG), EG1 – simulation of isolated ischemia-reperfusion syndrome (IRS) of the limb, EG2 – simulation of isolated volumetric blood loss, EG3 – combination of IRS of the limb with blood loss, EG4 – simulation of isolated mechanical injury of the thigh, EG5 – combination of IRS of the limb and mechanical injury. The variability of catalase level in liver was analyzed. Results. It was found that each of the experimental interventions has led to changes of catalase activity in the liver. The most expressed pathological expressions were observed on the 3rd after interventions, when the studied index in EG3 was lower than in EG1 and EG2 in 6,2 times and by 33,1 %. On the 7th day catalase activity in EG3 was in 9,4 times and by 44,5 % times lower than in EG1 and in EG2 data concordantly. The combination of limb ischemia-reperfusion with blood loss in EG3 led to exhausting of liver antioxydant enzyme catalase in the most critical posttraumatic period (day 3). The same, but less significant effect was registered in the group of combination of mechanical trauma with ischemia-reperfusion in EG5. This proved the role of the tourniquet as a factor that complicated the course of traumatic disease due to ischemic reperfusion. Conclusions. In this experiment, founded risk factors of combination of ischemia-reperfusion with heavy blood loss emphasized the importance and particular attention on such widespread method of bleeding tratment, as the imposition of a tourniquet, as in our experiment it triggered risk factors of ischemia-reperfusion. It was shown katalase activity depression respectively to the periods of increasing of lipid peroxydation. There was peculiarity, that on the base of isolated IRS catalase activity was increased in 2,5 times comparely to control group, whereas the hardest depression of it was found on the background of IRS, combined with blood loss – catalase activity was lower, comparely to KG – in 2,5 times. The importance of understanding the suppression of hepatocytes’ antyoxydants is great, as it might help in prevention the development of liver failure or hepatorenal syndrome on the background of limb ischemia-reperfusion.

scholarly journals Pycnogenol® Supplementation Attenuates Memory Deficits and Protects Hippocampal CA1 Pyramidal Neurons via Antioxidative Role in a Gerbil Model of Transient Forebrain Ischemia

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2477
Author(s):  
Bora Kim ◽  
Tae-Kyeong Lee ◽  
Cheol Woo Park ◽  
Dae Won Kim ◽  
Ji Hyeon Ahn ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Neuroprotective Effect ◽  
Ischemic Injury ◽  
Pyramidal Cells ◽  
Acid Oxidation ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Ca1 Region ◽  
Pine Tree ◽  
Before And After

Pycnogenol® (an extract of the bark of French maritime pine tree) is used for dietary supplement and known to have excellent antioxidative efficacy. However, there are few reports on neuroprotective effect of Pycnogenol® supplementation and its mechanisms against ischemic injury following transient forebrain ischemia (TFI) in gerbils. Now, we examined neuroprotective effect and its mechanisms of Pycnogenol® in the gerbils with 5-min TFI, which evokes a significant death (loss) of pyramidal cells located in the cornu ammonis (CA1) region of gerbil hippocampus from 4–5 days post-TFI. Gerbils were pretreated with 30, 40, and 50 mg/kg of Pycnogenol® once a day for 7 days before TFI surgery. Treatment with 50 mg/kg, not 30 or 40 mg/kg, of Pycnogenol® potently protected learning and memory, as well as CA1 pyramidal cells, from ischemic injury. Treatment with 50 mg/kg Pycnogenol® significantly enhanced immunoreactivity of antioxidant enzymes (superoxide dismutases and catalase) in the pyramidal cells before and after TFI induction. Furthermore, the treatment significantly reduced the generation of superoxide anion, ribonucleic acid oxidation and lipid peroxidation in the pyramidal cells. Moreover, interestingly, its neuroprotective effect was abolished by administration of sodium azide (a potent inhibitor of SODs and catalase activities). Taken together, current results clearly indicate that Pycnogenol® supplementation can prevent neurons from ischemic stroke through its potent antioxidative role.

Relaxin protects against renal ischemia-reperfusion injury

2013 ◽  
Vol 305 (8) ◽  
pp. F1169-F1176 ◽  
Author(s):  
Takuya Yoshida ◽  
Hiromichi Kumagai ◽  
Tetsuya Kohsaka ◽  
Naoki Ikegaya
Keyword(s):  
Structural Damage ◽  
Ischemia Reperfusion Injury ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Male Rats ◽  
Semiquantitative Assessment ◽  
Cell Counts ◽  
Significant Difference

Relaxin, a pregnancy hormone, has antiapoptotic and anti-inflammatory properties. The aim of this study was to determine the effects of relaxin on ischemia-reperfusion (IR)-induced acute kidney injury. Male rats underwent unilateral nephrectomy and contralateral renal IR (45 min of renal pedicle clamping). Rats were divided into three groups: 1) sham group, 2) IR group, and 3) IR-RLX group (rats treated with relaxin before ischemia). In this group, relaxin was infused at 500 ng/h via subcutaneous osmotic minipump for 24 h beginning 2 h before renal ischemia. At 24 h after reperfusion, renal function was assessed and kidneys were removed for analysis. There was no significant difference in blood pressure among the three groups. IR increased plasma levels of creatinine and urea nitrogen, and relaxin provided protection against the increases in these two parameters. Relaxin significantly decreased plasma TNF-α levels and renal TNF receptor 1 mRNA expression, compared with the IR group. Semiquantitative assessment of the histological lesions showed marked structural damage in IR rats compared with the IR-RLX rats. RLX significantly reduced apoptotic cell counts compared with the IR group. Overexpression of caspase-3 observed in the IR kidneys was reduced in the IR-RLX group. The results demonstrated that relaxin provided protection against IR-induced renal injury by reducing apoptosis and inflammation.

scholarly journals Effects of FK506 on Hippocampal CA1 Cells Following Transient Global Ischemia/Reperfusion in Wistar Rat

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Zahra-Nadia Sharifi ◽  
Farid Abolhassani ◽  
Mohammad Reza Zarrindast ◽  
Shabnam Movassaghi ◽  
Nasrin Rahimian ◽  
...  
Keyword(s):  
Single Dose ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Pyramidal Cells ◽  
Wistar Rat ◽  
Cell Number ◽  
Global Cerebral Ischemia ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Transient Global Cerebral Ischemia

Transient global cerebral ischemia causes loss of pyramidal cells in CA1 region of hippocampus. In this study, we investigated the neurotrophic effect of the immunosuppressant agent FK506 in rat after global cerebral ischemia. Both common carotid arteries were occluded for 20 minutes followed by reperfusion. In experimental group 1, FK506 (6 mg/kg) was given as a single dose exactly at the time of reperfusion. In the second group, FK506 was administered at the beginning of reperfusion, followed by its administration intraperitoneally (IP) 6, 24, 48, and 72 hours after reperfusion. FK506 failed to show neurotrophic effects on CA1 region when applied as a single dose of 6 mg/kg. The cell number and size of the CA1 pyramidal cells were increased, also the number of cell death decreased in this region when FK506 was administrated 48 h after reperfusion. This work supports the possible use of FK506 in treatment of ischemic brain damage.

scholarly journals Effect of Giving Mahkota Dewa Fruits (Phaleria Macrocarpa) Extract to Epithelialization In Incision Wound of White Rats (Rattus Norvegicus)

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Idola Perdana Sulistyoning Suharto
Keyword(s):  
Treatment Group ◽  
Rattus Norvegicus ◽  
Male Rats ◽  
Control Group ◽  
P Value ◽  
Control Group Design ◽  
White Rats ◽  
Significant Difference ◽  
Phaleria Macrocarpa ◽  
Incision Wound

The research purpose was to analysis effect of giving mahkota dewa fruits (Phaleria macrocarpa) extract to epithelialization in incision wound of white rats (Rattus norvegicus). The method was randomized posted-only control group design. There were 30 male rats (Rattus norvegicus) grouped on control and treatment group. Control group divided into three groups (KK1, KK2, KK3) and also treatment group divided into three groups (KP1, KP2, KP3). Control group just given CMC 1% peroral without mahkota dewa fruits extract, the treatment group given mahkota dewa fruits extract 22.5 mg/kg body weight. The data was analyzed by Kruskall Wallis. Based on Kruskall Wallis test, obtained result that there was a significant difference (p<0.05) epithelialization variable with p value p = 0.000 between control and treatment group. And based on One-way Anova test, obtained result that there was a significant difference (p<0.05) with p value p =0.000 between control and treatment group. The conclusion of this research was giving mahkota dewa fruits (Phaleria macrocarpa) extract can increase epithelialization in incision wound of white rats (Rattus norvegicus). Keywords : Mahkota Dewa Fruits (Phaleria Macrocarpa) Extract, Epithelialization, Incision Wound 

scholarly journals Photobiomodulation Promotes Hippocampal CA1 NSC Differentiation Toward Neurons and Facilitates Cognitive Function Recovery Involving NLRP3 Inflammasome Mitigation Following Global Cerebral Ischemia

2021 ◽  
Vol 15 ◽  
Author(s):  
Sihan Guo ◽  
Ruimin Wang ◽  
Jiewei Hu ◽  
Liping Sun ◽  
Xinru Zhao ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Neurological Recovery ◽  
Male Rats ◽  
Global Cerebral Ischemia ◽  
Inflammasome Activation ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1

Our recent study revealed that photobiomodulation (PBM) inhibits delayed neuronal death by preserving mitochondrial dynamics and function following global cerebral ischemia (GCI). In the current study, we clarified whether PBM exerts effective roles in endogenous neurogenesis and long-lasting neurological recovery after GCI. Adult male rats were treated with 808 nm PBM at 20 mW/cm2 irradiance for 2 min on cerebral cortex surface (irradiance ∼7.0 mW/cm2, fluence ∼0.8 J/cm2 on the hippocampus) beginning 3 days after GCI for five consecutive days. Cognitive function was evaluated using the Morris water maze. Neural stem cell (NSC) proliferation, immature neurons, and mature neurons were examined using bromodeoxyuridine (BrdU)-, doublecortin (DCX)-, and NeuN-staining, respectively. Protein expression, such as NLRP3, cleaved IL1β, GFAP, and Iba1 was detected using immunofluorescence staining, and ultrastructure of astrocyte and microglia was observed by transmission electron microscopy. The results revealed that PBM exerted a markedly neuroprotective role and improved spatial learning and memory ability at 58 days of ischemia/reperfusion (I/R) but not at 7 days of reperfusion. Mechanistic studies revealed that PBM suppressed reactive astrocytes and maintained astrocyte regeneration at 7 days of reperfusion, as well as elevated neurogenesis at 58 days of reperfusion, as evidenced by a significant decrease in the fluorescence intensity of GFAP (astrocyte marker) but unchanged the number of BrdU-GFAP colabeled cells at the early timepoint, and a robust elevation in the number of DCX-NeuN colabeled cells at the later timepoint in the PBM-treated group compared to the GCI group. Notably, PBM treatment protected the ultrastructure of astrocyte and microglia cells at 58 days but not 7 days of reperfusion in the hippocampal CA1 region. Furthermore, PBM treatment significantly attenuated the GCI-induced immunofluorescence intensity of NLRP3 (an inflammasome component), cleaved IL1β (reflecting inflammasome activation) and Iba1, as well as the colocalization of NLRP3/GFAP or cleaved IL-1β/GFAP, especially in animals subjected to I/R at 58 days. Taken together, PBM treatment performed postischemia exerted a long-lasting protective effect on astrocytes and promoted endogenous neurogenesis in the hippocampal CA1 region, which might contribute to neurological recovery after GCI.

Neuroprotective Effect of Nilotinib on Cortical Pyramidal Cells, Histological, Morphometric and Biochemical Study

2020 ◽  
pp. 23-33
Author(s):  
Ahmed S. Ahmed
Keyword(s):  
Cell Death ◽  
Antioxidant Enzymes ◽  
Antiepileptic Drug ◽  
Neuroprotective Effect ◽  
Latency Period ◽  
Neuronal Cell ◽  
Pyramidal Cells ◽  
Male Rats ◽  
Control Group ◽  
Cortical Tissue

Introduction: Death of neuronal cell and gliosis are the two main pathological hallmarks induced by nervous tissue stress like conditions such as status epilepticus. Previous studies have mentioned that neuronal cell death occur as a result of different mechanisms, namely, necrosis and apoptosis. Although more recent studies have explained the cell death on the basis of autophagy. Many antiepileptic drugs are marketed, taking into consideration the antioxidant role of nilotinib and support its use as a favorable antiepileptic drug. The aim of the present study is to assess the neuroprotective effect of antiepileptic drug nilotinib on cortical tissue in rats. Materials and Methods: Sixty adult male rats were divided into three groups: (1) Control group, (2) pentylenetetrazol group (injected with pentylenetetrazol 60 mg/kg, subcutaneously), (3) nilotinib and pentylenetetrazol group (pretreated with nilotinib, 25 mg/kg daily for seven days prior to pentylenetetrazol administration). Latency of seizure and level of either oxidant or antioxidant enzymes in the cortical tissue was assessed. The histopathological changes in the cerebral cortex were studied also using hematoxylin and eosin stain. Results: Nilotinib increased the latency period of convulsions, increased the antioxidant enzymes levels with regain of the normal histological features. Conclusions: Nilotinib proved to promote the antioxidant, antiapoptotic pathways, anti-inflammatory and inhibiting autophagy which favor its use as an anti-epileptic drug.

scholarly journals Dietary cottonseed consumption induced subfertility in male and female rats: a potent eco-friendly rodenticide compound

2021 ◽  
Author(s):  
Fariborz Nowzari ◽  
Farhad Rahmanifar ◽  
Nader Tanideh ◽  
Mohammad Reza Dorvash ◽  
Arezoo Khoradmehr ◽  
...  
Keyword(s):  
Treatment Group ◽  
Female Rats ◽  
Male Rats ◽  
Whole Body ◽  
Control Group ◽  
Cottonseed Flour ◽  
Male And Female ◽  
Treatment Groups ◽  
Male And Female Rats ◽  
Significant Difference

Abstract Effects of cottonseed flour in male and female rats’ fertility based on hormonal and histomorphometry changes were studied. Sixty-four Sprague-Dawley adult male and female rats were randomly divided into control and treatment groups. Treatment group was received diets containing cottonseed flour for 35 days. Control group was given standard rat food. Body and testis weights, epididymis semen evaluation indices and serum sex steroid hormones were determined. Histomorphometry alterations of testes and ovary were evaluated. Then, normal female and male rats were mated by rats in both groups and after 35 days, number of pups was measured. However, there was no significant difference in whole body and testes weights, sperm concentration and viability between the control and treatment groups, respectively. Moreover, sperm motility in the treatment rats was significantly lower than the control group. Serum hormones alterations were not significant, but histomorphometry evaluations of testes showed significant changes in the testis structures after chronic consumption of cottonseed flour. In the female rats, body weight did not have significant difference between the treatment and control groups. Histomorphometry data in female ovary showed significant reduction of primary follicle volume and number in the treatment group against control. Follicle stimulating hormone showed insignificant reduction in the treatment group. Number of pups was significantly reduced in the female rats fed by cottonseed flour. Cottonseed flour in rat diet had adverse effects on rat reproduction. Therefore, it can be used as an efficient product for control of the rat population as a natural rodenticide agent.

scholarly journals The Effects of Pentoxifylline on Memory in Male Rats Treated with Zinc Oxide NPs

2021 ◽  
Vol 25 (1) ◽  
pp. 1-10
Author(s):  
Niloufar Darbandi ◽  
◽  
Zeynab Vasheghani Farahani ◽  
Hamidreza Momeni ◽  
◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Zinc Oxide ◽  
Treatment Group ◽  
Blood Serum ◽  
Zinc Oxide Nanoparticles ◽  
Male Rats ◽  
Control Group ◽  
Oxide Nanoparticles ◽  
Zno Nps ◽  
Ca1 Region

Background: Zinc oxide Nanoparticles (NPs) present irreversible effects on the nervous system, memory, and learning. Objective: The current study aimed to investigate the effects of pentoxifylline on memory impairments, CA1 hippocampal pyramidal cells, and blood serum antioxidant enzymes in male rats treated with zinc oxide NPs. Methods: Male Wistar rats were divided into the control, zinc oxide NPs (1.25 mg/kg), pentoxifylline (50 mg/kg), and pentoxifylline with zinc oxide NPs groups. In all study groups, saline, zinc oxide NPs, and pentoxifylline were intraperitoneally injected 30 minutes before training. In the co-treatment group, pentoxifylline was injected one hour before injecting Zno NPs. After performing the behavioral test, the tested animals’ brains were fixed and the number of healthy neurons in the CA1 region of the hippocampus was counted. In all research groups, malondialdehyde levels, total antioxidant power, superoxide dismutase levels, and glutathione peroxidase in blood serum were measured. Results: Zinc oxide nanoparticles decreased memory and the number of healthy neurons in the CA1 region of the hippocampus and increased oxidative stress in blood serum, compared to the controls. In the co-treatment group, using pentoxifylline improved the above-mentioned factors and reached the level of the control group. Pentoxifylline alone presented no significant effect on the aforementioned characteristics, compared to the control group. Conclusion: ZnO NPs may decrease memory retrieval and cause cell death in the pyramidal neurons of the CA1 region of the hippocampus by increasing oxidative stress. Pentoxifylline, as a potent antioxidant, can prevent the harmful effects of ZnO NPs.

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