Apoptotic Mode of Cell Death in Substantia Nigra Following Intranigral Infusion of the Parkinsonian Neurotoxin, MPP+ in Sprague-Dawley Rats: Cellular, Molecular and Ultrastructural Evidences

AbstractSalsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline; Sal) is structurally similar to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is supposed to have a role in the development of Parkinson-like syndrome in both human and non-human subjects. In the human brain, the amount of (R)-enantiomer of Sal is much higher than (S)-enantiomer, suggesting that a putative enzyme may participate in the synthesis of (R)-salsolinol, called (R)-salsolinol synthase. In this study, the (R)-salsolinol synthase activity in the condensation of dopamine and acetaldehyde was investigated in the crude extracts from the brains of Sprague Dawley rats. Identification of the enzymatic reaction products and enzyme activity detection were achieved by HPLC-electrochemical detection. The discovery of this enzyme activity in rat’s brain indicates the natural existence of (R)-salsolinol synthase in the brains of humans and rats, and it is distributed in most brain regions of rat with higher activity in soluble proteins extracted from striatum and substantia nigra.

Download Full-text

High-Fat-High-Fructose Diet Decreases Hippocampal Neuron Number in Male Rats

The Indonesian Biomedical Journal ◽

10.18585/inabj.v12i1.865 ◽

2020 ◽

Vol 12 (1) ◽

pp. 1-7

Author(s):

Inggita Kusumastuty ◽

Frinny Sembiring ◽

Sri Andarini ◽

Dian Handayani

Keyword(s):

Cell Death ◽

Nerve Cell ◽

Hippocampal Neurons ◽

Sprague Dawley ◽

High Fat ◽

Group I ◽

Sprague Dawley Rats ◽

High Fructose ◽

Group Ii ◽

Nerve Cell Death

BACKGROUND: Consumption of foods and drinks high in energy, fat, and/or sugar beyond the recommended quantities can cause obesity, which triggers the incidence of brain nerve cell death related to oxidative stress, high levels of tumor necrosis factor (TNF)-α and triglycerides, and low high-density lipoprotein (HDL) levels. Progressive nerve cell death causes decreasing cognitive performance. This study aims to prove that an American Institute of Nutrition committee in 1993 (AIN-93M) diet modified with high-fat-high-fructose (HFHF) can decrease the number of hippocampal neurons. A decrease in the number of hippocampal neurons indicates progressive nerve cell death.METHODS: An experimental study using a post-test control group design was carried out using male Sprague Dawley rats. Samples were selected using simple random sampling to divide them into two groups, Group I was AIN-93M-modified HFHF diet (n=14) and Group II was AIN-93M standard (n=16). The number of visible neurons was measured in the hippocampus area of Sprague Dawley rats’ brains, stained with haemotoxylin and eosin (H&E) and scanned under 400x magnification. Neurons were counted in 10 visual fields using the "Cell_Count" application.RESULTS: The data were analysed by Pearson’s correlation test using SPSS. The results show that rats in Group I had a greater weight gain and fewer neurons than those in the Group II (p=0.023, r=-0.413).CONCLUSION: The consumption of foods high in fat and fructose can cause an increase in nerve cell death, as shown by the decrease in the number of hippocampal neurons.KEYWORDS: brain nerve cells, high fat, high fructose, increased body weight

Download Full-text

Inhalation of formaldehyde and xylene induces apoptotic cell death in the lung tissue

Toxicology and Industrial Health ◽

10.1177/0748233709106824 ◽

2009 ◽

Vol 25 (7) ◽

pp. 455-461 ◽

Cited By ~ 9

Author(s):

M. Sandikci ◽

K. Seyrek ◽

H. Aksit ◽

H. Kose

Keyword(s):

Cell Death ◽

Lung Tissue ◽

Lymphoid Tissue ◽

Apoptotic Cell ◽

Apoptotic Cells ◽

Sprague Dawley ◽

Control Groups ◽

Adult Rats ◽

Lymphoid Follicles ◽

Sprague Dawley Rats

The aim of this study was to determine the localization and number of apoptotic cells in lung tissue and bronchus-associated lymphoid tissue (BALT) of newborns, young, and adult rats exposed to formaldehyde (6 ppm) or technical xylene (300 ppm) for 6 weeks (8 h/day). A total of 27 female Sprague-Dawley rats were used. Apoptotic cells were mainly localized around the bronchus and bronchioles and relatively less frequently on the walls of alveoli and interalveolar septa both in control and experimental groups. In the BALT, reactive cells were localized in the area under the epithelium and distributed homogenously within the lymphoid follicles. The numbers of apoptotic cells in the lung tissue including the BALT were significantly higher in young and adult rats exposed to formaldehyde and xylene than those detected in control groups.

Download Full-text

Effect of Photobiomodulation in Rescuing Lipopolysaccharide-Induced Dopaminergic Cell Loss in the Male Sprague–Dawley Rat

Biomolecules ◽

10.3390/biom9080381 ◽

2019 ◽

Vol 9 (8) ◽

pp. 381 ◽

Cited By ~ 2

Author(s):

O’Brien ◽

Austin

Keyword(s):

Cell Death ◽

Cell Loss ◽

Lesion Size ◽

Motor Deficits ◽

Sprague Dawley ◽

Dopaminergic Cell ◽

Sprague Dawley Rats ◽

Neuroprotective Therapy ◽

Potential Benefits ◽

Inflammatory Component

Photobiomodulation (PBM) provides neuroprotection against dopaminergic cell death and associated motor deficits in rodent and primate models of Parkinson’s disease (PD). However, it has not yet been tested in the lipopolysaccharide (LPS) model of PD, which leads to dopaminergic cell death through microglia-evoked neuroinflammation. We investigated whether transcranial PBM could protect against dopaminergic cell death within the substantia nigra in male Sprague–Dawley rats following supranigral LPS injection. PBM fully protected rats from 10 µg LPS which would have otherwise caused 15% cell loss, but there was no significant neuroprotection at a 20 µg dose that led to a 50% lesion. Cell loss at this dose varied according to the precise site of injection and correlated with increased local numbers of highly inflammatory amoeboid microglia. Twenty microgram LPS caused motor deficits in the cylinder, adjusted stepping and rotarod tests that correlated with dopaminergic cell loss. While PBM caused no significant improvement at the group level, motor performance on all three tests no longer correlated with the lesion size caused by 20 µg LPS in PBM-treated rats, suggesting extranigral motor improvements in some animals. These results provide support for PBM as a successful neuroprotective therapy against the inflammatory component of early PD, provided inflammation has not reached a devastating level, as well as potential benefits in other motor circuitries.

Download Full-text

Abstract 211: Delayed Cell Death in CA1 Region in a Cardiac Arrest Rat Model: Continuing After 2 Weeks of Survival?

Circulation ◽

10.1161/circ.130.suppl_2.211 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Sandra Högler ◽

Ursula Teubenbacher ◽

Wolfgang Weihs ◽

Fritz Sterz ◽

Ingrid A M Magnet ◽

...

Keyword(s):

Cell Death ◽

Cardiac Arrest ◽

Brain Regions ◽

Spontaneous Circulation ◽

Sprague Dawley ◽

Ca1 Region ◽

Delayed Cell Death ◽

Time Period ◽

Sprague Dawley Rats ◽

Hematoxylin Eosin

Background: Evolution of histological lesions in selectively vulnerable brain regions in animal models of cardiac arrest (CA)give evidence of potential therapeutic windows. Delayed cell death is of special interest in this regard. Methods: In male Sprague-Dawley rats (350g) ventricular fibrillation (VF) CA was induced for 6 min followed by chest compressions, ventilation and drugs for 2 min. To achieve return of spontaneous circulation animals were defibrillated every 2 min. Animals were sacrificed after one week (n=5) or two weeks (n=7) of survival and compared to four sham animals. Brains were fixed in formalin, embedded in paraffin wax and cut into 3 μm thick coronary sections for histological examination. Viable neurons with nucleolus were counted in Hematoxylin-Eosin (HE)-stained sections in a 250 μm sector of the medial CA1 region. FluoroJade B staining was applied to count dying neurons in the same sector. Results: In HE-staining sham animals had 31±4 viable neurons. In one week survivors 11±9 viable neurons (p=0.003) and in two week survivors 7±7 viable neurons (p=0.001 vs sham, p=0.49 vs one week survivors) were counted. Furthermore, a lot of degenerated hypereosinophilic neurons were present in HE-staining in both CA-groups. FluoroJade B-staining was negative in sham animals. In one week survivors 29±8 dying neurons (p=0.006) and in two week survivors 33±13 dying neurons (p= 0.016 vs sham, p=0.343 vs one week survivors) were detectable. Conclusions: Consistent damage in the medial CA1 region was present after 6 min VFCA in both survival time groups. Lesions seemed to be constant, with no significant differences between time points. Contrary to expectations, FluoroJade B-staining was still positive after two weeks of survival, suggesting that delayed cell death might go on for a longer time period than assumed so far.

Download Full-text

Dopaminochrome induces neuroinflammation in the substantia nigra of Sprague Dawley rats

The FASEB Journal ◽

10.1096/fasebj.24.1_supplement.1053.8 ◽

2010 ◽

Vol 24 (S1) ◽

Author(s):

Julie Marie Breckenridge ◽

Daniel S Zahm ◽

Thomas C Westfall ◽

Heather Macarthur

Keyword(s):

Substantia Nigra ◽

Sprague Dawley ◽

Sprague Dawley Rats

Download Full-text

Cell Death in the Normal Epiphyseal Cartilage of the Rat

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100060210 ◽

1967 ◽

Vol 25 ◽

pp. 40-41

Author(s):

Aly Fahmy

Keyword(s):

Cell Death ◽

Epiphyseal Cartilage ◽

Base Line ◽

Long Bones ◽

Sprague Dawley ◽

Cartilaginous Tissues ◽

Intercellular Matrix ◽

Sprague Dawley Rats ◽

Secretory Products ◽

Tibial Epiphyseal

The ultrastructure of the upper tibial epiphyseal cartilage plate of weanling and plateaued Sprague-Dawley rats growing under normal conditions has been studied, in order to establish a base-line for the future investigation of the site and mechanism of action of certain hormones which are known to affect the growth and maturation of long bones.Observations have been made concerning the character and amount of the secretory products in the cells of the various zones, as well as the characteristics of the constituents of the intercellular matrix. Our findings have confirmed and amplified published observations on the ultrastructure of cartilaginous tissues in a variety of species in general.

Download Full-text

Intralesional Patterns of MRI ADC Maps Predict Outcome in Experimental Stroke

Cerebrovascular Diseases ◽

10.1159/000381727 ◽

2015 ◽

Vol 39 (5-6) ◽

pp. 293-301 ◽

Cited By ~ 8

Author(s):

Isabel Lestro Henriques ◽

María Gutiérrez-Fernández ◽

Berta Rodríguez-Frutos ◽

Jaime Ramos-Cejudo ◽

Laura Otero-Ortega ◽

...

Keyword(s):

Cell Death ◽

Functional Outcome ◽

Lesion Size ◽

Artery Occlusion ◽

Experimental Stroke ◽

Acute Ischemia ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Ischemic Tissue ◽

Cerebral Artery Occlusion

Background: After acute ischemia, the tissue that is at risk of infarction can be detected by perfusion-weighted imaging/diffusion-weighted imaging (PWI/DWI) mismatch but the time that is needed to process PWI limits its use. As DWI is highly sensitive to acute ischemic tissue damage, we hypothesized that different ADC patterns represent areas with a different potential for recovery. Methods: In a model of permanent middle cerebral artery occlusion (pMCAO), Sprague-Dawley rats were randomly distributed to sham surgery and pMCAO. We further separated the pMCAO group according to intralesional ADC pattern (homogeneous or heterogeneous). At 24 h after ischemia induction, we analyzed lesion size, functional outcome, cell death expression, and brain protection markers including ROS enzyme NOX-4. MRI included DWI (ADC maps), DTI (tractography), and PWI (CBF, CBV and MTT). Results: The lesion size was similar in pMCAO rats. Animals with a heterogeneous pattern in ADC maps showed better functional outcome in Rotarod test (p = 0.032), less expression of cell death (p = 0.014) and NOX-4 (p = 0.0063), higher intralesional CBF (p = 0.0026) and larger PWI/DWI mismatch (p = 0.007). Conclusions: In a rodent model for ischemic stroke, intralesional heterogeneity in ADC maps was related to better functional outcome in lesions of similar size and interval after pMCAO. DWI ADC maps may assist in the early identification of ischemic tissue with an increased potential for recovery as higher expression of acute protection markers, lower expression of cell death, increased PWI/DWI mismatch, and higher intralesional CBF were present in animals with a heterogeneous ADC pattern.

Download Full-text

Nicorandil inhibits TLR4/MyD88/NF-κB/NLRP3 signaling pathway to reduce pyroptosis in rats with myocardial infarction

Experimental Biology and Medicine ◽

10.1177/15353702211013444 ◽

2021 ◽

pp. 153537022110134

Author(s):

Feng Chen ◽

Zhi-Qing Chen ◽

Gui-Ling Zhong ◽

Ji-Jin Zhu

Keyword(s):

Myocardial Infarction ◽

Cell Death ◽

Myocardial Injury ◽

Inflammatory Cell ◽

Adenine Nucleotides ◽

Sprague Dawley ◽

Protein Levels ◽

Sprague Dawley Rats ◽

Cardioprotective Effects ◽

Inflammatory Effect

Pyroptosis is an inflammatory cell death that regulates cardiomyocyte loss after myocardial infarction. Reports indicate that nicorandil has a strong anti-inflammatory effect and protects the myocardium from myocardial infarction. However, its relationship with pyroptosis is largely unreported. Here, we investigated to influence and mechanism of action of nicorandil on cardiomyocyte pyroptosis. Forty Sprague Dawley rats were randomly assigned to sham, MI, MI + nicorandil, and MI + nicorandil + TAK242 groups (10 per group). Myocardial infarction modeling was performed through ligation of the anterior descending branch of the left coronary artery. The function of cardiac was evaluated through echocardiography, detection of myocardial adenine nucleotides, cTnI, LDH, TTC, and HE staining. Moreover, we used qRT-PCR, immunohistochemistry, and Western blotting to examine the expression of pyroptosis-related molecules and the inflammasome pathway of TLR4/MyD88/NF- κB/NLRP3. Myocardial infarction caused the activation of GSDMD, aggravated myocardial injury, and triggered cardiac dysfunction. Myocardial infarction induced pyroptotic cell death, manifested as upregulation in mRNA and protein levels associated with pyroptosis, including caspase-1 cleavage and increased expression of IL-1β and IL-18. These changes were mitigated by nicorandil. The achieved data implicate that myocardial infarction induces pyroptosis via the TLR4/MyD88/NF- κB/NLRP3 pathway, which can be inhibited by nicorandil pretreatment. Therefore, nicorandil exerts cardioprotective effects by activating KATP channels, and at least in part through inhibition of the TLR4/MyD88/NF- κB/NLRP3 pathway to reduce myocardial infarction-induced pyroptosis. As such, it is a potential therapy for ischemic heart disease.

Download Full-text

Divergent Effects of Resveratrol on Rat Cardiac Fibroblasts and Cardiomyocytes

Molecules ◽

10.3390/molecules24142604 ◽

2019 ◽

Vol 24 (14) ◽

pp. 2604

Author(s):

Xavier Lieben Louis ◽

Zach Meikle ◽

Laura Chan ◽

Garret DeGagne ◽

Rebecca Cummer ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Death ◽

Estrogen Receptor Alpha ◽

Cardiac Fibroblasts ◽

Dependent Manner ◽

Sprague Dawley ◽

Induce Cell Death ◽

Adult Rat ◽

Sprague Dawley Rats ◽

Apoptosis Assay

In this study, we tested the potential cardioprotective effects of the phytoalexin resveratrol (Rsv) on primary adult rat cardiac fibroblasts (CF), myofibroblasts (MF) and cardiomyocytes. Adult rat CF and cardiomyocytes were isolated from male 10-week old Sprague–Dawley rats, cultured for either 24 h (cardiomyocytes) or 48 h (CF) before treatments. To isolate MF, CF were trypsinized after 48 h in culture, seeded in fresh plates and cultured for 24 h prior to treatment. All three cells were then treated for a further 24 h with a range of Rsv doses. In CF and MF, cell proliferation, viability, apoptosis assays were performed with or without Rsv treatment for 24 h. In cardiomyocytes, cell viability and apoptosis assay were performed 24 h after treatment. In separate experiments, CF was pre-incubated with estrogen, tamoxifen and fulvestrant for 30 min prior to Rsv treatment. Rsv treatment decreased proliferation of both fibroblasts and myofibroblasts. Rsv treatment also increased the proportion of dead CF and MF in a dose dependent manner. However, treatment with Rsv did not induce cell death in adult cardiomyocytes. There was an increase in the percentage of cells with condensed nuclei with Rsv treatment in both CF and MF, but not in cardiomyocytes. Treatment with estrogen, tamoxifen and fulvestrant alone or in combination with Rsv did not have any additional effects on CF survival. Our results demonstrate that treatment with Rsv can inhibit cell proliferation and induce cell death in rat CF and MF, while not affecting cardiomyocyte survival. We also demonstrated that the induction of cell death in CF with Rsv treatment was independent of estrogen receptor alpha (ERα) signaling.

Download Full-text