scholarly journals Effects of Chronic Lithium Chloride and L-Arginine Treatment on Prevention of Streptozotocin Induced Cognitive Deficits by Ellagic Acid

2018 ◽  
Vol 11 (1) ◽  
pp. 53-65
Author(s):  
Manish Kumar ◽  
Nitin Bansal
Keyword(s):  
Oxidative Stress ◽  
Cognitive Deficits ◽  
Ellagic Acid ◽  
Oral Route ◽  
Cognitive Improvement ◽  
Ldh Activity ◽  
Tnf Α ◽  
Brain Oxidative Stress ◽  
Memory Enhancing ◽  
Nitrite Content

Administration of streptozotocin (STZ) through intracerebroventricular (ICV) route manifests AD symptoms in rats. STZ deregulates the control over GSK-3 and eNOS activities through disruption of phosphoinositides mediated signaling. We attempted to elucidate the functions of GSK-3 and eNOS in memory enhancing activity of ellagic acid (EGA) in STZ (ICV) triggered AD type dementia. A 3 mg/kg dose of STZ was injected gently in lateral cerebral ventricles of rats on day 1 and 3. The rats were given EGA (35 mg/kg b.w.) through oral route for four weeks daily. LiCl (GSK-3 inhibitor) and L-Arginine (NO precursor) were administered for four weeks to explore the modulation of GSK-3 and eNOS respectively by EGA in STZ (ICV) injected rats. MWM and EPM paradigms were utilized for evaluation of memory of rats. The rats were sacrificed on day 28 to determine markers of oxidative stress (TBARS, GSH, SOD, CAT), nitrite, AChE, LDH, TNF-α and eNOS in brain. STZ (ICV) initiated cognitive deficits through enhancement of brain oxidative stress, nitrite, TNF-α, AChE, LDH activity and reduction in eNOS levels. EGA attenuated the rise in oxidative stress, inflammation and LDH activity in STZ (ICV) treated rats. Decrease in nitrite content, AChE activity and resurrection of eNOS activity by EGA averted STZ (ICV) induced memory dysfunction in rats. Chronic inhibition of GSK-3 by LiCl (100 mg/kg, i.p.) enhanced these effects of EGA in STZ (ICV) injected rats which thereby exhibited marked cognitive improvement. L-Arginine group manifested inflation in brain oxidative stress, TNF-α content, AChE and LDH activities. L-Arginine (200 mg/kg, i.p.) surged the nitrite content even though eNOS expression was diminished in brain of EGA and STZ (ICV) administered rats resulting in profound loss of memory. It can be concluded that GSK-3 and eNOS are involved in memory enhancing activity of EGA in STZ (ICV) injected rats.

Tetraclinis articulata essential oil mitigates cognitive deficits and brain oxidative stress in an Alzheimer's disease amyloidosis model

Phytomedicine ◽  
2019 ◽  
Vol 56 ◽  
pp. 57-63 ◽  
Author(s):  
Fatima Zahra Sadiki ◽  
Mostafa El Idrissi ◽  
Oana Cioanca ◽  
Adriana Trifan ◽  
Monica Hancianu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Essential Oil ◽  
Cognitive Deficits ◽  
Tetraclinis Articulata ◽  
Brain Oxidative Stress

PDE3 Inhibition by Cilostazol Ameliorated Behavioral and Biochemical Deficits in Prenatal Alcohol Induced Experimental ADHD

2021 ◽  
Vol 17 ◽  
Author(s):  
Niti Sharma ◽  
Bhupesh Sharma ◽  
Neerupma Dhiman ◽  
Lalit K. Golani
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Ethyl Alcohol ◽  
Neuronal Survival ◽  
Brain Inflammation ◽  
Protein Markers ◽  
Tnf Α ◽  
Brain Oxidative Stress ◽  
Prenatal Alcohol ◽  
Pde3 Inhibitor

Background: Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder with complex aetiology and phenotypes. Maternal consumption of alcohol is known to produce deleterious effects in the progeny, generating ADHD related phenotypes. Phosphodiesterase-3 (PDE3) has been shown to provide benefits in various brain conditions. Objective: To investigate the role of a selective PDE3 inhibitor, effects of cilostazol administration on core phenotypes of prenatal alcohol exposure (PAE) model of ADHD were assessed. Methods: PAE was established by exposing animals to 6/4 g.kg-1 (weekdays/weekends) ethyl alcohol from gestational day 8-20 and cilostazol (30/60 mg.kg-1 p.o.) was administered to the offspring (PND21-48) of females exposed to ethyl alcohol. To identify probable mechanisms involved, the effects on protein markers of neuronal function such as, neuronal survival-BDNF, neuronal transcription factor-pCREB, brain inflammation (IL-6, IL-10 and TNF-α) and brain oxidative stress (TBARS and GSH) were studied in frontal cortex, cerebellum, and striatum. Also, effects on behaviour such as hyperactivity, inattention and anxiety were assessed. Result: PAE induced hyper-locomotion, inattention, and anxiety in tested animals. Administration of cilostazol to PAE group of animals resulted in amelioration of behavioural deficits. Also, cilostazol resulted in a significant increase in the levels of BDNF, pCREB, IL-10 and GSH along with significant decrease in TNF-α, IL-6 and TBARS in different brain areas of PAE group. Conclusion: Cilostazol, a selective PDE3 inhibitor rectified behavioural phenotypes associated with ADHD, possibly by altering protein markers associated with neuronal survival, neuronal transcription factor, brain inflammation, and brain oxidative stress.

Ellagic Acid Administration Negated the Development of Streptozotocin-Induced Memory Deficit in Rats

Drug Research ◽  
2017 ◽  
Vol 67 (07) ◽  
pp. 425-431 ◽  
Author(s):  
Nitin Bansal ◽  
Pushplata Yadav ◽  
Manish Kumar
Keyword(s):  
Morris Water Maze ◽  
Cognitive Deficits ◽  
Ellagic Acid ◽  
Water Maze ◽  
Elevated Plus Maze ◽  
Morris Water Maze Test ◽  
Elevated Plus Maze Test ◽  
Maze Test ◽  
Tnf Α ◽  
Plus Maze

AbstractRampant production of pro-oxidants and inadequate antioxidant availability in brain exert oxidative stress, which in synergism with impaired glucose metabolism and inflammation leads to neurodegeneration and cognitive deficits. Ellagic acid (EGA) is a phenolic compound present in various fruits and is reported to possess robust antioxidant and anti-inflammatory properties. The present study investigated the effect of EGA administration on streptozotocin (STZ) induced dementia in rats. Bilateral intracerebroventricle (ICV) injection of STZ (3 mg/kg) was given to Wistar rats (200 g) on day 1 and 3. EGA (17.5 and 35 mg/kg) was administered orally to rats for 28 days daily. The spatial memory of rats was quantified by using Morris water maze and elevated plus maze. Brain TBARS, GSH and TNF-α were also measured. Administration of EGA prevented the induction of STZ-ICV triggered cognitive deficits as evident by a significant (p<0.05) reduction in mean escape latency during acquisition trial and increased (p<0.05) time spent in target quadrant during retrieval trial in Morris water maze test, and reduction (p<0.05) in transfer latency in elevated plus maze test. Furthermore, both the doses of EGA attenuated STZ-ICV induced rise in brain TBARS as well as TNF-α and simultaneously enhanced the GSH content. Thus, EGA ameliorated STZ-induced dementia by probably restoring the balance between cellular pro-oxidants and anti-oxidants in brain of rats.

scholarly journals Ellagic Acid Alleviates Rheumatoid Arthritis in Rats through Inhibiting MTA1/HDAC1-Mediated Nur77 Deacetylation

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Huanjin Song ◽  
Hao Wu ◽  
Jun Dong ◽  
Sihua Huang ◽  
Jintao Ye ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Ellagic Acid ◽  
Oxidative Stress Marker ◽  
Dependent Manner ◽  
Histone Deacetylase 1 ◽  
Protein Levels ◽  
Tnf Α ◽  
And Oxidative Stress

Ellagic acid (EA) was reported to play protective roles in rheumatoid arthritis (RA). It was found that the level of metastasis-associated gene 1 (MTA1)/histone deacetylase 1 (HDAC1) protein complex was downregulated by polyphenols in several human disorders. Notably, inhibition of MTA1 or HDAC1 has anti-inflammatory effects on RA. Therefore, our study is aimed at investigating whether EA prevents RA progression through regulating the MTA1/HDAC1 complex. Herein, the human fibroblast-like synoviocyte (FLS) cell line MH7A was treated with TNF-α to induce an inflammation model in vitro and then incubated with different concentrations of EA. Western blot analysis showed that EA reduced MTA1 expression in a dose-dependent manner in MH7A cells. Then, TNF-α-treated MH7A cells were incubated with EA alone or together with MTA1 overexpression plasmid (pcDNA-MTA1), and we found that EA inhibited proliferation, inflammation cytokine levels, and oxidative stress marker protein levels and promoted apoptosis in MH7A cells, while MTA1 overexpression abolished these effects. Moreover, coimmunoprecipitation assay verified the interaction between MTA1 and HDAC1. EA downregulated the MTA1/HDAC1 complex in MH7A cells. MTA1 knockdown inhibited proliferation, inflammation, and oxidative stress and promoted apoptosis in MH7A cells, while HDAC1 overexpression reversed these effects. Moreover, chromatin immunoprecipitation assay indicated that EA inhibited HDAC1-mediated Nur77 deacetylation. Rescue experiments demonstrated that Nur77 knockdown reversed the effects of EA on MH7A cell biological behaviors. Additionally, EA treatment attenuated arthritis index, paw swelling, synovial hyperplasia, and inflammation in collagen-induced arthritis (CIA) rats. In conclusion, EA inhibited proliferation, inflammation, and oxidative stress and promoted apoptosis in MH7A cells and alleviated the severity of RA in CIA rats though downregulating MTA1/HDAC1 complex and promoting HDAC1 deacetylation-mediated Nur77 expression.

Inhibition of microRNA-155 Alleviates Neurological Dysfunction Following Transient Global Ischemia and Contribution of Neuroinflammation and Oxidative Stress in the Hippocampus

2020 ◽  
Vol 25 (40) ◽  
pp. 4310-4317 ◽  
Author(s):  
Lichao Sun ◽  
Shouqin Ji ◽  
Jihong Xing
Keyword(s):  
Oxidative Stress ◽  
Brain Edema ◽  
Severity Score ◽  
Global Ischemia ◽  
Signal Pathways ◽  
Neurological Severity Score ◽  
Tnf Α ◽  
Transient Global Ischemia ◽  
And Oxidative Stress

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.

TA-65, A Telomerase Activator improves Cardiovascular Markers in Patients with Metabolic Syndrome

2018 ◽  
Vol 24 (17) ◽  
pp. 1905-1911 ◽  
Author(s):  
Maria Luz Fernandez ◽  
Minu Sara Thomas ◽  
Bruno S. Lemos ◽  
Diana M. DiMarco ◽  
Amanda Missimer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Plasma Lipids ◽  
Disease Risk ◽  
Glycosylated Hemoglobin ◽  
Cardiovascular Disease Risk ◽  
Hdl Cholesterol ◽  
Double Blind ◽  
Tnf Α ◽  
Luminex Technology

Background: Telomerase Activator 65 (TA-65), a compound extracted from Astragalus membranaceus has been used in Chinese traditional medicine for extending lifespan. Scarce information exists on the effects of TA-65 on parameters of metabolic syndrome (MetS). Methods: We recruited 40 patients with MetS to determine the effects of TA-65 on dyslipidemias, hypertension, and oxidative stress in this at-risk population. The study was a double-blind, randomized crossover design in which patients were allocated to consume either 16 mg daily of a TA-65 supplement or a placebo for 12 weeks. Following a 3-week washout, participants were allocated to the alternate treatment for an additional 12 weeks. Anthropometric and biological markers were measured at the end of each treatment. Plasma lipids, glucose, CReactive Protein (CRP), liver enzymes, and glycosylated hemoglobin were measured using a Cobas c-111. Inflammatory cytokines were measured by Luminex technology and markers of oxidative stress by the use of spectroscopy. Results: Compared to the placebo period, HDL cholesterol (HDL-C) was higher while body mass index, waist circumference, and the LDL/HDL ratio were lower (p < 0.05) during TA-65 treatment. In addition, plasma tumor necrosis factor-α (TNF-α) was lower during the TA-65 period (p< 0.05). Positive correlations were observed in changes between the placebo and the TA-65 periods in HDL-C and CRP (r = -0.511, p < 0.01), alanine aminotransferase (r = -0.61, p < 0.001) and TNF-α (r = -0.550, p < 0.001) suggesting that the favorable changes observed in HDL were associated with decreases in inflammation. Conclusion: TA-65 improved key markers of cardiovascular disease risk, which were also associated with reductions in inflammation.

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