scholarly journals Neuroprotective Effect of Syringic Acid by Modulation of Oxidative Stress and Mitochondrial Mass in Diabetic Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Marzieh Rashedinia ◽  
Mahshid Alimohammadi ◽  
Nazgol Shalfroushan ◽  
Mohammad Javad Khoshnoud ◽  
Mitra Mansourian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Energy Metabolism ◽  
Mrna Expression ◽  
Mitochondrial Biogenesis ◽  
Neuroprotective Effect ◽  
Syringic Acid ◽  
Diabetic Rats ◽  
Sciatic Nerves ◽  
The Brain

Diabetes is a metabolic complaint associated with oxidative stress and dysfunction of mitochondria. One of the most common complications of diabetes mellitus is neuropathy. This study evaluated the possible neuroprotective effects of syringic acid (SYR), a natural polyphenolic derivative of benzoic acid, on oxidative damage and mitochondria in the brain, spinal cord, and sciatic nerve of streptozotocin-induced diabetic rats. Different groups of rats including normal control, diabetics (induced by streptozotocin), diabetic groups treated with 25, 50, and 100 mg/kg of SYR, and non-diabetic group treated with only 100 mg/kg of SYR were treated for 6 weeks. Learning and memory function, physical coordination, and acetylcholinesterase (AChE) and antioxidant indexes, as well as mRNA expression of mitochondrial biogenesis, were measured in the brain, spinal cord, and sciatic nerves. Diabetic rats treated with 100 mg/kg SYR exhibited significantly improved learning, memory, and movement deficiency ( p < 0.05 ). SYR 100 mg/kg also significantly upregulated the brain mRNA expression of PGC-1α and NRF-1, the key regulators of energy metabolism, oxidative phosphorylation, and mitochondrial biogenesis. In addition, SYR 100 mg/kg and SYR 50 mg/kg increased the mtDNA/nDNA ratio in the brain and the spinal cord of diabetic rats, respectively ( p < 0.05 ). SYR attenuated the lipid peroxidation in all the tissues, but not significant effects were observed on GSH, AChE, catalase, and superoxide dismutase activity. In all the tests, nonsignificant differences were observed between the control and SYR 100 mg/kg groups. Moreover, SYR reduced inflammation and demyelination in sciatic nerves. This is the first study to reveal the regulation of mitochondrial biogenesis and energy metabolism by SYR, beyond its antioxidant role in the diabetic rats’ brain and spinal tissues.

Syringic acid: A potential natural compound for the management of renal oxidative stress and mitochondrial biogenesis in diabetic rats

2020 ◽  
Vol 17 ◽  
Author(s):  
Marzieh Rashedinia ◽  
Mohammad Javad Khoshnoud ◽  
Bahman khalvati Fahlyan ◽  
Seyedeh-Sara Hashemi ◽  
Mahshid Alimohammadi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Mrna Expression ◽  
Mitochondrial Biogenesis ◽  
Treated Group ◽  
Syringic Acid ◽  
Diabetic Rats ◽  
Diabetic Group ◽  
Renal Diseases ◽  
Tbars Level

Background: Diabetic nephropathy can lead to renal diseases, and oxidative stress and mitochondrial dysfunction have critical roles in its development. Objectives: In this study, the effect of syringic acid (SYR), natural phenolic acid on diabetic nephropathy and mitochondrial biogenesis were examined. Methods: Diabetes was induced in rats by injecting streptozotocin. SYR (25, 50 and 100 mg/kg/day) was orally administered for 6 weeks. SYR effects on factors, such as antioxidant activity and mRNA expression level of mitochondrial biogenesis indexes were evaluated. Results: In SYR-treated rats, blood glucose and ALP level were significantly reduced. SYR increased kidney GSH content in the diabetic group. Elevated renal catalase and superoxide dismutase activities in diabetic rats were restored to normal levels after treatment. The SYR significantly reduced renal TBARS level, which had increased in diabetic rats. This compound also significantly upregulated renal mRNA expression of PGC-1α and NRF-1, and increased mtDNA/nDNA ratio in diabetic rats. These values were reduced in non-treated diabetic group. The result show improvement of histopathological damages of kidney in SYR treated group in comparison with the diabetic group. Conclusion: According to the results, SYR alters renal antioxidant defense mechanisms. Also, it could be considered as a novel approach by targeting mitochondria in renal diabetic complications.

scholarly journals Protective Effects of Beta Glucan and Gliclazide on Brain Tissue and Sciatic Nerve of Diabetic Rats Induced by Streptozosin

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Harun Alp ◽  
Sefer Varol ◽  
Muhammet Murat Celik ◽  
Murat Altas ◽  
Osman Evliyaoglu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Sciatic Nerve ◽  
Neuroprotective Effect ◽  
Diabetic Rats ◽  
Nerve Tissue ◽  
Stress Index ◽  
Diabetic Rat ◽  
Beta Glucan ◽  
The Brain ◽  
Antioxidant Effects

There have not been yet enough studies about effects of beta glucan and gliclazide on oxidative stress created by streptozotocin in the brain and sciatic nerve of diabetic rats. The aim of this paper was to investigate the antioxidant effects of gliclazide and beta glucan on oxidative stress and lipid peroxidation created by streptozotosin in brain and sciatic nerve. Total of 42 rats were divided into 6 groups including control, diabetic untreated (DM) (only STZ, diabetic), STZ (DM) + beta glucan, STZ (DM) + gliclazide, only beta glucan treated (no diabetic), and only gliclazide treated (no diabetic). The brain and sciatic nerve tissue samples were analyzed for malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and paraoxonase (PON-1) levels. We found a significant increase in MDA, TOS, and OSI along with a reduction in TAS level, catalase, and PON-1 activities in brain and sciatic nerve of streptozotocin-induced diabetic rats. Also, this study shows that in terms of these parameters both gliclazide and beta glucan have a neuroprotective effect on the brain and sciatic nerve of the streptozotocin-induced diabetic rat. Our conclusion was that gliclazide and beta glucan have antioxidant effects on the brain and sciatic nerve of the streptozotocin-induced diabetic rat.

The effects of crocin (active contstituent of saffron) treatment on brain antioxidant enzyme mRNA levels in diabetic rats / Diyabetik ratlarda safranın aktif içeriği olan krosin tedavisinin beyindeki antioksidan enzimlerin mRNA seviyeleri üzerine etkisi

2016 ◽  
Vol 41 (2) ◽  
Author(s):  
Eyüp Altınöz ◽  
Cemal Ekici ◽  
Berna Özyazgan ◽  
Yılmaz Çiğremiş
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Mrna Expression ◽  
Antioxidant Enzyme ◽  
Diabetic Rats ◽  
Control Group ◽  
Mrna Levels ◽  
The Brain ◽  
And Oxidative Stress

AbstractObjective: The aim of the present study is to evaluate the effect of crocin on mRNA expression of antioxidant enzymes, SOD, CAT and GPX in the brain of the STZ induced diabetic rats.Methods: Thirty animals randomized in three groups containing ten animals in each group as follows; control (non-diabetic rats), DM (STZ-induced untreated diabetic rats), DM+crocin (STZ-induced diabetic rats treated with crocin,). Crocin was given at a dose of 20 mg/kg bw/day by gavage for 21 days.Results: STZ injection caused a significant increase in mRNA expression of antioxidant enzymes, SOD, CAT and GPX when compared to control group. Crocin given to diabetic rats significantly decreased mRNA expression of antioxidant enzymes, SOD, CAT and GPX when compared to DM group.Conclusion: The present study demonstrates that crocin can modulate mRNA expression of antioxidant enzymes, SOD, CAT and GPX and oxidative stress in the brain of the STZ induced diabetic rats.

scholarly journals Syringic acid improves oxidative stress and mitochondrial biogenesis in the liver of streptozotocin-induced diabetic rats

2020 ◽  
Vol 10 (3) ◽  
pp. 111 ◽  
Author(s):  
Marzieh Rashedinia ◽  
Zahra Sabahi ◽  
MohammadJavad Khoshnoud ◽  
Bahman Khalvati ◽  
Seyedeh-Sara Hashemi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Biogenesis ◽  
Syringic Acid ◽  
Diabetic Rats

Abstract 814: Atorvastatin Attenuates Oxidative Stress And Improves Neuronal Nitric Oxide Synthase In The Brain Stem Of Heart Failure Mice

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Joseph Francis ◽  
Li Yu ◽  
Anuradha Guggilam ◽  
Srinivas Sriramula ◽  
Irving H Zucker
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Brain Stem ◽  
Mrna Expression ◽  
Natriuretic Peptide ◽  
Left Ventricular ◽  
Neuronal Nos ◽  
The Brain

3-Hydroxyl-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been shown to reduce the incidence of myocardial infarction independent of their lipid-lowering effects. Nitric oxide (NO) in the central nervous system contributes to cardiovascular regulatory mechanisms. Imbalance between nitric oxide (NO) and superoxide anion (O 2 . − ) in the brain may contribute to enhanced sympathetic drive in heart failure (HF). This study was done to determine whether treatment with atorvastatin (ATS) ameliorates the imbalance between NO and O 2 . − production in the brain stem and contributes to improvement of left ventricular (LV) function. Methods and Results: Myocardial infarction (MI) was induced by ligation of the left coronary artery or sham surgery. Subsequently, mice were treated with ATS (10 μg/kg) (MI + ATS), or vehicle (MI + V). After 5 weeks, echocardiography revealed left ventricular dilatation in MI mice. Realtime RT-PCR indicated an increase in the mRNA expression of the LV hypertrophy markers, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Neuronal NOS (nNOS) and endothelial NOS (eNOS) mRNA expression were significantly reduced, while that of NAD(P)H oxidase subunit (gp91phox) expression was elevated in the brain stem of MI mice. Compared with sham-operated mice, ATS-treated mice showed reduced cardiac dilatation, decreased ANP and BNP in the LV. ATS also reduced gp91phox expression and increased nNOS mRNA expression in the brain stem, while no changes in eNOS and iNOS were observed. Conclusion: These findings suggest that ATS reduces oxidative stress and increases neuronal NOS in the brain stem, and improves left ventricular function in heart failure.

scholarly journals Neuroprotective effect of melatonin in mice with toxic cuprizone model of demyelination and possible pathways of its realization

2018 ◽  
Vol 6 (2) ◽  
Author(s):  
I. Labunets ◽  
A. Rodnichenko ◽  
N. Melnyk ◽  
N. Utko
Keyword(s):  
Spinal Cord ◽  
Immune System ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Neuroprotective Effect ◽  
Nissl Staining ◽  
Spinal Cord Neurons ◽  
Malondialdehyde Content ◽  
Brain And Spinal Cord ◽  
The Brain

The search for tools that increase the effectiveness of cell therapy of demyelinating pathology is relevant. They may be preparations that affect the pathogenetic factors of this pathology, in particular, the pineal hormone melatonin.The purpose of the work is to evaluate the involvement of immune system and antioxidant defense in the implementation of the protective effects of melatonin on morpho-functional disorders in the central nervous system induced by neurotoxin cuprizone.Materials and methods. The toxic demyelination model was induced on 129/Sv mice at the age of 3-5 months by adding cuprizone to food for 3 weeks. Since the 7th day of cuprizone administration, melatonin was injected intraperitoneally at 18:00 daily, at a dose of 1 mg/kg. In the brain of mice, the proportion of CD3+, Nestin+ cells and phagocytic macrophages, the content of malondialdehyde and the activity of antioxidant enzymes was determined. Blood serum was tested for thymic hormone thymulin levels. In the animals, we evaluated the structure of the brain and spinal cord neurons by Nissl staining of histological sections as well as analyzed behavioural reactions in the "open field" test.Results. In the brain of the mice received cuprizone, the proportion of CD3+ and Nestin+ cells, active macrophages and malondialdehyde content increases, glutathione peroxidase and glutathione reductase levels decreases. In the brain and spinal cord of the mice with a cuprizone diet, the proportion of altered neurons increases, and motor and emotional activity decreases. The introduction of melatonin results in a decrease in the relative number of CD3+ cells, active macrophages and malondialdehyde content, increased activity of glutathione peroxidase, glutathione reductase and level of thymulin. In such mice, the proportion of unchanged neurons increases as the number of Nestin+ cells decreases and behavioural responses are also improved.Conclusions. The neuroprotective effect of melatonin in demyelinating pathology is realized through the factors of the immune system and oxidative stress. The results may be useful in the development of new biotechnological approaches to the treatment of demyelinating pathology, in particular, multiple sclerosis.

Genistein and Momordica charantia L. prevents oxidative stress and upregulate proglucagon and insulin receptor mRNA in diabetic rats.

2021 ◽  
Author(s):  
Wusa Makena ◽  
Abdullahi Ibrahim Iliya ◽  
Joseph Olajide Hambolu ◽  
James Abrak Timbuak ◽  
Uduak Emmanuel Umana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Insulin Receptor ◽  
Mrna Expression ◽  
Insulin Signaling ◽  
Diabetic Rats ◽  
Momordica Charantia ◽  
Receptor Mrna ◽  
Group I

Type 2 diabetes (T2D) occur as a result of insulin resistance and malfunction in insulin signaling. Controlling hyperglycemia and activation of insulin signaling are important in the management of T2D. The study aimed to evaluate the effect of Genistein and Momordica charantia L. fruit on oxidative stress, markers of inflammation, and their role on proglucagon and insulin receptor mRNA expression by RT-PCR in diabetic rats. Thirty-five albino rats were divided into seven groups (n=5). Group I (non-diabetic) and group II (diabetic control) were treated with distilled water, groups III and IV received 250mg/kg and 500mg/kg lyophilized MCF respectively. Groups V and VI received 10mg/kg and 20mg/kg Genistein respectively while group VII received 500mg/kg Metformin. The administration lasted for 28 days. MCF and Genistein significantly reduced IL-1β and TNFα levels that was elevated in serum of diabetic rats. Treatment with MCF and Genistein significant increased the expression of proglucagon mRNA in the small intestine and insulin receptor mRNA in the liver of diabetic rats. In conclusion, MCF and Genistein ameliorate type 2 diabetes complications by preventing the loss of insulin-positive cells, inhibiting IL-1β and TNFα and up-regulating proglucagon and insulin receptor mRNA expression. Novelty: • MCF and Genistein has an inhibitory effect on diabetic induced IL-1β and TNFα production. • MCF and Genistein up-regulates proglucagon and insulin receptor mRNA expression.

Abstract 276: Angiotensin AT1 Receptor Blockade Reverses Age-Related Changes in Myocardial Energy Metabolism and Increases Mitochondrial Biogenesis

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Peter M Abadir ◽  
Ashwin Akki ◽  
Robert Carey ◽  
Ashish Gupta ◽  
Vadappuram Chacko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Mitochondrial Biogenesis ◽  
Energy Production ◽  
Nuclear Gene ◽  
At1 Receptor ◽  
Resonance Spectroscopy ◽  
Receptor Blockade ◽  
Lv Mass ◽  
Old Mice

Aging and mitochondrial function have been closely linked. We recently reported the identification of a mitochondrial angiotensin system. We hypothesized that angiotensin AT1 receptor blockade would increase energy production and mitochondrial biogenesis and reduce oxidative stress in aging hearts. We used Magnetic resonance spectroscopy to measure cardiac energy metabolism and function in young (20 wks old), aged (150 wks old) mice at baseline and after 4 weeks of losartan (50 mg/kg/day). For mitobiogenesis, qPCR was used to calculate CytB (mitochondrial gene)/GAPDH (nuclear gene) ratio and to measure mito-survival genes Sirt1, Sirt3, Nampt, and PGC-1α. Cardiomyocyte mitochondria from young, aged and treated mice were examined with electron microscopy. The expression of nitrotyrosine was quantified by immunohistochemistry. Older animals hearts (n=9) exhibited increase in LV mass (103±9 mg versus 120±8 mg, young (n=8) versus old (n=9), P<0.002). The mean cardiac PCr/ATP was reduced in older animals (1.5±0.2) than that of young mice (2.0±0.3, P<0.0004). Losartan abolished the LV mass increase in older animals (109±11 mg vs 101±7 mg, young versus old, P<0.1) and improved the impaired energy metabolism of the older hearts increasing the PCr/ATP ratios towards those observed in younger animals (1.94±0.01 vs 1.87±0.4, control versus old, P<0.7). Losartan increased EF in older animals (56±5% vs 63±5%, old versus old treated, P<0.01). Losartan increased mitobiogenesis in the hearts of treated young and old mice (3.8+2.5 folds, P<0.02 and 4.3+ 0.9 folds, P<0.0001). Mito-survival genes in the heart were not increased but PGC-1α was up-regulated by 2.8+1.6-fold, P<0.05 and 7+ 1.9-fold, P<0.001 in young and old treated mice. Electron micrograph analysis revealed that aging was associated with swollen cardiac mitochondria and disrupted cristae, which were reversed by Losartan. Losartan in older animals significantly reduced oxidative damage as evidenced by less Nitrotyrosine staining score in cardiomyocytes (2.5±0.5 vs. 1.3±0.4, old versus old treated, P<0.0009). Our results indicate that Losartan in aging increased mitobiogenesis, reduced oxidative stress, improved energy production and restored cardiac function to the healthy young adult level.

Protocatechuic acid protects brain mitochondrial function in streptozotocin-induced diabetic rats

2015 ◽  
Vol 40 (10) ◽  
pp. 1078-1081 ◽  
Author(s):  
Yoswaris Semaming ◽  
Jirapas Sripetchwandee ◽  
Piangkwan Sa-nguanmoo ◽  
Hiranya Pintana ◽  
Patchareewan Pannangpetch ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glycemic Control ◽  
Mitochondrial Dysfunction ◽  
Stress Reduction ◽  
Mitochondrial Function ◽  
Protocatechuic Acid ◽  
Diabetic Rats ◽  
Brain Oxidative Stress ◽  
The Brain ◽  
Brain Mitochondrial Function

Brain mitochondrial dysfunction has been demonstrated in diabetic animals with neurodegeneration. Protocatechuic acid (PCA), a major metabolite of anthocyanin, has been shown to exert glycemic control and oxidative stress reduction in the heart. However, its effects on oxidative stress and mitochondrial function in the brain under diabetic condition have never been investigated. We found that PCA exerted glycemic control, attenuates brain mitochondrial dysfunction, and contributes to the prevention of brain oxidative stress in diabetic rats.

Sign in / Sign up

Export Citation Format

Share Document