scholarly journals Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Chelating Activity and Inhibition of Oxidative Stress

Biomolecules ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. 453 ◽  
Author(s):  
Kabeer Abubakar ◽  
Maryam Muhammad Mailafiya ◽  
Abubakar Danmaigoro ◽  
Samaila Musa Chiroma ◽  
Ezamin Bin Abdul Rahim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Treatment Group ◽  
Lead Acetate ◽  
Curcuma Longa ◽  
Oral Treatment ◽  
Active Constituent ◽  
Sod Activity ◽  
Chelating Activity ◽  
Histological Architecture ◽  
Pb Concentration

Lead (Pb) is a toxic, environmental heavy metal that induces serious clinical defects in all organs, with the nervous system being its primary target. Curcumin is the main active constituent of turmeric rhizome (Curcuma longa) with strong antioxidant and anti-inflammatory properties. This study is aimed at evaluating the therapeutic potentials of curcumin on Pb-induced neurotoxicity. Thirty-six male Sprague Dawley rats were randomly assigned into five groups with 12 rats in the control (normal saline) and 6 rats in each of groups, i.e., the lead-treated group (LTG) (50 mg/kg lead acetate for four weeks), recovery group (RC) (50 mg/kg lead acetate for four weeks), treatment group 1 (Cur100) (50 mg/kg lead acetate for four weeks, followed by 100 mg/kg curcumin for four weeks) and treatment group 2 (Cur200) (50 mg/kg lead acetate for four weeks, followed by 200 mg/kg curcumin for four weeks). All experimental groups received oral treatment via orogastric tube on alternate days. Motor function was assessed using a horizontal bar method. The cerebellar concentration of Pb was evaluated using ICP-MS technique. Pb-administered rats showed a significant decrease in motor scores and Superoxide Dismutase (SOD) activity with increased Malondialdehyde (MDA) levels. In addition, a marked increase in cerebellar Pb concentration and alterations in the histological architecture of the cerebellar cortex layers were recorded. However, treatment with curcumin improved the motor score, reduced Pb concentration in the cerebellum, and ameliorated the markers of oxidative stress, as well as restored the histological architecture of the cerebellum. The results of this study suggest that curcumin attenuates Pb-induced neurotoxicity via inhibition of oxidative stress and chelating activity.

scholarly journals Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Inhibition of Oxidative Stress and Chelating Activity

2019 ◽  
Author(s):  
Kabeer Abubakar ◽  
Maryam Muhammad Mailafiya ◽  
Abubakar Danmaigoro ◽  
Samaila Musa Chiroma ◽  
Ezamin Abdul Bin Rahim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Treatment Group ◽  
Lead Acetate ◽  
Curcuma Longa ◽  
Sprague Dawley ◽  
Active Constituent ◽  
Sod Activity ◽  
Chelating Activity ◽  
Histological Architecture ◽  
Pb Concentration

Lead (Pb) is a toxic environmental heavy metal that induces serious clinical defect on all organs with the nervous system being the primary target. Curcumin is the main active constituent of turmeric rhizome (Curcuma longa) with strong antioxidant and anti-inflammatory properties. This study is aimed at evaluating the therapeutic potentials of curcumin on Pb-induced neurotoxicity. Thirty six male Sprague Dawley rats were randomly assigned into five (5) groups with 12 rats in the control (normal saline) and 6 rats for the lead treated group (LTG) (50 mg/kg lead acetate for 4 weeks), recovery group (RC) (50 mg/kg lead acetate for 4 weeks), treatment group 1 (Cur100) (50 mg/kg lead acetate for 4 weeks, followed by 100 mg/kg curcumin for 4 weeks) and treatment group 2 (Cur200) (50 mg/kg lead acetate for 4 weeks, followed by 200 mg/kg curcumin for 4 weeks) groups each. All experimental groups received the oral treatments through orogastric-tube on alternate days. Motor function was assessed using horizontal bar method while Pb concentration in the cerebellum of the rats were evaluated using ICP-MS techniques. Pb-administered rats showed significant decrease in motor scores, SOD activity with increase MDA levels and Pb concentration in their cerebellum with marked alterations in the histological architecture of the cerebellar cortex layers. However, treatment with curcumin improved the motor score, reduced Pb concentration in the cerebellum and ameliorates the markers of oxidative stress as well as restored the histological architecture of the cerebellum. The results this in study suggested that curcumin attenuates Pb-induced neurotoxicity via inhibition of oxidative stress and chelating activity.

scholarly journals Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Inhibition of Oxidative Stress and Chelating Activity

2019 ◽  
Author(s):  
Kabeer Abubakar ◽  
Maryam Muhammad Mailafiya ◽  
Abubakar Danmaigoro ◽  
Samaila Musa Chiroma ◽  
Ezamin Abdul Rahim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Treatment Group ◽  
Lead Acetate ◽  
Curcuma Longa ◽  
Sprague Dawley ◽  
Active Constituent ◽  
Sod Activity ◽  
Chelating Activity ◽  
Histological Architecture ◽  
Pb Concentration

Lead (Pb) is a toxic environmental heavy metal that induces serious clinical defect on all organs with the nervous system being the primary target. Curcumin is the main active constituent of turmeric rhizome (Curcuma longa) with strong antioxidant and anti-inflammatory properties. This study is aimed at evaluating the therapeutic potentials of curcumin on Pb-induced neurotoxicity. Thirty six male Sprague Dawley rats were randomly assigned into five (5) groups with 12 rats in the control (normal saline) and 6 rats for the lead treated group (LTG) (50 mg/kg lead acetate for 4 weeks), recovery group (RC) (50 mg/kg lead acetate for 4 weeks), treatment group 1 (Cur100) (50 mg/kg lead acetate for 4 weeks, followed by 100 mg/kg curcumin for 4 weeks) and treatment group 2 (Cur200) (50 mg/kg lead acetate for 4 weeks, followed by 200 mg/kg curcumin for 4 weeks) groups each. All experimental groups received the oral treatments through orogastric-tube on alternate days. Motor function was assessed using horizontal bar method while Pb concentration in the cerebellum of the rats were evaluated using ICP-MS techniques. Pb-administered rats showed significant decrease in motor scores, SOD activity with increase MDA levels and Pb concentration in their cerebellum with marked alterations in the histological architecture of the cerebellar cortex layers. However, treatment with curcumin improved the motor score, reduced Pb concentration in the cerebellum and ameliorates the markers of oxidative stress as well as restored the histological architecture of the cerebellum. The results this in study suggested that curcumin attenuates Pb-induced neurotoxicity via inhibition of oxidative stress and chelating activity.

scholarly journals ACTI ON OF N- ACETYLCYSTEI NE ON ASYMMETRI C DIMETHYLARGININE AND ALBUMINURIA IN STAGE 1-4 NONDIABETIC CHRONIC KIDNEY DISEASE PATIENTS

2010 ◽  
Vol 1 (3) ◽  
pp. 146
Author(s):  
MOCHAMMAD THAHA ◽  
Widodo Widodo ◽  
Moh. Yogiantoro ◽  
WENNY PUTRI NILAMSARI ◽  
MOCHAMAD YUSUF ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Treatment Group ◽  
Kidney Disease ◽  
Day Treatment ◽  
Oral Treatment ◽  
Control Group ◽  
Adma Level ◽  
Ckd Stage ◽  
Stage 1

Background: Uremic patients are in a pro-oxidant state and show an increased level of asymmetric dimethylarginine (ADMA), which is due to increased PRMT1 activity and reduced dimethylarginine dimethylaminohydrolase (DDAH) as degradation enzymes. Reactive oxidant species may play an important role in increasing the action of PRMT1 and in inhibiting the action of DDAH. Albuminuria and ADMA are closely correlated with progression of cardiovascular disease in chronic kidney disease (CKD) patients as well as indicators for decreasing renal function. Although ACEIs and/or ARBs reduced albuminuria in CKD patients, the results are still conflicting. Several factors in these patients may play important roles in the mechanism of albuminuria such as oxidative stress. The antioxidant N-acetylcysteine may prove to have beneficial therapeutic effect, because it can reduce oxidative stress as shown by evidence in humans, and subsequently increase ADMA. The objective of the present study is to explore the contribution of the antioxidant N-acetylcysteine (NAC) to the decrease of ADMA and albuminuria in non-diabetic CKD patients. Material and Methods: Patients with non-DM CKD stage 1–4 with albuminuria were randomized to receive ACEI and/or ARB alone (control group) or with antioxidant NAC 600 mg orally twice a day (treatment group). Observations were performed for 3 months to measure ADMA and albuminuria before and after-treatment. 80 patients in total 40 in the control group and 40 in the treatment group were used. Results: After oral treatment with NAC, the plasma level of ADMA in the treatment group increased from 0.604 µmol/l to 0.689 µmol/l, whereas ADMA level in the control group exhibited a higher increase from 0.561 µmol/l to 0.743 µmol/l. The increases in these groups were significantly different (p < 0.02). Moreover, the level of albuminuria was reduced from 148.12 µg/mg • cr to 132.7 µg/mg • cr in the treatment group, and from 75.25 µg/mg • cr to 71.85 µg/mg • cr in the control group. The difference was significant (p < 0.001). Conclusion: The anti-oxidant N-acetylcysteine can be used as adjuvant therapy to inhibit the progression of CKD in patients by decreasing the ADMA level and albuminuria.

The Neuroprotective Effect of Picroside II from Hu-Huang-Lian against Oxidative Stress

2007 ◽  
Vol 35 (04) ◽  
pp. 681-691 ◽  
Author(s):  
Ting Li ◽  
Jian-Wen Liu ◽  
Xiao-Dong Zhang ◽  
Ming-Chuan Guo ◽  
Guang Ji
Keyword(s):  
Oxidative Stress ◽  
Pc12 Cells ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Active Constituent ◽  
Sod Activity ◽  
Picroside Ii ◽  
Pre Treatment

Picroside II is an active constituent extracted from the traditional Chinese medicine (TCM) Hu-Huang-Lian. To evaluate the neuroprotective effect of picroside II, PC12 cells were treated with glutamate in vitro and male ICR mice were treated with AlCl 3in vivo. Pre-treatment of PC12 cells with picroside II could enhance the cell viability and decrease the level of intracellular reactive oxygen species (ROS) induced by glutamate. By DNA fragmentation and flow cytometry assay, picroside II (1.2 mg/ml) significantly prevented glutamate-induced cell apoptosis. In the animal study, amnesia was induced in mice by AlCl 3 (100 mg/kg/d, i.v.). Pricroside II, at the dose of 20 and 40 mg/kg/d (i.g.), markedly ameliorated AlCl 3-induced learning and memory dysfunctions and attenuated AlCl 3-induced histological changes. This was associated with the significant increased superoxide dismutase (SOD) activity in the brain of experimental mice. All these results indicated that picroside II possessed the therapeutic potential in protecting against neurological injuries damaged by oxidative stress.

scholarly journals Effect of dexmedetomidine on oxidative stress response and expression of intracellular adhesion factor-1 (ICAM-1) and S100B in patients

2021 ◽  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Stress Response ◽  
Treatment Group ◽  
Oxidative Stress Response ◽  
Stress Index ◽  
Control Group ◽  
Sod Activity ◽  
Gcs Score ◽  
Adhesion Factor

[Abstract] Objective: To study the effect of dexmedetomidine on oxidative stress response and the expression of intracellular adhesion factor-1 (ICAM-1) and S100B in patients with traumatic brain injury (TBI). Method: TBI patients treated in our hospital from May 2017 to April 2019 were enrolled in the study and divided into control group and treatment group by random number table method. The treatment group was administered with dexmedetomidine injection via intravenous pump on the basis of conventional treatment in the control group. Glasgow coma scale (GCS) and Glasgow outcome scale (GOS) were used to evaluate patients’ injury, recovery and prognosis. ELISA method was taken to detect 4 oxidative stress index levels including serum superoxide dismutase (SOD), lipid peroxidation (LPO), malondialdehyde (MDA) and total antioxidant capacity (TAC), as well as ICAM-1 and S100B levels at admission and at different time points after operation. Results: At 3d and 14 d after operation, the treatment group had higher GCS score than the control group (P<0.05).At 30 d, 90 d and 180 d after discharge, the treatment group had higher GOS score than the control group (P<0.05). At 3d, 5d, and 14d after operation, the treatment group had higher SOD activity than the control group (P<0.05). Immediately after operation, at 3d, 5d, and 14d after operation, the treatment group had higher LPO level than the control group (P<0.05); at 3d, 5d, and 14d after operation, blood MDA level gradually decreased in both groups, which was lower in the treatment group than in the control group (P<0.05); at 3d, 5d and 14d after operation, the treatment group had higher TAC activity in the blood than the control group (P<0.05). At 3d, 5d and 14d after operation, the treatment group had lower S100B level than the control group (P<0.05). Conclusion: Dexmedetomidine can relieve TBI-induced oxidative stress state and reduce the levels of brain injury markers (ICAM-1, S100B), which has a protective effect on the brain tissue with TBI.

Biocompatible Iron Sulphide Nanoparticles Against Neuroinflammation for Intracerebral Haemorrhage and Long-term Neurological Functional Recovery

2021 ◽  
Author(s):  
Song Zhang ◽  
Tianqing Xiong ◽  
Yuan Yuan ◽  
Wenwen Zhuang ◽  
Yijun Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Treatment Group ◽  
Intracerebral Haemorrhage ◽  
Neuronal Apoptosis ◽  
Iron Sulphide ◽  
Sod Activity ◽  
Haematoma Volume ◽  
H 26 ◽  
Pre Treatment

Abstract BackgroundMass effects of haematoma, neuroinflammation, oxidative stress, and neuronal apoptosis are the major causes of poor prognosis of intracerebral haemorrhage (ICH). Our previous study suggests that biocompatible iron sulphide nanoparticles possess peroxidase-like activity and can release hydrogen polysulfanes, which may inhibit brain injury. The purpose of this study was to investigate the neuroprotective efficacy of diallyl disulfide (DADS)-nFeS in mice after ICH and preliminarily illustrate the potential mechanism. MethodsAdult male C57BL/6 mice (n = 176) were injected with bacterial collagenase in the striatum. In the first part, DADS-nFeS at different doses (25, 50, or 100 mg/kg) was intragastrically administered 2 h, 26 h, and 50 h before ICH. In the second and third parts, DADS-nFeS (50 mg/kg) was administered 2 h, 26 h, and 50 h before and after the induction of ICH in the pre-treatment group and post-treatment group, respectively. H&E staining was performed to detect drug toxicity. Haematoma volume measurement, Fluoro-Jade C (F-JC) staining, Nissl staining, immunofluorescence staining, western blotting, terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining, malondialdehyde (MDA) and superoxide dismutase (SOD) assays, and neurobehavioural tests were performed. ResultsAll three doses of DADS-nFeS had neuroprotective effects, and 50 mg/kg resulted in the best outcome. DADS-nFeS reduced the haematoma volume and MDA content, inhibited the activation of microglia and astrocytes, progressive neuronal degeneration, and apoptosis, increased SOD activity and neuronal survival, and improved both short-term and long-term neurological functions in perihaematomal areas after ICH. Moreover, DADS-nFeS was associated with the downregulation of Iba-1, GFAP, TNF-α, IL-1β, 4-hydroxynonenal (4-HNE), and Bax/Bcl-2 levels in perihaematomal areas after ICH. Finally, post-treatment with DADS-nFeS had a better effect than pre-treatment with DADS-nFeS. ConclusionsOur study indicated that gavage administration of DADS-nFeS decreased the haematoma volume, suppressed neuroinflammation, oxidative stress, and neuronal apoptosis, and improved short- and long-term neurological functions, which was, at least in part, realized by inhibiting the activation of microglia and astrocytes, enhancing local SOD activity, and decreasing the recruitment of reactive oxygen species. Therefore, DADS-nFeS may serve as a potential therapeutic strategy via the diet against central nervous system diseases.

scholarly journals Gingerol Fraction from Zingiber officinale Protects against Gentamicin-Induced Nephrotoxicity

2014 ◽  
Vol 58 (4) ◽  
pp. 1872-1878 ◽  
Author(s):  
Francisco A. P. Rodrigues ◽  
Mara M. G. Prata ◽  
Iris C. M. Oliveira ◽  
Natacha T. Q. Alves ◽  
Rosa E. M. Freitas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitrosative Stress ◽  
Oral Treatment ◽  
Control Group ◽  
Mrna Levels ◽  
Sod Activity ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Ifn Γ ◽  
Nephroprotective Effect

ABSTRACTNephrotoxicity is the main complication of gentamicin (GM) treatment. GM induces renal damage by overproduction of reactive oxygen species and inflammation in proximal tubular cells. Phenolic compounds from ginger, called gingerols, have been demonstrated to have antioxidant and anti-inflammatory effects. We investigated if oral treatment with an enriched solution of gingerols (GF) would promote a nephroprotective effect in an animal nephropathy model. The following six groups of male Wistar rats were studied: (i) control group (CT group); (ii) gingerol solution control group (GF group); (iii) gentamicin treatment group (GM group), receiving 100 mg/kg of body weight intraperitoneally (i.p.); and (iv to vi) gentamicin groups also receiving GF, at doses of 6.25, 12.5, and 25 mg/kg, respectively (GM+GF groups). Animals from the GM group had a significant decrease in creatinine clearance and higher levels of urinary protein excretion. This was associated with markers of oxidative stress and nitric oxide production. Also, there were increases of the mRNA levels for proinflammatory cytokines (tumor necrosis factor alpha [TNF-α], interleukin-1β [IL-1β], IL-2, and gamma interferon [IFN-γ]). Histopathological findings of tubular degeneration and inflammatory cell infiltration reinforced GM-induced nephrotoxicity. All these alterations were attenuated by previous oral treatment with GF. Animals from the GM+GF groups showed amelioration in renal function parameters and reduced lipid peroxidation and nitrosative stress, in addition to an increment in the levels of glutathione (GSH) and superoxide dismutase (SOD) activity. Gingerols also promoted significant reductions in mRNA transcription for TNF-α, IL-2, and IFN-γ. These effects were dose dependent. These results demonstrate that GF promotes a nephroprotective effect on GM-mediated nephropathy by oxidative stress, inflammatory processes, and renal dysfunction.

Assessment of Oxidative Stress Effect of Withania somnifera in Rats after 28 Days Repeated Oral Treatment

2015 ◽  
Vol 22 (3) ◽  
pp. 52
Author(s):  
P. V. Prabhakar ◽  
Utkarsh Addi Reddy ◽  
M. F. Rahman ◽  
Paramjit Grover ◽  
Mohammed Mahboob
Keyword(s):  
Oxidative Stress ◽  
Withania Somnifera ◽  
Oral Treatment ◽  
Stress Effect

Effect of Opuntia dejecta (Salm-Dyck) flowers in liver of fructose-fed rats: Biochemicals, enzymatic and histological studies

2021 ◽  
pp. 096032712110134
Author(s):  
O Zouaoui ◽  
K Adouni ◽  
A Jelled ◽  
A Thouri ◽  
A Ben Chrifa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Body Weight ◽  
Diabetes Type 2 ◽  
Male Rats ◽  
Control Group ◽  
Standard Drug ◽  
High Fructose ◽  
Group A ◽  
Histological Architecture

Phytochemical composition and antioxidant activity of flowers decoction at post-flowering stage (F3D) of Opuntia dejecta were determined. The obtained findings demonstrate that F3D has a marked antioxidant activity in all tested assays. Furthermore, the present study was designed to test the protective activity of F3D against induced Diabetes type 2 (DT2) in male rats. Those metabolic syndromes were induced by a high-fructose diet (HFD) (10% fructose solution) for a period of 20 weeks. F3D was administered orally (100 and 300 mg/kg body weight) daily for the last 4 weeks. Metformin (150 mg/kg body weight) was used as a standard drug and administrated orally for the last 4 weeks. The results showed a significant increase in blood glucose, triglycerides and hepatic markers (ALAT, ASAT and ALK-P) in HFD group. A significant increase in hepatic TBARS and a significant decrease in SOD, CAT and GPX were observed in fructose fed rats compared to control group. Administration of F3D showed a protective effect in biochemical and oxidative stress parameters measured in this study. Also, oral administration of F3D restored the histological architecture of rat liver in comparison with rats fed HFD. In conclusion, F3D attenuated hepatic oxidative stress in fructose-fed rats.

scholarly journals Curcumin activates Nrf2 through PKCδ-mediated p62 phosphorylation at Ser351

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jee-Yun Park ◽  
Hee-Young Sohn ◽  
Young Ho Koh ◽  
Chulman Jo
Keyword(s):  
Oxidative Stress ◽  
Crucial Role ◽  
Curcuma Longa ◽  
Expression Plasmid ◽  
Expression Of Genes ◽  
Nrf2 Activation ◽  
First Time ◽  
Nrf2 Protein ◽  
Endogenous Defense ◽  
In Cells

AbstractCurcumin, a phytochemical extracted from Curcuma longa rhizomes, is known to be protective in neurons via activation of Nrf2, a master regulator of endogenous defense against oxidative stress in cells. However, the exact mechanism by which curcumin activates Nrf2 remains controversial. Here, we observed that curcumin induced the expression of genes downstream of Nrf2 such as HO-1, NQO1, and GST-mu1 in neuronal cells, and increased the level of Nrf2 protein. Notably, the level of p62 phosphorylation at S351 (S349 in human) was significantly increased in cells treated with curcumin. Additionally, curcumin-induced Nrf2 activation was abrogated in p62 knockout (−/−) MEFs, indicating that p62 phosphorylation at S351 played a crucial role in curcumin-induced Nrf2 activation. Among the kinases involved in p62 phosphorylation at S351, PKCδ was activated in curcumin-treated cells. The phosphorylation of p62 at S351 was enhanced by transfection of PKCδ expression plasmid; in contrast, it was inhibited in cells treated with PKCδ-specific siRNA. Together, these results suggest that PKCδ is mainly involved in curcumin-induced p62 phosphorylation and Nrf2 activation. Accordingly, we demonstrate for the first time that curcumin activates Nrf2 through PKCδ-mediated p62 phosphorylation at S351.

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