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 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 Decreased Oxidative Stress, Inhibited NF-κB Activation, and Improved Liver Pathology in Ethanol-Induced Liver Injury in Rats

2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Suchittra Samuhasaneeto ◽  
Duangporn Thong-Ngam ◽  
Onanong Kulaputana ◽  
Doungsamon Suyasunanont ◽  
Naruemon Klaikeaw
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Early Stage ◽  
Control Group ◽  
Liver Pathology ◽  
Sprague Dawley ◽  
Hepatocyte Apoptosis ◽  
Sod Activity ◽  
Ethanol Group ◽  
Liver Histopathology

To study the mechanism of curcumin-attenuated inflammation and liver pathology in early stage of alcoholic liver disease, female Sprague-Dawley rats were divided into four groups and treated with ethanol or curcumin via an intragastric tube for 4 weeks. A control group treated with distilled water, and an ethanol group was treated with ethanol (7.5 g/kg bw). Treatment groups were fed with ethanol supplemented with curcumin (400 or 1 200 mg/kg bw). The liver histopathology in ethanol group revealed mild-to-moderate steatosis and mild necroinflammation. Hepatic MDA, hepatocyte apoptosis, and NF-κB activation increased significantly in ethanol-treated group when compared with control. Curcumin treatments resulted in improving of liver pathology, decreasing the elevation of hepatic MDA, and inhibition of NF-κB activation. The 400 mg/kg bw of curcumin treatment revealed only a trend of decreased hepatocyte apoptosis. However, the results of SOD activity, PPARγprotein expression showed no difference among the groups. In conclusion, curcumin improved liver histopathology in early stage of ethanol-induced liver injury by reduction of oxidative stress and inhibition of NF-κB activation.

scholarly journals IL-23 Promotes Myocardial I/R Injury by Increasing the Inflammatory Responses and Oxidative Stress Reactions

2016 ◽  
Vol 38 (6) ◽  
pp. 2163-2172 ◽  
Author(s):  
Xiaorong Hu ◽  
Ruisong Ma ◽  
Jiajia Lu ◽  
Kai Zhang ◽  
Weipan Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Tunel Staining ◽  
Ischemia And Reperfusion ◽  
Stress Reactions ◽  
Sprague Dawley ◽  
Sod Activity ◽  
Myocardial Ischemia And Reperfusion ◽  
Tnf Α ◽  
And Oxidative Stress

Background/Aims: Inflammation and oxidative stress play an important role in myocardial ischemia and reperfusion (I/R) injury. We hypothesized that IL-23, a pro-inflammatory cytokine, could promote myocardial I/R injury by increasing the inflammatory response and oxidative stress. Methods: Male Sprague-Dawley rats were randomly assigned into sham operated control (SO) group, ischemia and reperfusion (I/R) group, (IL-23 + I/R) group and (anti-IL-23 + I/R) group. At 4 h after reperfusion, the serum concentration of lactate dehydrogenase (LDH), creatine kinase (CK) and the tissue MDA concentration and SOD activity were measured. The infarcte size was measured by TTC staining. Apoptosis in heart sections were measured by TUNEL staining. The expression of HMGB1 and IL-17A were detected by Western Blotting and the expression of TNF-α and IL-6 were detected by Elisa. Results: After 4 h reperfusion, compared with the I/R group, IL-23 significantly increased the infarct size, the apoptosis of cardiomyocytes and the levels of LDH and CK (all P < 0.05). Meanwhile, IL-23 significantly increased the expression of eIL-17A, TNF-α and IL-6 and enhanced both the increase of the MDA level and the decrease of the SOD level induced by I/R (all P<0.05). IL-23 had no effect on the expression of HMGB1 (p > 0.05). All these effects were abolished by anti-IL-23 administration. Conclusion: The present study suggested that IL-23 may promote myocardial I/R injury by increasing the inflammatory responses and oxidative stress reaction.

Benefit Agmatine Effects in Experimental Multiple Sclerosis. CNS Nitrosative and Oxidative Stress Suppression / Protektivni Efekti Agmatina U Eksperimentalnoj Multiploj Sklerozi. Supresija Nitrozativnog I Oksidativnog Stresa U CNS-U

2014 ◽  
Vol 31 (4) ◽  
pp. 233-243
Author(s):  
Ivana Stojanović ◽  
Srđan Ljubisavljević ◽  
Ivana Stevanović ◽  
Slavica Stojnev ◽  
Radmila Pavlović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Clinical Symptoms ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Autoimmune Encephalomyelitis ◽  
Sod Activity ◽  
Neuroprotective Effects ◽  
Sprague Dawley Rats ◽  
And Oxidative Stress

Summary The aim of this study was to investigate the exogenous agmatine influence on nitrosative and oxidative stress parameters in acute phase of multiple sclerosis (MS) experimental model, experimental autoimmune encephalomyelitis (EAE). EAE was induced by subcutaneous injection of myelin basic protein (50 μg per animal). Sprague-Dawley rats were divided into five groups: I group - (CG), treated by PBS (i.p.), II group - (EAE), III group - (CFA), treated with Complete Freund’s adjuvant (0.2 ml subcutaneously), IV group - (EAE+AGM), treated by agmatine (75 mg/kg bw i.p.) upon EAE induction and V group - (AGM), received only agmatine in the same dose. The animals were treated every day during experiment - from day 0 to 15, and clinically scored every day. They were sacrificed on day 16 from MBP application. NO2+NO3, S-nitrosothiols (RSNO), malondyaldehide (MDA) and reduced glutathione (GSH) concentrations and superoxide dismutase (SOD) activity were determined in rat whole encephalitic mass (WEM) and cerebellum homogenates. Agmatine exerted strong protective effects on EAE clinical symptoms (p<0.05). In EAE brain homogenates, NO2+NO3, RSNO and MDA concentrations were increased compared to CG values. Agmatine treatment diminished NO2+NO3, RSNO and MDA levels in EAE animals (p<0.05). In EAE rats, GSH level and SOD activity were decreased compared to CG values, but agmatine treatment increased both parameters compared to EAE untreated animals (p<0.05). Immunohistochemical staining supported the clinical and biochemical findings in all groups. The CNS changes in EAE are successfully supressed by agmatine application, which could be the the new aspect of the neuroprotective effects of agmatine.

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 Remote Inflammatory Preconditioning Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Inhibition of Intrinsic Apoptosis in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yong Liu ◽  
Jiahang Xu ◽  
Liang Zhao ◽  
Jing Cheng ◽  
Baojun Chen
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Animal Experiments ◽  
Intrinsic Apoptosis ◽  
Sprague Dawley ◽  
Sod Activity ◽  
Lung Protection ◽  
Sprague Dawley Rats ◽  
The Right

Background. Acute lung injury (ALI) always leads to severe inflammation. As inflammation and oxidative stress are the common pathological basis of endotoxin-induced inflammatory injury and ischemic reperfusion injury (IRI), we speculate that remote ischemic preconditioning (RIPC) can be protective for ALI when used as remote inflammatory preconditioning (RInPC). Method. A total of 21 Sprague-Dawley rats were used for the animal experiments. Eighteen rats were equally and randomly divided into the control (NS injection), LPS (LPS injection), and RInPC groups. The RInPC was performed prior to the LPS injection via tourniquet blockage of blood flow to the right hind limb and adopted three cycles of 5 min tying followed by 5 min untying. Animals were sacrificed 24 hours later. There were 2 rats in the LPS group and 1 in the RInPC group who died before the end of the experiment. Supplementary experiments in the LPS and RInPC groups were conducted to ensure that 6 animals in each group reached the end of the experiment. Results. In the present study, we demonstrated that the RInPC significantly attenuated the LPS-induced ALI in rats. Apoptotic cells were reduced significantly by the RInPC, with the simultaneous improvement of apoptosis-related proteins. Reduction of MPO and MDA and increasing of SOD activity were found significantly improved by the RInPC. Increasing of TNF-α, IL-1β, and IL-6 induced by the LPS was inhibited, while IL-10 was significantly increased by RInPC, compared to the LPS group. Conclusion. RInPC could inhibit inflammation and attenuate oxidative stress, thereby reducing intrinsic apoptosis and providing lung protection in the LPS-induced ALI in rats.

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.

scholarly journals Red Guava Juice (Psidium guajava L.) Reduce Oxidative Stress of Toll Gate Collector

2019 ◽  
Vol 39 (4) ◽  
pp. 333
Author(s):  
Riva Mustika Anugrah ◽  
Sugeng Maryanto ◽  
Kusmiyati Tjahjono ◽  
Martha Irene Kartasurya
Keyword(s):  
Oxidative Stress ◽  
Treatment Group ◽  
Initial Conditions ◽  
Thiobarbituric Acid ◽  
Psidium Guajava ◽  
T Test ◽  
Wilcoxon Test ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Exposure to air pollution can increase the occurrence of oxidative stress. Research showed that guava can reduce oxidative stress in Sprague Dawley rats. This experiment investigated the effect of red guava juice on oxidative stress in toll collectors. The subjects were 20 toll collectors in the treatment group and 20 in the control group. The treatment group received 250 mL red guava juice for 21 days while the controls did not receive anything. Malondialdehyde (MDA) was measured with thiobarbituric acid (TBA) reaction, food consumption was measured by 3×24 hours’ recall. The data were analyzed by paired t-test, Wilcoxon test, independent t-test, Mann Whitney test, and general linear model. The results showed that the effect of red guava juice on the MDA level was significant in the treatment group (p<0.05). A multivariate analysis showed that the effect of red guava juice to MDA level was significant after controlled by age, carbohydrate intake and initial conditions (p<0.05). Red guava juices of 250 mL for 21 days could reduce malondialdehyde (MDA) levels of toll collectors.

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