scholarly journals Effect of sitagliptin on depression in male wistar rats

Author(s):  
Vidya M. Mahalmani ◽  
Anil P. Hogade ◽  
Sanjay K. Mishra

Background: Growing evidence supports relationship between depression and inflammation. The hypothesis of involvement of inflammatory pathways in depression is supported by the findings of increased levels of proinflammatory cytokines. So, we decided to evaluate the effect of sitagliptin on depression using forced swim test (FST) and possible effects of sitagliptin on serum oxidative stress markers and cytokine gene expression in rat hippocampus.Methods: FST model was used to evaluate antidepressant effect in male wistar rats. Rats in group I (control group) were given normal saline, group II (standard group) were given fluoxetine, group III and IV (test groups) were given sitagliptin 5 mg/kg and sitagliptin 9 mg/kg respectively. All the drugs in all groups were given per orally. At the end, animals were sacrificed and blood was collected. Hippocampus of rat brain was dissected out. Serum oxidative stress markers and hippocampal pro inflammatory cytokine gene expression analysis was carried out.Results: Sitagliptin 5 mg/kg and 9 mg/kg showed reduction in depressive symptoms and hippocampal cytokine gene expression in comparison to control. In case of serum oxidative stress markers, there was statistically significant reduction in nitric oxide levels with stagliptin 9 mg/kg. Although there was a decrease in the levels of catalase and increase in the levels of glutathione with standard and test groups, the results were not statistically significant.Conclusions: The present study showed significant antidepressant effect activity of standard and test groups. Hence, further research should be carried out to substantiate above results.

2014 ◽  
Vol 66 (3) ◽  
pp. 1075-1081
Author(s):  
Ivan Simic ◽  
Violeta Iric-Cupic ◽  
Rada Vucic ◽  
Marina Petrovic ◽  
Violeta Mladenovic ◽  
...  

The aim of the present study was to evaluate the subchronic effects of 3,4-methylenedioxymethamphetamine on several oxidative stress markers: index of lipid peroxidation (ILP), superoxide dismutase (SOD) activity, superoxide radical (O2.-) levels, and reduced glutathione (GSH) levels in the frontal cortex, striatum and hippocampus of the rat. The study included 64 male Wistar rats (200-250g). The animals were treated per os with of 5, 10, or 20 mg/kg of 3,4-methylenedioxymethamphetamine (MDMA) every day for 15 days. The subchronic administration of MDMA resulted in an increase in ILP, SOD and O2.-, and a decrease in GSH, from which we conclude that oxidative stress was induced in rat brain.


Author(s):  
Ijeoma Ezebuiro ◽  
Chibuike Obiandu ◽  
Friday Saronee ◽  
Adesua C. Obiandu

Introduction: Cnidoscolus aconitifolius is considered to be an important and effective medicinal plant in folklore remedies where it has been applied as an alternative therapy for the treatment of various ailments. Aim: The present study aims to determine the effects of Cnidoscolus aconitifolius on lipid profile and some oxidative stress markers of male Wistar rats. Methodology: A total of 15 male wistar rats were procured for the study and randomly assigned into three groups of 5 rats each. Group 1 served as control and received distilled water only. Group 2 received 200 mg/kg and group 3 received 400mg/kg of the hydromethanolic (1:4) extract of Cnidoscolus aconitifolius which was administered as single daily dose using oral cannula. On completion of treatment, blood samples were collected by cardiac puncture for determination of some serum lipid parameters and oxidative stress markers. Results: Results showed that there were no significant difference in the serum level of total cholesterol, triglyceride, low density lipoprotein cholesterol and high density lipoprotein cholesterol at both doses of the extract, compared to control. However, compared to control, there was a significant (p<0.05) increase in the activity of superoxide dismutase and glutathione reductase but significant reduction in malondialdehyde level. The catalase enzyme activity was not significant. Conclusion: The result obtained suggest that the extract may be useful in reducing oxidative stress by improving some antioxidant enzyme activities and may also prevent cell death due to lipid peroxidation.


2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Olufunke Olorundare ◽  
Adejuwon Adeneye ◽  
Akinyele Akinsola ◽  
Sunday Soyemi ◽  
Alban Mgbehoma ◽  
...  

Trastuzumab (TZM) is a humanized monoclonal antibody that has been approved for the clinical management of HER2-positive metastatic breast and gastric cancers but its use is limited by its cumulative dose and off-target cardiotoxicity. Unfortunately, till date, there is no approved antidote to this off-target toxicity. Therefore, an acute study was designed at investigating the protective potential and mechanism(s) of CVE and IGE in TZM-induced cardiotoxicity utilizing cardiac enzyme and oxidative stress markers and histopathological endpoints. 400 mg/kg/day CVE and IGE dissolved in 5% DMSO in sterile water were investigated in Wistar rats injected with 2.25 mg/kg/day/i.p. route of TZM for 7 days, using serum cTnI and LDH, complete lipid profile, cardiac tissue oxidative stress markers assays, and histopathological examination of TZM-intoxicated heart tissue. Results showed that 400 mg/kg/day CVE and IGE profoundly attenuated increases in the serum cTnI and LDH levels but caused no significant alterations in the serum lipids and weight gain pattern in the treated rats. CVE and IGE profoundly attenuated alterations in the cardiac tissue oxidative stress markers’ activities while improving TZM-associated cardiac histological lesions. These results suggest that CVE and IGE could be mediating its cardioprotection via antioxidant, free radical scavenging, and antithrombotic mechanisms, thus, highlighting the therapeutic potentials of CVE and IGE in the management of TZM-mediated cardiotoxicity.


2020 ◽  
Vol 11 (2) ◽  
pp. 88-98
Author(s):  
Babatunde Ogunlade ◽  
◽  
Olasumbo Afolayan ◽  
Sunday Adelakun ◽  
◽  
...  

Lead (Pb) exposure induces oxidative stress causing imbalance in antioxidant enzymes, cognitive impairments and neurodegeneration. This study investigated the neuroprotective and antioxidant properties of sulphoraphane (SFN) on Pb-induced neurotoxicity of adult Wistar rats. Forty animals (150 ± 20 g) were divided into four groups (n=10): Group A received normal saline as placebo; Group B received 50 mg/kg body weight (bw) of Lead only; Group C received a combination of 50 mg/kg bw of Lead and 50 mg/kg bw of SFN; Group D received 50 mg/kg bw of SFN only. All administration was through oral gavages for 28 days; animals underwent behavioural tests (Morris water and Y- mazes); and thereafter sacrificed and brains extracted. Biochemical estimations of antioxidants (superoxide dismutase, reduced glutathione, and catalase), oxidative stress markers (malondialdehyde, nitric oxide, and hydrogen peroxide), neurotransmitters (dopamine, serotonin, and norepinephrine) and hippocampal histology were done. The results showed significant increase in escape latency, norepinephrine and oxidative stress markers with concomitant decrease percentage correct alternation, serotonin, dopamine and antioxidant enzymes in Pb exposed rats compared with the control. However, the co-administration of SFN and Pb significantly attenuated Pb neurotoxicity. Sulphoraphane is capable of ameliorating oxidative stress induced neurobehavioural deficits and hippocampal neurochemistry caused by Pb exposure in Alzheimer’s type animal model of neurodegenerative disorder.


2021 ◽  
Vol 15 (4) ◽  
pp. 249-256
Author(s):  
Taiwo Adekemi Abayomi ◽  
◽  
Olorunfemi Samuel Tokunbo ◽  
Moyinoluwa Ajayi ◽  
Olawale Ayobami Abayomi ◽  
...  

Background: Although ethanol exerts its neurotoxic effect on the brain through inflammatory and oxidative processes, the effect of Riboceine on the brain following ethanol neurotoxicity is yet to be elucidated. Therefore, this study was designed to evaluate the effects of riboceine on the cellular, behavioral, and molecular impairments induced by ethanol toxicity in rats. Methods: A total of 24 male Wistar rats weighing between 160-170 grams were used for the study, and were divided into four groups of six rats each. After completion of the administration of ethanol and riboceine, and testing for motor impairment, the rats were sacrificed. The cerebellum was excised and processed for oxidative stress analyses, based on oxidative stress markers and histological examinations. The immunohistochemical expression of astrocytes in the cerebellum was examined, using Glial Fibrillary Acidic Protein (GFAP) stain. Results: This study demonstrated that ethanol-induced neurotoxicity in the cerebellum, characterized by increased oxidative stress profile, astrocyte activation, and neuronal death in the cerebellum, especially the Purkinje layer. Necrosis, significant decrease in Superoxide Dismutase (SOD), Catalase (CAT) and Gluathione (GSH) activities (P<0.05) as well as astrogliosis was associated with ethanol treatment. However, riboceine was observed to significantly increase the cerebellar SOD, CAT and GSH activities with significantly reduced Malondialdehyde (MDA) levels (P<0.05). It also attenuated the histomorphological alteration of the cerebellum and reduced the cerebellar astrocytes activation following ethanol-induced neurotoxicity, thus leading to the attenuation of motor impairment. Conclusion: Riboceine attenuated motor impairment caused by chronic ethanol-induced neurotoxicity, suggestive of its anti-oxidative and anti-inflammatory properties.


Author(s):  
Binitha P Purushothaman ◽  
Gayathri Valsan ◽  
Ramadasan Kuttan

Objective: Elucidation of the protective effect of lutein against carbofuran induced toxicity in Wistar rats.Methods: Male Wistar rats were assigned into 5 groups of five animals. Group I normal received sunflower oil, Group 2 received carbofuran (5 mg/kg b. w.) alone. Group 3-5 received carbofuran plus lutein (50, 100 and 200 mg/kg body weight) respectively. Carbofuran and lutein administration were continued for 14 d. Neurobehavioural markers such as rotarod, grip strength test and pain threshold tests were carried out. After sacrifice, tissues were analysed for marker enzymes, antioxidant enzymes as well as oxidative stress markers.Results: Low dose of carbofuran was found to produce neurobehavioral problems as seen from the decreased retention time during rotarod test, endurance capacity in grip strength test and increased endurance capacity in pain threshold test. They were found to be significantly reversed by oral lutein administration. Administration of lutein restored the decreased acetylcholinesterase produced by carbofuran. Serum and tissue marker enzymes such as lactate dehydrogenase, creatine kinase and gamma-glutamyltransferase, which were increased by carbofuran were decreased by lutein administration. Lutein administration also reduced oxidative stress parameters which were increased by carbofuran.Conclusion: The results showed that carbofuran induced toxicity in male Wistar rats was reversed by carotenoid lutein.


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