scholarly journals Neuroprotective potential of hydroethanolic hull extract of Juglans regia L. on isoprenaline induced oxidative damage in brain of Wistar rats

2021 ◽  
Vol 8 ◽  
pp. 223-229
Author(s):  
Priyanka Sharma ◽  
Pawan K. Verma ◽  
Shilpa Sood ◽  
Nrip K. Pankaj ◽  
Sanjay Agarwal ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Felipe Ornell ◽  
Samira S. Valvassori ◽  
Amanda V. Steckert ◽  
Pedro F. Deroza ◽  
Wilson R. Resende ◽  
...  

The effects of modafinil (MD) on behavioral and oxidative damage to protein and lipid in the brain of rats were evaluated. Wistar rats were given a single administration by gavage of water or MD (75, 150, or 300 mg/kg). Behavioral parameters were evaluated in open-field apparatus 1, 2, and 3 h after drug administration. Thiobarbituric acid reactive substances (TBARS) and protein carbonyl formation were measured in the brain. MD increased locomotor activity at the highest dose 1 and 3 h after administration. MD administration at the dose of 300 mg/kg increased visits to the center of open-field 1 h after administration; however, 3 h after administration, all administered doses of MD increased visits to the open-field center. MD 300 mg/kg increased lipid damage in the amygdala, hippocampus, and striatum. Besides, MD increased protein damage in the prefrontal cortex, amygdala, and hippocampus; however, this effect varies depending on the dose administered. In contrast, the administration of MD 75 and 300 mg/kg decreased the protein damage in the striatum. This study demonstrated that the MD administration induces behavioral changes, which was depending on the dose used. In addition, the effects of MD on oxidative damage parameters seemed to be in specific brain region and doses.


Author(s):  
Insha Amin ◽  
Ishraq Hussain ◽  
Muneeb U. Rehman ◽  
Bilal Ahmad Mir ◽  
Showkat Ahmad Ganaie ◽  
...  

Author(s):  
Pawan K. Verma ◽  
Rajinder Raina ◽  
Shahid Prawez ◽  
Mudasir Sultana ◽  
Maninder Singh ◽  
...  

2016 ◽  
Vol 33 (S1) ◽  
pp. S527-S527
Author(s):  
D. Martín Hernández ◽  
Á.G. Bris ◽  
K.S. MacDowell ◽  
A. Sayd ◽  
D. Azpiazu ◽  
...  

IntroductionPatients with major depression who are otherwise medically healthy have activated inflammatory pathways. It has been described that depression is not only escorted by inflammation but also by induction of multiple oxidative/nitrosative stress pathways. Nevertheless, there are finely regulated mechanisms involved in preserving cells from damage, such as the nuclear factor Nrf2.AimsTo explore in a depression-like model the Nrf2 pathway in the prefrontal cortex (PFC) and the hippocampus of rats and to analyze which classic antidepressants affect the antioxidant activity of the Nrf2 pathway.MethodsMale Wistar rats were exposed to chronic mild stress (CMS) and some of them were treated with desipramine, escitalopram or duloxetine. We studied the expression in the PFC and hippocampus of upstream and downstream elements of the Nrf2 pathway and the oxidative damage induced by the CMS.ResultsAfter exposure to a CMS protocol, in the PFC, there is an inhibition of upstream and downstream elements of the Nrf2 pathway. Moreover, antidepressant treatments, particularly desipramine and duloxetine, are able to recover some of these elements and to reduce the oxidative damage induced by the depression model. In the hippocampus however, Nrf2 pathways are not that affected and antidepressants do not have many actions.ConclusionsNrf2 pathway is differentially regulated by antidepressants in the PFC and hippocampus. The Nrf2 pathway is involved in the oxidative/nitrosative damage detected in the PFC after CMS exposure. However, it seems that Nrf2 is not very involved in the effects caused by the CMS in the hippocampus.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2010 ◽  
Vol 23 (2) ◽  
pp. 257-263 ◽  
Author(s):  
Rajamani Karthikeyan ◽  
T. Manivasagam ◽  
P. Anantharaman ◽  
T. Balasubramanian ◽  
S. T. Somasundaram

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 1681-1693
Author(s):  
Kapil Kumar ◽  
Praveen K Dixit ◽  
Harshit Takru ◽  
Nagarajan K

The present study explored the assessment of the antidiabetic potential of Tinospora cordifolia & Juglans regia composite extract in STZ induced diabetes in wistar rats. As streptozotocin -associated infiltrations of increase glucose level has been reported to be responsible for diabetes. We evaluated the glucose lowering potential of Tinospora cordifolia & Juglans regia on the basis of its anti-diabetic property. Rats were administered streptozotocin (55 mg/kg i.p., once) with nicotinamide (120mg/kg) to induce experimental toxicity. The development of diabetes was assessed biochemically as well as histologically 72 hours after induction of diabetes. Body weight and blood glucose levels were determined in (0, 7th, 14th, 21st, 28th) days. Serum lipid profile and enzyme estimated, (kidney, liver, pancreas) tissue was measured at the end of the experimental period. Treatment with composite extracts TCAE high dose (350 gm/kg b.w.) & JRAE high dose (800 mg/kg b.w.) and TCHE high dose (350 gm/kg b.w.) & JRHE high dose (800 mg/kg b.w.) were noted to be more effective against the streptozotocin- induced toxicity as compared to Glibenclamide (5 mg/kg b.w.). it may be concluded that streptozotocin-induced glucose may be accountable for the induction of diabetes toxicity in rats. Interestingly, improvement in body weight, glucose level, lipid profiles, biochemical parameters and histopathological changes in kidney, liver and pancreas was observed following herbal treatment in STZ induced diabetic rats. Furthermore, composite extract of TCAE (350mg/kg b.w.) & JRAE (800mg/kg b.w.) was found to be efficacious than the composite extract of TCHE (350mg/kg b.w.) & JRHE (800mg/kg b.w.).


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