Withania somnifera attenuates nicotine induced locomotor sensitization and withdrawal symptoms in mice

2018 ◽  
Vol 7 (2) ◽  
pp. 180-184
Author(s):  
Nitin G Dumore ◽  
◽  
Milind J Umekar ◽  
Brijrsh G Taksande ◽  
Manish M Aglawe ◽  
...  

Objective: To investigate the effect of withania somnifera extract (WSE) on nicotine mediated reinforcement effect and withdrawal symptoms which attributed for the addiction liabilities of nicotine. Methods: In Swiss albino mice nicotine mediated locomotor sensitization and anxiogenic effects of chronic and acute nicotine treatment respectively was tested per se or in combination with WSE. In addition, nicotine withdrawal induced anxiety-like behavior was also studied. Locomotor sensitization was tested by employing open field test (OFT), while symptoms of anxiety were evaluated by subjecting mice to elevated plus maze (EPM). Results: Daily treatment with nicotine (subcutaneous) for 7 days showed gradual increase in the locomotor activity in OFT as compared to saline group indicating the development of locomotor sensitization. Following 3 days of drug free period, nicotine challenge on day 11 also showed rise in locomotor activity depicting expression of sensitization. WSE pretreatment inhibited the nicotine induced development and expression of locomotor sensitization. WSE+nicotine treated group showed decreased ambulations as compared to per se nicotine group on day 1-7 and day 8 (P<0.05). In EPM, acute nicotine treated mice spend more time in open arms as compared to saline indicating the anxiolytic behavior. WSE pretreatment reversed this anxiolytic effect. Nicotine withdrawal mice showed significant increase in the number of entries in arm and total time spend in closed arm indicating anxiety-like behavior. WSE treatment in nicotine withdrawal mice inhibited the nicotine withdrawal induced increased number of entries and time spend in closed arms. Conclusion: These results indicated that WSE may serve an effective herbal medicine in arresting nicotine mediated reinforcement and withdrawal signs

2013 ◽  
Author(s):  
T. R. Schlam ◽  
M. E. Piper ◽  
J. W. Cook ◽  
M. C. Fiore ◽  
T. B. Baker

1997 ◽  
Vol 82 (4) ◽  
pp. 1119-1125 ◽  
Author(s):  
G. S. Supinski ◽  
D. Stofan ◽  
R. Ciufo ◽  
A. Dimarco

Supinski, G. S., D. Stofan, R. Ciufo, and A. DiMarco. N-acetylcysteine administration alters the response to inspiratory loading in oxygen-supplemented rats. J. Appl. Physiol. 82(4): 1119–1125, 1997.—Based on recent studies, it has been suggested that free radicals are elaborated in the respiratory muscles during strenuous contractions and contribute to the development of muscle fatigue. If this theory is correct, then it should be possible to attenuate the development of diaphragm fatigue and/or delay the onset of respiratory failure during loaded breathing by administering a free radical scavenger. The purpose of the present experiment was, therefore, to examine the effect of N-acetylcysteine (NAC), a free radical scavenger and glutathione precursor, on the evolution of respiratory failure in decerebrate unanesthetized rats breathing against a large inspiratory resistive load. We compared the inspiratory volume and pressure generation over time in animals pretreated with either saline or NAC (150 mg/kg) and then loaded until respiratory arrest. After arrest, the diaphragm was excised, and samples were assayed for reduced (GSH) and oxidized glutathione. As a control, we also assessed respiratory function and glutathione concentrations in groups of nonloaded saline- and NAC-treated animals. We found that NAC-treated animals were able to tolerate loading better than the saline-treated group, maintaining higher inspiratory pressures and sustaining higher inspired volumes. Administration of NAC also increased the time that animals could tolerate loading before the development of respiratory arrest. In addition, although saline-treated loaded animals had significant reductions in diaphragmatic GSH levels compared with unloaded controls, the magnitude of this reduction was blunted by NAC administration (i.e., GSH averaged 965 ± 113, 568 ± 83, 907 ± 39, and 784 ± 61 nmol/g for unloaded-saline, loaded-saline, unloaded-NAC, and loaded-NAC groups, P< 0.05, with the value for the loaded-saline group lower than the values for the two unloaded groups; GSH for the loaded-NAC group was not different, however, from unloaded controls). These data demonstrate that administration of NAC, a free radical scavenger, slows the rate of development of respiratory failure during inspiratory resistive loading.


2018 ◽  
Vol 27 (2) ◽  
pp. 122-128 ◽  
Author(s):  
N. Marefati ◽  
N. Eftekhar ◽  
M. Kaveh ◽  
J. Boskabadi ◽  
F. Beheshti ◽  
...  

Objectives: To evaluate the effects of Allium cepa (A. cepa) on levels of oxidants, antioxidants, and immunological markers in bronchoalveolar lavage fluids (BALF) of sensitized rats. Materials and Methods: Oxidant/antioxidant markers and cytokines in BALF of control rats treated with saline (group C), ovalbumin-sensitized rats (group S), rats treated with 1.25 μg/mL dexamethasone and 3 doses of A. cepa extract (35, 70, and 140 mg/kg body weight [BW]/day) (S + AC) were investigated. Comparison of the results between groups was performed using analysis of variance with the Tukey-Kramer post hoc test. Results: The oxidant markers nitrogen dioxide (NO2), nitrate (NO3–), and malondialdehyde (MDA), and immunological markers interleukin (IL)-4 and immunoglobulin E (IgE) were significantly higher, but the antioxidant markers superoxide dismutase (SOD), catalase (CAT), thiol, and interferon (IFN)-γ, and the IFN-γ/IL-4 ratio were lower in sensitized rats compared to control rats (p < 0.001 to p < 0.01). Compared to group S, the levels of the following markers were significantly lower: NO2, NO3–, and IgE in groups treated with the A. cepa extract, MDA and IL-4 levels in groups treated with 70 and 140 mg/kg BW/day of the A. cepa extract, and all these markers as well as IFN-γ in rats treated with dexamethasone (p < 0.001 to p < 0.05). However, there were significantly higher levels of SOD and CAT and an increased IFN-γ/IL-4 ratio (groups treated with 70 and 140 mg/kg BW/day of the A. cepa extract), and levels of thiol and IFN-γ (group treated with 140 mg/kg BW/day of the A. cepa extract) as well as SOD, CAT, and thiol (dexamethasone-treated group) versus group S (p < 0.00 to p < 0.05). Conclusion: A. cepa showed antioxidant and immunomodulatory properties in sensitized rats.


2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Vijay R. Ambiye ◽  
Deepak Langade ◽  
Swati Dongre ◽  
Pradnya Aptikar ◽  
Madhura Kulkarni ◽  
...  

Ashwagandha (Withania somnifera) has been described in traditional Indian Ayurvedic medicine as an aphrodisiac that can be used to treat male sexual dysfunction and infertility. This pilot study was conducted to evaluate the spermatogenic activity of Ashwagandha root extract in oligospermic patients. Forty-six male patients with oligospermia (sperm count < 20 million/mL semen) were enrolled and randomized either to treatment (n=21) with a full-spectrum root extract of Ashwagandha (675 mg/d in three doses for 90 days) or to placebo (n=25) in the same protocol. Semen parameters and serum hormone levels were estimated at the end of 90-day treatment. There was a 167% increase in sperm count (9.59 ± 4.37 × 106/mL to 25.61 ± 8.6 × 106/mL;P<0.0001), 53% increase in semen volume (1.74 ± 0.58 mL to 2.76 ± 0.60 mL;P<0.0001), and 57% increase in sperm motility (18.62 ± 6.11% to 29.19 ± 6.31%;P<0.0001) on day 90 from baseline. The improvement in these parameters was minimal in the placebo-treated group. Furthermore, a significantly greater improvement and regulation were observed in serum hormone levels with the Ashwagandha treatment as compared to the placebo. The present study adds to the evidence on the therapeutic value of Ashwagandha (Withania somnifera), as attributed in Ayurveda for the treatment of oligospermia leading to infertility.


2018 ◽  
Vol 115 (16) ◽  
pp. 4282-4287 ◽  
Author(s):  
Julia K. Brynildsen ◽  
Bridgin G. Lee ◽  
Isaac J. Perron ◽  
Sunghee Jin ◽  
Sangwon F. Kim ◽  
...  

Cigarette smoking is the leading cause of preventable disease and death in the United States, with more persons dying from nicotine addiction than any other preventable cause of death. Even though smoking cessation incurs multiple health benefits, the abstinence rate remains low with current medications. Here we show that the AMP-activated protein kinase (AMPK) pathway in the hippocampus is activated following chronic nicotine use, an effect that is rapidly reversed by nicotine withdrawal. Increasing pAMPK levels and, consequently, downstream AMPK signaling pharmacologically attenuate anxiety-like behavior following nicotine withdrawal. We show that metformin, a known AMPK activator in the periphery, reduces withdrawal symptoms through a mechanism dependent on the presence of the AMPKα subunits within the hippocampus. This study provides evidence of a direct effect of AMPK modulation on nicotine withdrawal symptoms and suggests central AMPK activation as a therapeutic target for smoking cessation.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Swati Dongre ◽  
Deepak Langade ◽  
Sauvik Bhattacharyya

Background.Many women experience sexual dysfunction where there are orgasm disorders and sexual difficulties. Ashwagandha (Withania somnifera) is a herb known to improve the body’s physical and psychological condition.Objective.The purpose of the study was to determine the efficacy and safety of a high-concentration ashwagandha root extract (HCARE) supplementation for improving sexual function in healthy females.Methods.In this pilot study, 50 study subjects were randomized to either (i) HCARE-treated group or (ii) placebo- (starch-) treated group. The subjects consumed either HCARE or placebo capsules of 300mg twice daily for 8 weeks. Sexual function was assessed using two psychometric scales, the Female Sexual Function Index (FSFI) Questionnaire and the Female Sexual Distress Scale (FSDS), and by the number of total and successful sexual encounters.Results.The analysis indicates that treatment with HCARE leads to significantly higher improvement, relative to placebo, in the FSFI Total score (p<0.001), FSFI domain score for “arousal” (p<0.001), “lubrication” (p<0.001), “orgasm” (p=0.004), and “satisfaction” (p<0.001), and also FSDS score (p<0.001) and the number of successful sexual encounters (p<0.001) at the end of the treatment.Conclusions.This study demonstrated that oral administration of HCARE may improve sexual function in healthy women. The present study is registered in the Clinical Trial Registry, Government of India, with a numberCTRI/2015/07/006045.


2013 ◽  
Vol 25 (7) ◽  
pp. 986-997 ◽  
Author(s):  
Benjamin Becker ◽  
Eva M. Klein ◽  
Nadine Striepens ◽  
Yoan Mihov ◽  
Thomas E. Schlaepfer ◽  
...  

Hippocampal learning is thought to induce metaplasticity, which can facilitate subsequent learning. Administered at single low doses, the N-methyl-d-aspartate-type glutamate receptor antagonist memantine predominantly blocks α7 nicotinic acetylcholine receptors (α7 nAChRs). Placebo-controlled administration of a single low dose of memantine in a pharmaco-fMRI experiment may thus help characterize the role of α7 nAChRs in hippocampal metaplasticity. We hypothesized that if α7 nAChRs contribute to learning-induced metaplasticity in the hippocampus, blockade of these receptors with low-dose memantine would selectively interfere with a facilitation of subsequent learning without impairing hippocampal learning per se. To specifically test this hypothesis, we devised a randomized controlled trial in which healthy volunteers were administered a 20-mg single oral dose of memantine or placebo and scanned on three subsequent runs of a hippocampal learning task. Our results indicate no discrepancies in behavioral learning between low-dose memantine- and placebo-treated participants in the first and second run of this task. In the third run, however, only the placebo-treated group showed facilitated behavioral learning, an effect paralleled by decreased neural responses in the hippocampal cornu ammonis region. Our findings suggest that blockade of α7 nAChRs selectively interfered with a learning-induced facilitation of subsequent learning while leaving unimpaired hippocampal learning per se. Taken together, our results provide support for a relevant contribution of α7 nAChRs to learning-associated metaplasticity in the hippocampus.


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