University Institute of Pharmaceutical science

Chandigarh, India

University Institute of Pharmaceutical science

Chandigarh, India
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Patent
University Institute Of Pharmaceutical Science | Date: 2013-01-09

The present invention relates to a simple and convenient process for preparing solid lipid sustained release nanoparticles for delivery of drugs/vitamins, preferably fat soluble vitamins and more specifically Vitamin D_(3 )and retinoic acid (RA). The process involves microemulsion technique. The nanoparticles of Vitamin D_(3 )and RA obtained by the process of the present invention have utility in treatment of diseases like tuberculosis. Use may be extended to other diseases like AMD, diabetic retinopathy, cancers, hyperpigmentation, acne, and osteoporosis.


Sharma A.,Rayat Bahra Institute of Pharmacy | Piplani P.,University Institute of Pharmaceutical science
Central Nervous System Agents in Medicinal Chemistry | Year: 2013

In view of the large libraries of acetylcholinesterase inhibitors (AChEIs) that are now being handled in organic synthesis, the identification of drug biological activity is advisable prior to synthesis and this can be achieved by employing predictive biological property methods. In this sense, Quantitative Structure-Activity Relationships (QSAR) or docking approaches have emerged as promising tools. The intention of this review is to summarize the present knowledge concerning computational predictions of AChEIs and AChE. © 2013 Bentham Science Publishers.


Dhingra M.S.,University Institute of Pharmaceutical science | Dhingra S.,University of the West Indies | Chadha R.,University Institute of Pharmaceutical science | Singh T.,Panjab University | Karan M.,University Institute of Pharmaceutical science
Medicinal Chemistry Research | Year: 2014

In our effort to identify the effective gastric sparing and protective anti-inflammatory agents, a series of gallic acid esters were synthesized, characterized, and studied to assess their physicochemical properties. Subsequently, the esters were evaluated for their anti-inflammatory activity and effect on gastric mucosa by most active compounds. All the compounds exhibited promising antiinflammatory activity in carrageenan-induced rat paw edema model. In particular, 7a, 7c, 7f, and 7h emerged as the most active compounds in the series. The findings of gastric ulcer and antioxidant studies suggested these compounds as non-ulcerogenic and gastroprotective. Further, the predicted ADME properties of all the tested compounds were found to be in the ranges as predicted by QikProp for 95 % of known oral drugs and also satisfy the Lipinski's rule of five. © Springer Science+Business Media New York 2014.


Kumar A.,University Institute of Pharmaceutical science | Lalitha S.,University Institute of Pharmaceutical science | Mishra J.,University Institute of Pharmaceutical science
Indian Journal of Pharmacology | Year: 2014

Aim: Epilepsy is a chronic neurological disorder with complex pathophysiology. Several evidences suggest a role of oxidative stress and mitochondrial dysfunction in pathophysiology of epilepsy. Hesperidin (Hesp) acts as a powerful anti-oxidant agent against superoxide, singlet oxygen, and hydroxyl radicals. Thus, this study was undertaken to evaluate the possible neuroprotective mechanism of Hesp against pentylenetetrazole (PTZ)-induced convulsions in mice. Materials and Methods: Sixty males Laca mice (20-25 g) were randomly divided into 10 treatment groups (n = 6). Seven days pretreatment of Hesp (100, 200 mg/kg, p.o.) was carried out before PTZ (80 mg/kg, intraperitoneal [i.p.]) challenge, whereas diazepam (DZP) (0.2, 0.5 mg/kg) and gabapentin (Gbp) (10, 20 mg/kg) were administered i.p. 30 min before PTZ administration, that is, on 7 th day. Following PTZ challenge, severity of convulsions (onset of jerks, myoclonic seizures, extensor phase and death), brain anti-oxidant enzyme levels and mitochondrial complex enzymes activities were estimated. Results: Single i.p. PTZ (80 mg/kg) challenge demonstrated severe convulsions, oxidative damage (raised lipid peroxidation [LPO], nitrite concentration as well as depleted reduced glutathione, superoxide dismutase and catalase levels), and depletion of mitochondrial enzyme Complex (I, II, IV) activities. Hesp (200 mg/kg), DZP (0.5 mg/kg) and Gbp (20 mg/kg) pretreatments attenuated PTZ induced behavioral, biochemical and mitochondrial alterations. However, administration of Hesp (100 mg/kg) in combination with DZP (0.2 mg/kg) or Gbp (10 mg/kg) potentiated their neuroprotective effect, which was significant as compared to their effects in PTZ treated animals. Conclusion: Hesp possesses potent anticonvulsant activity which might be mediated through modulation of gamma-amino butyric acid/benzodiazepine receptor action.


Gaur V.,University Institute of Pharmaceutical science | Kumar A.,University Institute of Pharmaceutical science
Brain Research | Year: 2010

The present study has been designed to explore the nitric oxide mechanism in the protective effect of desipramine, venlafaxine and trazodone against I/R induced oxidative stress and mitochondrial dysfunction in mice. Vitamin E was taken as standard antioxidant. Laca mice (25-30 g) were subjected to twice BCCAO occlusion (5 min) at the interval of 10 min, followed by 96 h reperfusion. The drug treatments were started from the day of surgery and continued for the next four days. After 96 h the animals were sacrificed for biochemical (malondialdehyde, nitrite concentration, superoxidedismutase, catalase, redox ratio and GST) and mitochondrial enzyme complex (NADH dehydrogenase, succinate dehydrogenase, MTT assay and cytochrome c oxidase) estimations. Ischemia caused significant oxidative damage and mitochondrial enzyme dysfunction after 96 h of reperfusion as compared to sham operated animals. Antidepressant (desipramine, venlafaxine and trazodone) treatment significantly attenuated oxidative damage and restored mitochondrial enzyme complex activities as compared to control (I/R) group. Further, protective effects of desipramine (15 mg/kg) and/or venlafaxine (5 mg/kg) were attenuated by l-arginine (100 mg/kg) or sildenafil (5 mg/kg) pretreatment. Further, L-NAME (10 mg/kg) or 7-NI (10 mg/kg) pretreatment with desipramine (15 mg/kg) and/or venlafaxine (5 mg/kg) significantly potentiated their protective effect which was significant as compared to their effect alone. The present study highlights the involvement of nitric oxide mechanism in the protective effects of desipramine and venlafaxine against I/R induced oxidative stress and mitochondrial dysfunction in mice. © 2010 Elsevier B.V. All rights reserved.


Kumar A.,University Institute of Pharmaceutical science | Garg R.,University Institute of Pharmaceutical science | Gaur V.,University Institute of Pharmaceutical science | Kumar P.,University Institute of Pharmaceutical science
Brain Research | Year: 2010

Present study has been designed to elucidate the nitric oxide modulatory mechanism of venlafaxine in experimental model of chronic behavior despair in mice. Animals (male albino laca mice) were forced to swim daily for 6 min test session for 7 days and immobility period of each animal was measured on every alternate days. Six minutes forced swimming test session for 7 days caused anxiety-like behavior (as assessed by mirror chamber and plus maze tests) and impairment in locomotor activity followed by oxidative damage (increased lipid peroxidation, nitrite concentration, depleted reduced glutathione and catalase activity) as compared to naïve animals. Seven days venlafaxine (5 and 10 mg/kg) treatment significantly caused anti-anxiety-like effect, improved locomotor activity and attenuated oxidative damage (reduced lipid peroxidation, nitrite concentration and caused restoration of reduce glutathione and catalase activity) as compared to control. Caffeine (10 mg/kg) pretreatment with venlfaxine (5 mg/kg) did not produce any significant effect on locomotor activity, immobility period and oxidative damage as compared to their effect per se. Further, l-NAME (5 mg/kg) and methylene blue (10 mg/kg) pretreatment with sub effective dose of venlafaxine (5 mg/kg) potentiated its protective effect which was significant as compared to their effect per se. However, l-arginine (100 mg/kg) pretreatment with venlafaxine (5 mg/kg) significantly reversed the protective effect of venlafaxine (P < 0.05). Present study suggests that nitric oxide modulation might be involved in the protective effects of venlafaxine. © 2009 Elsevier B.V. All rights reserved.


Prakash A.,Jawaharlal Institute of Postgraduate Medical Education & Research | Chopra K.,University Institute of Pharmaceutical science | Medhi B.,Jawaharlal Institute of Postgraduate Medical Education & Research
Indian Journal of Pharmacology | Year: 2013

Introduction: The present study was designed to evaluate the effect of granulocyte-colony stimulating factor (G-CSF) in the treatment of Parkinson′s disease (PD), the second most common neurodegenerative disease characterized by muscle and movement disorder, often associated with depression. PD is very difficult to treat. Hence, the present study was aimed to evaluate the effect of G-CSF in PD associated with depression. Materials and Methods: Adult Wistar male rats weighing about 180-250 g were selected and divided into five groups in parallel designed method namely; control group (n = 5); sham operated group (n = 5); Vehicle group (n = 5); G-CSF group (70 μg/kg, s.c.) (n = 5) and L-DOPA group (n = 5). The rats were treated with 6-hydroxydopamine (6-OHDA) on day 0 and then treatment was continued for 14 day of L-DOPA/carbidopa, whereas G-CSF (70 μg/kg, s.c.) was given from day 1 to 6. Thereafter, adhesive removal and forced swim tests were conducted to evaluate the behavioral outcome of G-CSF treatment. The finding was correlated and analyzed with Nissl staining findings for the final conclusion. Results: The behavioral parameters were assessed and found to be ameliorate the symptoms of Parkinson′s and reduced the depression like behavior in PD. The histological findings were supported the behavioral findings and showed pathological improvement. Conclusion: As a preliminary work, the present study first time suggested that G-CSF have a potential role in PD and associated depression.


Kumar A.,University Institute of Pharmaceutical science | Rinwa P.,University Institute of Pharmaceutical science | Kaur G.,University Institute of Pharmaceutical science | MacHawal L.,University Institute of Pharmaceutical science
Journal of Pharmacy and Bioallied Sciences | Year: 2013

Stress, both physical and psychological, is attracting increasing attention among neuroresearchers. In the last 20 decades, there has been a surge of interest in the research of stress-induced manifestations and this approach has resulted in the development of more appropriate animal models for stress-associated pathologies and its therapeutic management. These stress models are an easy and convenient method for inducing both psychological and physical stress. To understand the behavioral changes underlying major depression, molecular and cellular studies are required. Dysregulation of the stress system may lead to disturbances in growth and development, and may this may further lead to the development of various other psychiatric disorders. This article reviews the different types of stress and their neurobiology, including the different neurotransmitters affected. There are various complications associated with stress and their management through various pharmacological and non-pharmacological techniques. The use of herbs in the treatment of stress-related problems is practiced in both Indian and Western societies, and it has a vast market in terms of anti-stress medications and treatments. Non-pharmacological techniques such as meditation and yoga are nowadays becoming very popular as a stress-relieving therapy because of their greater effectiveness and no associated side effects. Therefore, this review highlights the changes under stress and stressor and their impact on different animal models in understanding the mechanisms of stress along with their effective and safe management.


Kumar P.,University Institute of Pharmaceutical science | Kalonia H.,University Institute of Pharmaceutical science | Kumar A.,University Institute of Pharmaceutical science
Basic and Clinical Pharmacology and Toxicology | Year: 2010

Sesamol (SML) (Sesamum indicum, Linn, Pedaliaceae) has been used traditionally as a health supplement in India and other countries for a long time. It is a well-known antioxidant, currently being tried against several neurological disorders. The present study was designed to evaluate the potential of sesamol treatment against 3-nitropropionic acid (3-NP)-induced cognitive impairment and oxidative damage in striatal, cortex and hippocampal regions of the rat. The memory performance was assessed by Morris water maze and elevated plus maze paradigms. The oxidative damage was assessed by estimating the total glutathione, reduced glutathione, oxidized glutathione levels and glutathione redox ratio. Glutathione-S-transferase and lactate dehydrogenase enzymes were also measured in different brain areas. 3-NP significantly impaired memory performance as assessed in Morris water maze and elevated plus maze, which was significantly attenuated by sesamol (5, 10 and 20 mg/kg) pre-treatment. On the other hand, 3-NP significantly induced oxidative stress and depleted total glutathione, reduced glutathione, glutathione-S-transferase, lactate dehydrogenase enzyme levels and redox ratio in the striatum, cortex and hippocampal regions as compared to the vehicle-treated group. Sesamol pre-treatment restored oxidative defence possibly by its free radical scavenging activity as compared to the 3NP-treated group. The present study suggests that sesamol could be used as an effective agent in the management of Huntington's disease. © 2010 Nordic Pharmacological Society.


Kumar A.,University Institute of Pharmaceutical science | Prakash A.,University Institute of Pharmaceutical science | Dogra S.,University Institute of Pharmaceutical science
Food and Chemical Toxicology | Year: 2010

Role of mitochondrial dysfunction and oxidative stress has been well documented in aging and related disorders such as Alzheimer's disease. Bioflavonoids have been reported to have a therapeutic potential against several age related processes. Bioflavonoids are being used as a neuroprotectants in the treatment of various neurological disorders including aging. Therefore, present study has been conducted in order to explore the possible role of naringin against d-galactose induced cognitive dysfunction, oxidative damage and mitochondrial dysfunction in mice. Chronic administration of d-galactose (100 mg/kg) for 6 weeks significantly impaired cognitive performance (both in Morris water maze and elevated plus maze), locomotor activity, oxidative defense and mitochondrial complex (I, II and III) enzymes activities as compared to sham group. Six weeks naringin (40 and 80 mg/kg) treatment significantly improved cognitive performance, oxidative defense and restored mitochondria complex enzyme activities as compared to control (d-galactose). Naringin treatment significantly attenuated acetylcholine esterase activity in d-galactose treated mice. In conclusion, present study highlights the potential role of naringin against d-galactose induced cognitive impairment, biochemical and mitochondrial dysfunction in mice. Crown Copyright © 2009.

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