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ABSTRACTS
Year : 2014  |  Volume : 46  |  Issue : 7  |  Page : 6-7
 

Prof. Manjeet Singh Prize



Date of Web Publication26-Dec-2014

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Source of Support: None, Conflict of Interest: None


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How to cite this article:
. Prof. Manjeet Singh Prize. Indian J Pharmacol 2014;46, Suppl S1:6-7

How to cite this URL:
. Prof. Manjeet Singh Prize. Indian J Pharmacol [serial online] 2014 [cited 2020 Sep 28];46, Suppl S1:6-7. Available from: http://www.ijp-online.com/text.asp?2014/46/7/6/147657


PZM-1

Carnosic acid Inhibits Osteoclastogenesis by Up-Regulating the Nrf2 and Suppressing the NF-KB and MAPK Signaling


V.G.M.Naidu 1 *, Dinesh Thummuri 1 , Harishankar Nemani 2

1 Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Balanagar, Hyderabad, Andhra Pradesh, India, 2 National Centre for Laboratory Animal Sciences, National Institute of Nutrition, Habsiguda, Hyderabad, Andhra Pradesh, India

Objective: To investigate the effect of carnosic acid (CA) on receptor activator of NF-KB ligand (RANKL), cancer induced osteoclastogenesis and LPS induced bone resorption model in C57BL/6J mice. Materials and Methods: RANKL and cancer induced osteoclastogenesis was performed in RAW 264.7 (macrophage) cells by treating with RANKL (100ng/ml) for 5 days or by co-culture with breast (MDA-MB 231) or multiple myeloma (U266) cancer cells. In vivo osteolysis was developed in C57BL/6J mice by injecting (i.p route) LPS (5 μg/g body weight) on day 1 and day 4. CA was orally administered at a dose of 25 mg/kg and 50 mg/kg, one day prior to the injection of LPS and continued for 8 days. The effect of CA on LPS induced bone resorption was determined by DXA analysis by measuring the bone mineral content (BMC) and bone mineral density (BMD). Results: CA significantly inhibited RANKL and cancer induced osteoclastogenesis in dose dependent manner without causing toxicity to the macrophages. Mechanistically CA blocked the RANKL triggered phosphorylation of mitogen activated protein kinases (MAPKs), Phophorylation and nuclear translocation of NF-KB. Pretreatment of CA inhibited the RANKL induced osteoclast specific gene expression of TRAP, NFATc1, c-FOS, DC-STAMP. Consistent with in-vitro results, the DXA analysis in mice have shown that administration of CA prevents the LPS induced bone loss. Conclusion: Taken together, our results demonstrated that CA suppresses RANKL and cancer induced osteoclastogenesis via NF-KB, MAPK and Nrf2 signaling pathways. Therefore CA may be considered as a novel therapeutic strategy against bone lytic diseases. Key words: Carnosic acid, Osteoclastogenesis, RANKL, NF-KB.

PZM-2

Mechanism based efficacy study of standardized extract of Centella asiatica (L.) Urban leaves on testosterone induced benign prostatic hyperplasia in male Wistar rats


Urmila Aswar*,Umesh Mahajan 1 , Geetanjali Nerurkar 1 , Manoj Aswar 1 , Amit Kandhare 1 , V. Mohan 2 , Prasad Thakurdesai 3

1 Department of Pharmacology, Sinhgad Institute of Pharmacy, Narhe, Pune, India, 2 Poona College of Pharmacy, Bharati Vidyapeeth Deemed University, Pune, India, 3 Indus Biotech Private Limited, 1, Rahul Residency, off Salunke Vihar Road, Kondhwa, Pune, India

Objective: The present study aimed to understand the molecular mechanism of standardized extract of Centella asiatica (L.) Urban leaves (INDCA) on testosterone induced benign prostatic hyperplasia (BPH) in male Wistar rats. Materials and Methods: BPH was developed in male Wistar rat by administration of testosterone (3 mg/kg, s.c.) in olive oil for 4 weeks. The effects of INDCA (15, 30 or 60 mg/kg, p.o.) for four weeks alone and in combination with finasteride (10 mg/kg, p.o.) followed by testosterone administration were studied. Normal group received only vehicle. At the end of treatment animals were sacrificed, prostate tissues were removed, weighed. The molecular (mRNA expression parameters) and histology parameters in prostate tissues and PSA levels in serum were measured. Result: Twenty-eight days administration of testosterone in rats induced BPH (elevated serum PSA levels). Subacute (28 days) administration of INDCA (30 and 60 mg/kg) treatment significantly reduced serum PSA levels. The expression of PSA, FXR, RAS, PGC 1α, smad7, EGF, IGF 1, TGF α, bFGF, NF-kB, PCNA and PTEN in INDCA treated rats were significantly reversed as compared to BPH control rats. The ameliorating properties of INDCA against experimental BPH is supported by histopathology of prostate tissues. Conclusion: The therapeutic effect of INDCA against BPH related parameters are mediated through regulating the expression of PSA, FXR, RAS, PGC 1α, smad7, EGF, IGF 1, TGF α, bFGF, NF-kB, PCNA and PTEN in prostate tissues.

PZM-3

Lithium chloride, a GSKβ inhibitor attenuates insulin resistance induced cognitive impairment in mice


Rajeev Taliyan*, Sorabh Sharma

Department of Pharmacy Birla Institute of Technology and Science, Pilani, Rajasthan, India

Objective: To evaluate the effect of Lithium chloride, a GSK3β inhibitor in insulin resistance induced cognitive impairment in mice. Materials and Methods: Swiss albino mice (n=12) were subjected to high fat diet (HFD) for 8 weeks to induce insulin resistance like condition. Following HFD feeding, Lithium chloride (LiCl) was administered (60 mg/kg and 120 mg/kg i.p). once daily for one week. Behaviorally, morris water maze task was used to assess cognitive impairment in mice. Biochemically, levels of oxidative stress markers, anitioxidant enzymes, neuroinflammatory markers and acetylcholinesterase activity were measured in brain homogenates. Further, levels of brain insulin and brain derived neurotrophic factor (BDNF) were measured to explore the molecular mechanism involved in HFD induced neurodegenerative process. Results: After 8 weeks of diet feeding the mice exhibited characteristic features of insulin resistance viz. increased serum glucose, triglycerides, cholesterol and insulin levels. Moreover, these mice showed cognitive impairment and elevated oxidative stress markers along with elevated neuroinflammatory markers. The observed changes occurred concurrently with reduced brain derived neurotrophic factor. In contrast, the mice treated with lithium chloride (60 and 120 mg/ kg i.p.) showed dose dependent improvement in insulin resistance and associated cognitive decline. Moreover, LiCl dose dependently augment the brain insulin and BDNF levels in HFD fed mice. Conclusion: Based upon these findings it could be suggested that GSK3 β inhibition could prove to be beneficial in insulin resistance induced cognitive deficits.




 

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