@article {745, title = {The study of aqueous extract of Ficus religiosa Linn. on cytokine TNF-α in type 2 diabetic rats}, journal = {Pharmacognosy Research}, volume = {3}, year = {2011}, month = {April 2011}, pages = {30-34}, type = {Original Article}, chapter = {30}, abstract = {

Background:\ Chronic systemic inflammation is an early process in pathogenesis of type 2 diabetes. Hence the present study was aimed to investigate the effect of traditionally known plant\ Ficus religiosa\ on elevated glucose and inflammatory marker namely tumor necrosis factor (TNF)-α in type 2 diabetic rats.\ Methods:\ Type 2 diabetes was induced by administering streptozotocin (90 mg/kg, i.p.) in neonatal rat model. Aqueous extract of\ F. religiosa\ at a dose of 100 and 200 mg/kg was given orally to desired group of animals for a period of 4 weeks. After 4 weeks of drug treatment, parameters such as fasting blood glucose, postprandial blood glucose and TNF-α in serum were analyzed.\ Results:\ Aqueous extract of\ F. religiosa\ at both dose levels i.e., 100 and 200 mg/kg decreased the elevated glucose and TNF-α in type 2 diabetic rats. The extract at 200 mg/kg had more pronounced effect.\ Conclusion:\ Modulation of cytokine TNF-α by the aqueous extract of\ F. religiosa\ indicates that the anti-inflammatory and immunomodulatory property of the plant is related with its potential anti-diabetic activity.

}, keywords = {Ficus religiosa, Inflammation, TNF-α, type 2 diabetes}, doi = {10.4103/0974-8490.79112}, author = {H Kirana and MV Jali and BP Srinivasan} } @article {754, title = {Dipeptidyl Peptidase-IV (DPP-IV) Inhibitory Activity of Parotid Exudate of Bufo melanostictus}, journal = {Pharmacognosy Research}, volume = {1}, year = {2009}, month = {January 2010 }, pages = {98-101}, type = {Original Article}, chapter = {98}, abstract = {

Type 2 diabetes arises as a result of -cell failure combined with concomitant insulin resistance. Glucagon-like peptide-1 is a gastrointestinal hormone that is released postprandially from the L cells of the gut and exerts a glucose- dependent and direct insulinotropic effect on the pancreatic  cell. Which activate adenylate cyclase and enhances insulin secretion. GLP-1 is rapidly degraded by DPP-IV to GLP-1(9-37) amide following release from gut L cells. GLP-1 directly enhances glucose-dependent insulin secretion via an increase in -cell cAMP. Dipeptidyl peptidase IV (DPP-IV) is a plasma membrane glycoprotein ectopeptidase. In mammals, DPP-IV was widely expressed on the surface of endothelial and epithelial cells and highest levels in humans have been reported to occur in the intestine, bone marrow and kidney. Inhibiting DPP-IV reduces its rapid degradation of GLP-1, increasing circulating levels of the active hormone in vivo and prolonging its beneficial effects. The IC50 value of parotid exudate was found to be 9.4 2g/ml. The maximum \% inhibition (61.8) was showed at a concentration of 122g/ml. Parotid exudate through inhibition of DPP-IV, improves glucose tolerance and enhances insulin secretion. DPP-IV inhibitors are a novel class of oral hypoglycemic agents with a potential to improve pancreatic beta cell function and the clinical course of type 2 diabetes.

}, keywords = {DPP-IV, GLP-1, Parotid exudate, type 2 diabetes}, doi = {Nil}, author = {Allenki Venkatesham and Neerati Prasad and Devarakonda R Krishna and Yellu Narsimha Reddy} }