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Articles by Harlokesh Narayan Yadav
Total Records ( 3 ) for Harlokesh Narayan Yadav
  Harlokesh Narayan Yadav , Manjeet Singh , P.L. Sharma , Dhiraj Mittal , Tapan Behl and Atinder Pal Kaur
  Background: Recently it has been noted that Cyclooxygenase-2 (COX-2) is involved in early phase of ischemic preconditioning (IPC) induced cardioprotection. The present study was designed to investigate the role of COX-2 in the cardioprotective effect of remote aortic preconditioning (RAPC) in rat. RAPC was given by 4 times of 5’ occlusion of abdominal aorta. Materials and Methods: Isolated perfused rat heart was subjected to global ischemia of 30 min., followed by reperfusion for 120 min. Coronary effluent was analyzed for LDH and CK release to access the degree of cardiac injury. Myocardial infarct size was estimated macroscopically using TTC staining. Results: RAPC produced a significant decrease in LDH and CK release and decrease in the myocardial infarct size, as compared to ischemia/reperfusion (I/R) control group. Pretreatment with celecoxib, a selective COX-2 inhibitor and glibenclamide, a blocker of KATP channels, given separately significantly attenuated the RAPC-induced cardioprotection. The cardioprotective effect of celecoxib and glibenclamide, administered in combination was almost equal to the sum total of the effect produced by these drugs when administered singly. Conclusion: On the basis of these results it was concluded that the cardioprotective effect of RAPC may be mediated through upregulation of COX-2 and subsequent activation of KATP channels.
  Harlokesh Narayan Yadav , Vibhav Varshney , Niraj Kumar Singh and Pyare Lal Sharma
  Background and Objective: Glycogen synthase kinase (GSK-3β) play central role in Ischemic Pre Conditioning (IPC) mediated early as well as late effect of cardioprotection. The signaling pathway of IPC gets diminished during diabetes mellitus. The present study was designed to investigate the whether GSK-3β inhibitors, administered 24 h before the ischemia, would exert the cardioprotection in diabetic rat. Methods: Diabetes Mellitus (DM) was induced by single administration of streptozotocin (STZ) (50 mg kg-1, i.p.). Rat heart was isolated and mounted on Langendroff’s apparatus and subjected to 30 min of ischaemia followed by 120 min of reperfusion. Myocardial infarct size was estimated by triphenyltetrazolium chloride (TTC) staining, lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) were measured for the extent of myocardial damage. Results: Administration of GSK-3β inhibitors, SB 216763 (SB, 0.6 mg kg-1, i.p.) and indirubin-3 monooxime (IND, 0.4 mg kg-1, i.p.), 24 h before, not 12 h before the isolation of heart, significantly attenuated I/R-induced infarct size, release of LDH and CK-MB, as compared to vehicle treated group. However, this observed cardioprotection was significantly attenuated by administration of quercetin (4 mg kg-1, i.p) an inhibitor of heat shock protein 72 (HSP-72) 1h before the treatment of either drugs. Conclusion: Administration of GSK-3β inhibitors 24 h before the ischemic insult produces the cardioprotection in diabetic rat heart which may be mediated through HSP-72, since it was significantly attenuated by pretreatment with quercetin.
  Uma Shankar Sharma , Harlokesh Narayan Yadav , Vishwa Mohini Khare , Surender Singh , Yogendra Kumar Gupta and Amit K. Tiwari
  Background and Objective: Cisplatin is a potent anti-cancer agent, however, its usage is limited due to its nephrotoxicity. To prevent cisplatin induced kidney toxicity we used a combination of dietary plant extracts, particularly, hydro-alcoholic extract of Tribulus terrestris (TT), Boerhaavia diffusa (BD) and Terminalia chebula (TC) in rats. Materials and Methods: Animals (n = 6 per group) were randomly assigned into six groups: A normal control, cisplatin control, the drug-combination armat doses of 198, 300 and 600 mg kg1 of equal ratio of each of TT, BD and TC and the combination of 300 mg kg1 per se group. All treatments were given orally once a day for 10 days. Nephrotoxicity was induced by single dose of cisplatin 8 mg kg1, i.p on the 7th day. Blood urea nitrogen (BUN), serum creatinine, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) and glutathione peroxidase (GPx), renal histopathology, liver fatty acid binding protein (L-FAB), kidney injury molecule-1 (Kim-1) and platinum accumulation in kidney tissue were determined. Results: The pre-treatment of the combination of equal ratio of TT, BD and TC at 198, 300 and 600 mg kg1 significantly (p<0.05) attenuated the cisplatin-induced nephrotoxicity, as indicated by decrease in BUN, serum creatinine, MDA and an increase in the concentration of GSH, SOD and GPx whereas combination100 and 200 mg kg1 significantly decreases Kim and L-FABP and combination of 600 mg kg1 significantly decreases the platinum accumulation in treated groups as compare to cisplatin control group. Conclusion: Our results suggest that the combination of TT, BD and TC may be efficacious in attenuating cisplatin-induced nephrotoxicity by decreasing the renal level of platinum, reactive oxygen species (ROS) and oxidative stress.
 
 
 
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