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Muthuraman A.,Akal Toxicology Research Center | Kaur P.,Akal Toxicology Research Center
Current Drug Targets | Year: 2016

Renin-Angiotensin-Aldosterone System (RAAS) is well established in renovascular and cardiovascular functions. The modulators of this system are significantly used for regulating elevated blood pressure in human and animals. Recently, it has also been documented to produce neurological actions. The abnormalities of this system raise renin, angiotensin (AT), angiotensin converting enzyme (ACE) activity, and aldosterone in circulation and nerve tissues. In the nervous system, abundant rise of these components cause neuronal damage and neurodegeneration. ACE contributes to degradation of β-amyloid in the brain, that is responsible for Alzheimer disease (AD). But, angiotensin converting enzyme-2 (ACE-2) mediated release of angiotensin1-7 (AT1-7) peptide in nerve tissue has potential neuroprotective actions. This review focuses on the current perspectives of the RAAS in neurodegeneration along with possible cellular and molecular mechanisms. Also, we have discussed the current evidence of RAAS modulators in the management of neuropathic pain in human and animals. Thus, we believe that, in the future, RAAS modulators may play a great role in the management of neuropathic pain and other neurodegenerative disorders such as AD, Parkinson disease (PD) and amyotrophic lateral sclerosis. But, more extensive clinical research is required for utilizing RAAS modulators in neurode-generative disorders. © 2016 Bentham Science Publishers. Source

Muthuraman A.,Akal Toxicology Research Center | Kaur P.,Akal Toxicology Research Center | Singh H.,Akal Toxicology Research Center | Boparai P.S.,Akal Toxicology Research Center
Life Sciences | Year: 2015

Aims The present study has been designed to investigate the ameliorative potential of vitamin P, and digoxin in ischemic-reperfusion (I/R)-induced renal injury in isolated rat kidney preparations by using the Langendorff apparatus. Main methods Vitamin P (50 and 100 mg/kg; p.o.) was administered to rats for 5 consecutive days. On the 6th day, isolated kidneys were subjected to 30 min of ischemia followed by 120 min of reperfusion by constant flow (8 ml/min). The total renal effluent was collected at various time intervals (i.e., basal, 0, 15, 30, 45 and 60 min). In addition, urea, creatinine, and creatine kinase (CK) activity were evaluated in the renal effluent, and TBARS, GSH, and Na+-K+-ATPase activity were evaluated in tissue. Key findings I/R of renal tissue produced a rise in the activity of CK and the levels of urea and creatinine in the renal effluent, as well as in the activity of Na+-K+-ATPase and levels of TBARS in the tissue. Additionally, it decreased GSH levels when compared with the sham control group. Digoxin served as positive control in the present work. Treatment with vitamin P (100 mg/kg), and digoxin (500 μg/kg) produced a significant (P < 0.05) ameliorative effect against the I/R induced changes in biomarkers. Significance The renoprotective effect of vitamin P is caused by its inhibition of Na+-K+-ATPase activity, which subsequently results in free radical scavenging and anti-infarct properties. Therefore, this vitamin can be useful in the management of renovascular disorders. © 2015 Elsevier Inc. All rights reserved. Source

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