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      The Pharmacological Potential of Rutin

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          Abstract

          The contemporary scientific community has presently recognized flavonoids to be a unique class of therapeutic molecules due to their diverse therapeutic properties. Of these, rutin, also known as vitamin P or rutoside, has been explored for a number of pharmacological effects. Tea leaves, apples, and many more possess rutin as one of the active constituents. Today, rutin has been observed for its nutraceutical effect. The present review highlights current information and health-promoting effects of rutin. Along with this, safety pharmacology issues and SAR of the same have also been discussed.

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          Reactive species mechanisms of cellular hypoxia-reoxygenation injury.

          Chuanyu Li, Robert M Jackson (2002)
          Exacerbation of hypoxic injury after restoration of oxygenation (reoxygenation) is an important mechanism of cellular injury in transplantation and in myocardial, hepatic, intestinal, cerebral, renal, and other ischemic syndromes. Cellular hypoxia and reoxygenation are two essential elements of ischemia-reperfusion injury. Activated neutrophils contribute to vascular reperfusion injury, yet posthypoxic cellular injury occurs in the absence of inflammatory cells through mechanisms involving reactive oxygen (ROS) or nitrogen species (RNS). Xanthine oxidase (XO) produces ROS in some reoxygenated cells, but other intracellular sources of ROS are abundant, and XO is not required for reoxygenation injury. Hypoxic or reoxygenated mitochondria may produce excess superoxide (O) and release H(2)O(2), a diffusible long-lived oxidant that can activate signaling pathways or react vicinally with proteins and lipid membranes. This review focuses on the specific roles of ROS and RNS in the cellular response to hypoxia and subsequent cytolytic injury during reoxygenation.
          Article 0 comments Cited 191 times – based on 0 reviews     Review now
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            Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis.

            Prabal Deb, Suash Sharma, K.M. Hassan (2010)
            Stroke is a serious neurological disease, and constitutes a major cause of death and disability throughout the world. The pathophysiology of stroke is complex, and involves excitotoxicity mechanisms, inflammatory pathways, oxidative damage, ionic imbalances, apoptosis, angiogenesis and neuroprotection. The ultimate result of ischemic cascade initiated by acute stroke is neuronal death along with an irreversible loss of neuronal function. Therapeutic strategies in stroke have been developed with two main aims: restoration of cerebral flow and the minimization of the deleterious effects of ischemia on neurons. Intense research spanning over the last two decades has witnessed significant therapeutic advances in the form of carotid endarterectomy, thrombolytics, anticoagulant therapy, antiplatelet agents, neuroprotective agents, and treating associated risk factors such as hypertension and hyperlipidemia. However, the search for an effective neuroprotectant remains frustrating, and the current therapeutic protocols remain suboptimal. Till date only one FDA-approved drug is available for ischemic stroke; i.e., the serine protease tissue-type plasminogen activator (tPA), utility of which is limited by short therapeutic window. The objective of this review is to critically evaluate the major mechanisms underlying stroke pathophysiology, with emphasis on potential novel targets for designing newer therapeutic modalities. Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.
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              Parathyroid hormone and teriparatide for the treatment of osteoporosis: a review of the evidence and suggested guidelines for its use.

              D. Dempster, Larry Dian, Thomas A. Miller … (2005)
              All therapies currently recommended for the management of osteoporosis act mainly to inhibit bone resorption and reduce bone remodeling. PTH and its analog, teriparatide [recombinant human PTH(1-34)], represent a new class of anabolic therapies for the treatment of severe osteoporosis, having the potential to improve skeletal microarchitecture. Significant reductions in both vertebral and appendicular fracture rates have been demonstrated in the phase III trial of teriparatide, involving elderly women with at least one prevalent vertebral fracture before the onset of therapy. However, there is as yet no evidence that the antifracture efficacy of PTH will be superior to the bisphosphonates, whereas cost-utility estimates suggest that teriparatide is significantly more expensive. Teriparatide should be considered as treatment for postmenopausal women and men with severe osteoporosis, as well as for patients with established glucocorticoid-induced osteoporosis who require long-term steroid treatment. Teriparatide should also be considered for the management of individuals at particularly high risk for fractures, including subjects who are younger than age 65 and who have particularly low bone mineral density measurements (T scores < or = 3.5). Teriparatide therapy is not recommended for more than 2 yr, based, in part, on the induction of osteosarcoma in a rat model of carcinogenicity. Total daily calcium intake from both supplements and dietary sources should be limited to 1500 mg together with adequate vitamin D intake (< or =1000 U/d). Monitoring of serum calcium may be safely limited to measurement after 1 month of treatment; mild hypercalcemia may be treated by withdrawing dietary calcium supplements, reducing the dosing frequency of PTH, or both. At present, concurrent therapy with antiresorptive therapy, particularly bisphosphonates, should be avoided, although sequential therapy with such agents may consolidate the beneficial effects upon the skeleton after PTH is discontinued.
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                Author and article information

                Contributors
                Aditya Ganeshpurkar
                Journal
                Journal ID (nlm-ta): Saudi Pharm J
                Journal ID (iso-abbrev): Saudi Pharm J
                Title: Saudi Pharmaceutical Journal : SPJ
                Publisher: Elsevier
                ISSN (Print): 1319-0164
                ISSN (Electronic): 2213-7475
                Publication date PMC-release: 30 April 2016
                Publication date (Print): February 2017
                Publication date (Electronic): 30 April 2016
                Volume: 25
                Issue: 2
                Pages: 149-164
                Affiliations
                [a ]Faculty of Pharmacy, Gujarat Technological University, Ahmedabad, Gujarat, India
                [b ]Shri Ram Institute of Technology-Pharmacy, Jabalpur, Madhya Pradesh, India
                [c ]A.R. College of Pharmacy, Vallabh Vidyanagar, Gujarat, India
                Author notes
                [* ]Corresponding author at: A.R. College of Pharmacy, Vallabh Vidyanagar, Gujarat, India. Tel.: +91 2692 230788.A.R. College of PharmacyVallabh VidyanagarGujaratIndia adityaganeshpurkar@ 123456gmail.com
                Article
                Publisher ID: S1319-0164(16)30026-3
                DOI: 10.1016/j.jsps.2016.04.025
                PMC ID: 5355559
                PubMed ID: 28344465
                SO-VID: 0017e870-b595-4009-a382-3216c7c524d9
                Copyright © © 2016 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 26 March 2016
                Date accepted : 24 April 2016
                Categories
                Subject: Review

                Keywords: anticancer,antidiabetic,antimicrobial,organ protection,rutin
                Data availability:
                Keywords: anticancer, antidiabetic, antimicrobial, organ protection, rutin

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