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      Natural compounds from traditional medicinal herbs in the treatment of cerebral ischemia/reperfusion injury

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          Abstract

          More and more attention in the field of drug discovery has been focused on the neuroprotection of natural compounds from traditional medicinal herbs. Cerebral ischemia is a complex pathological process involving a series of mechanisms, and a framework for the development of neuroprotectants from traditional herb medicine is a promising treatment for cerebral ischemia. Natural compounds with the effects of anti-oxidation, anti-inflammation, calcium antagonization, anti-apoptosis, and neurofunctional regulation exhibit preventive or therapeutic effects on experimental ischemic brain injury. According to the pharmacological mechanisms underlying neuroprotection, we evaluated natural products from traditional medicinal herbs that exhibit protective effects on ischemic brain injury and characterized the promising targets.

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          Exercise and the brain: something to chew on.

          Henriette van Praag (2009)
          Evidence is accumulating that exercise has profound benefits for brain function. Physical activity improves learning and memory in humans and animals. Moreover, an active lifestyle might prevent or delay loss of cognitive function with aging or neurodegenerative disease. Recent research indicates that the effects of exercise on the brain can be enhanced by concurrent consumption of natural products such as omega fatty acids or plant polyphenols. The potential synergy between diet and exercise could involve common cellular pathways important for neurogenesis, cell survival, synaptic plasticity and vascular function. Optimal maintenance of brain health might depend on exercise and intake of natural products.
          Article 0 comments Cited 160 times – based on 0 reviews     Review now
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            Inflammatory mediators and stroke: new opportunities for novel therapeutics.

            Frank C. Barone, Giora Feuerstein (1999)
            Contrary to previous dogmas, it is now well established that brain cells can produce cytokines and chemokines, and can express adhesion molecules that enable an in situ inflammatory reaction. The accumulation of neutrophils early after brain injury is believed to contribute to the degree of brain tissue loss. Support for this hypothesis has been drawn from many studies where neutrophil-depletion blockade of endothelial-leukocyte interactions has been achieved by various techniques. The inflammation reaction is an attractive pharmacologic opportunity, considering its rapid initiation and progression over many hours after stroke and its contribution to evolution of tissue injury. While the expression of inflammatory cytokines that may contribute to ischemic injury has been repeatedly demonstrated, cytokines may also provide "neuroprotection" in certain conditions by promoting growth, repair, and ultimately, enhanced functional recovery. Significant additional basic work is required to understand the dynamic, complex, and time-dependent destructive and protective processes associated with inflammation mediators produced after brain injury. The realization that brain ischemia and trauma elicit robust inflammation in the brain provides fertile ground for discovery of novel therapeutic agents for stroke and neurotrauma. Inhibition of the mitogen-activated protein kinase (MAPK) cascade via cytokine suppressive anti-inflammatory drugs, which block p38 MAPK and hence the production of interleukin-1 and tumor necrosis factor-alpha, are most promising new opportunities. However, spatial and temporal considerations need to be exercised to elucidate the best opportunities for selective inhibitors for specific inflammatory mediators.
            Article 0 comments Cited 152 times – based on 0 reviews     Review now
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              NADPH oxidase is the primary source of superoxide induced by NMDA receptor activation.

              Norman Lee, A. J. Brennan, Jun S Suh … (2009)
              Neuronal NMDA receptor (NMDAR) activation leads to the formation of superoxide, which normally acts in cell signaling. With extensive NMDAR activation, the resulting superoxide production leads to neuronal death. It is widely held that NMDA-induced superoxide production originates from the mitochondria, but definitive evidence for this is lacking. We evaluated the role of the cytoplasmic enzyme NADPH oxidase in NMDA-induced superoxide production. Neurons in culture and in mouse hippocampus responded to NMDA with a rapid increase in superoxide production, followed by neuronal death. These events were blocked by the NADPH oxidase inhibitor apocynin and in neurons lacking the p47(phox) subunit, which is required for NADPH oxidase assembly. Superoxide production was also blocked by inhibiting the hexose monophosphate shunt, which regenerates the NADPH substrate, and by inhibiting protein kinase C zeta, which activates the NADPH oxidase complex. These findings identify NADPH oxidase as the primary source of NMDA-induced superoxide production.
              Article 0 comments Cited 152 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Acta Pharmacol Sin
                Journal ID (iso-abbrev): Acta Pharmacol. Sin
                Title: Acta Pharmacologica Sinica
                Publisher: Nature Publishing Group
                ISSN (Print): 1671-4083
                ISSN (Electronic): 1745-7254
                Publication date (Print): December 2010
                Publication date (Electronic): 03 December 2010
                Volume: 31
                Issue: 12
                Pages: 1523-1531
                Affiliations
                [1 ]Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology , Wuhan 430030, China
                [2 ]Key Laboratory of Neurological Diseases (HUST), Ministry of Education of China , Wuhan 430030, China
                [3 ]Institutes of Biomedicine and Drug Discovery, Huazhong University of Science and Technology , Wuhan 430030, China
                [4 ]Hubei Key Laboratory of Natural Drug Chemistry and Evaluation (HUST) , Wuhan 430030, China
                Author notes
                Article
                Publisher Item ID: aps2010186
                DOI: 10.1038/aps.2010.186
                PMC ID: 4002952
                PubMed ID: 21127495
                SO-VID: b8f13020-9cfe-4457-8393-d5223d862ca7
                Copyright © Copyright © 2010 CPS and SIMM
                History
                Date received : 13 July 2010
                Date accepted : 28 September 2010
                Categories
                Subject: Review

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: cerebral ischemia,natural compounds,traditional medicinal herb
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: cerebral ischemia, natural compounds, traditional medicinal herb

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