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      The Effects of Baicalin and Baicalein on Cerebral Ischemia: A Review

      review-article
      , , *
      Aging and Disease
      JKL International LLC
      baicalin, baicalein, cerebral ischemia, neuronal protection

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          Abstract

          Ischemic stroke, producing a high mortality and morbidity rate, is a common clinical disease. Enhancing the prevention and control of ischemic stroke is particularly important. Baicalin and its aglycon baicalein are flavonoids extracted from Scutellaria baicalensis, an important traditional Chinese herb. In recent years, a growing body of evidences has shown that baicalin and baicalein could be effective in the treatment of cerebral ischemia. Pharmacokinetic studies have shown that baicalin could penetrate the blood-brain barrier and distribute in cerebral nuclei. Through a variety of in vitro and in vivo models of ischemic neuronal injury, numerous studies have demonstrated that baicalin and baicalein have salutary effect for neuroprotection. Especially, the studies on the pharmacological mechanism showed that baicalin and baicalein have several pharmacological activities, which include antioxidant, anti-apoptotic, anti-inflammatory and anti-excitotoxicity effects, protection of the mitochondria, promoting neuronal protective factors expression and adult neurogenesis effects and many more. This review focuses on the neuroprotective effects of baicalin and baicalein in ischemia or stroke-induced neuronal cell death. We aimed at collecting all important information regarding the neuroprotective effect and its pharmacological mechanism of baicalin and baicalein in various in vivo and in vitro experimental models of ischemic neuronal injury.

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          Glycogen synthase kinase-3 (GSK3) is implicated in the regulation of several physiological processes, including the control of glycogen and protein synthesis by insulin, modulation of the transcription factors AP-1 and CREB, the specification of cell fate in Drosophila and dorsoventral patterning in Xenopus embryos. GSK3 is inhibited by serine phosphorylation in response to insulin or growth factors and in vitro by either MAP kinase-activated protein (MAPKAP) kinase-1 (also known as p90rsk) or p70 ribosomal S6 kinase (p70S6k). Here we show, however, that agents which prevent the activation of both MAPKAP kinase-1 and p70S6k by insulin in vivo do not block the phosphorylation and inhibition of GSK3. Another insulin-stimulated protein kinase inactivates GSK3 under these conditions, and we demonstrate that it is the product of the proto-oncogene protein kinase B (PKB, also known as Akt/RAC). Like the inhibition of GSK3 (refs 10, 14), the activation of PKB is prevented by inhibitors of phosphatidylinositol (PI) 3-kinase.
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            Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis.

            Apoptosis plays an important role during neuronal development, and defects in apoptosis may underlie various neurodegenerative disorders. To characterize molecular mechanisms that regulate neuronal apoptosis, the contributions to cell death of mitogen-activated protein (MAP) kinase family members, including ERK (extracellular signal-regulated kinase), JNK (c-JUN NH2-terminal protein kinase), and p38, were examined after withdrawal of nerve growth factor (NGF) from rat PC-12 pheochromocytoma cells. NGF withdrawal led to sustained activation of the JNK and p38 enzymes and inhibition of ERKs. The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells. Therefore, the dynamic balance between growth factor-activated ERK and stress-activated JNK-p38 pathways may be important in determining whether a cell survives or undergoes apoptosis.
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              Peroxynitrite--the product of the diffusion-controlled reaction of nitric oxide with superoxide radical--is a short-lived oxidant species that is a potent inducer of cell death. Conditions in which the reaction products of peroxynitrite have been detected and in which pharmacological inhibition of its formation or its decomposition have been shown to be of benefit include vascular diseases, ischaemia-reperfusion injury, circulatory shock, inflammation, pain and neurodegeneration. In this Review, we first discuss the biochemistry and pathophysiology of peroxynitrite and then focus on pharmacological strategies to attenuate the toxic effects of peroxynitrite. These include its catalytic reduction to nitrite and its isomerization to nitrate by metalloporphyrins, which have led to potential candidates for drug development for cardiovascular, inflammatory and neurodegenerative diseases.
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                Author and article information

                Contributors
                Journal
                Aging Dis
                Aging Dis
                Aging and Disease
                JKL International LLC
                2152-5250
                December 2017
                1 December 2017
                : 8
                : 6
                : 850-867
                Affiliations
                [1-ad-8-6-850]Department of Traditional Chinese Medicine, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China
                [2-ad-8-6-850]Department of Traditional Chinese Medicine, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China
                [3-ad-8-6-850]Department of Traditional Chinese Medicine, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China #These authors equally contributed to this work.
                Author notes
                [* ]Correspondence should be addressed to: Dr. Wenqiang Chen, Department of Traditional Chinese Medicine, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Beijing, 100053, China. E-mail: wenqiang_chen@ 123456msn.com
                [#]

                These authors equally contributed to this work

                Article
                ad-8-6-850
                10.14336/AD.2017.0829
                5758355
                29344420
                04406fc3-f3ed-463b-8071-e3577062b1ac
                Copyright: © 2017 Liang et al.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

                History
                : 5 February 2017
                : 29 July 2017
                : 29 August 2017
                Categories
                Review

                baicalin,baicalein,cerebral ischemia,neuronal protection

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