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Neuropharmacological Potential of Gastrodia elata Blume and Its Components.

Jang JH, Son Y, Kang SS, Bae CS, Kim JC, Kim SH, Shin T, Moon C - Evid Based Complement Alternat Med (2015)

Bottom Line: Several neurodegenerative models are characterized by oxidative stress and inflammation in the brain, which lead to cell death via multiple extracellular and intracellular signaling pathways.The blockade of certain signaling cascades may represent a compensatory therapy for injured brain tissue.Specifically, GE rhizome extract and its components have been shown to protect neuronal cells and recover brain function in various preclinical brain injury models by inhibiting oxidative stress and inflammatory responses.

View Article: PubMed Central - PubMed

Affiliation: College of Veterinary Medicine and Animal Medical Institute, Chonnam National University, Gwangju 500-757, Republic of Korea ; Cheongju Hamsoa Oriental Clinic, Cheongju 361-814, Republic of Korea.

ABSTRACT
Research has been conducted in various fields in an attempt to develop new therapeutic agents for incurable neurodegenerative diseases. Gastrodia elata Blume (GE), a traditional herbal medicine, has been used in neurological disorders as an anticonvulsant, analgesic, and sedative medication. Several neurodegenerative models are characterized by oxidative stress and inflammation in the brain, which lead to cell death via multiple extracellular and intracellular signaling pathways. The blockade of certain signaling cascades may represent a compensatory therapy for injured brain tissue. Antioxidative and anti-inflammatory compounds isolated from natural resources have been investigated, as have various synthetic chemicals. Specifically, GE rhizome extract and its components have been shown to protect neuronal cells and recover brain function in various preclinical brain injury models by inhibiting oxidative stress and inflammatory responses. The present review discusses the neuroprotective potential of GE and its components and the related mechanisms; we also provide possible preventive and therapeutic strategies for neurodegenerative disorders using herbal resources.

No MeSH data available.


Related in: MedlinePlus

Schematic representation of the neuropharmacological effects of Gastrodia elata (GE). Multiple disease mechanisms, such as neurotransmitter imbalance, oxidative damage, and neuroinflammation, reportedly induce a variety of neurodegenerative disorders. GE has the potential to positively restore the neuronal cell damage in neurodegenerative diseases via the upregulation of inhibitory neurotransmitters and downregulation of oxidative stress and neuroinflammation. ASK-1: apoptosis signal-regulating kinase-1; CaMKII: Ca2+/calmodulin-dependent kinase II; COX-2: cyclooxygenase-2; GABA-T: gamma aminobutyric acid transaminase; GAD: glutamate decarboxylase; GE: Gastrodia elata; iNOS: inducible nitric oxide synthase; JNK: c-jun N-terminal kinases; MAPK: mitogen-activated protein kinase; NO: nitric oxide; SOD: superoxide dismutase; SSADH: succinic semialdehyde dehydrogenase.
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fig5: Schematic representation of the neuropharmacological effects of Gastrodia elata (GE). Multiple disease mechanisms, such as neurotransmitter imbalance, oxidative damage, and neuroinflammation, reportedly induce a variety of neurodegenerative disorders. GE has the potential to positively restore the neuronal cell damage in neurodegenerative diseases via the upregulation of inhibitory neurotransmitters and downregulation of oxidative stress and neuroinflammation. ASK-1: apoptosis signal-regulating kinase-1; CaMKII: Ca2+/calmodulin-dependent kinase II; COX-2: cyclooxygenase-2; GABA-T: gamma aminobutyric acid transaminase; GAD: glutamate decarboxylase; GE: Gastrodia elata; iNOS: inducible nitric oxide synthase; JNK: c-jun N-terminal kinases; MAPK: mitogen-activated protein kinase; NO: nitric oxide; SOD: superoxide dismutase; SSADH: succinic semialdehyde dehydrogenase.

Mentions: Many patients suffer from incurable neurodegenerative disorders, but there are few therapeutic drugs for treating these diseases. The pathological mechanisms involved in neurodegenerative diseases are mediated by neurotransmitter imbalance, oxidative stress, and neuroinflammation; however, treatment efficacy is not satisfactory. Herbal decoctions including GE rhizome have been used in oriental medicine in East Asia to treat a variety of diseases. To reveal the active components within such herbal decoctions, numerous studies have investigated cellular and molecular mechanisms using GE and its components. In this review, we summarized the protective effects of GE against neurodegenerative disorders and proposed the underlying mechanisms of the neuropharmacological potential of GE and its components. These mechanisms may be related to the correction of neurotransmitter imbalance and inhibition of oxidative response and neuroinflammation (Figure 5). In addition, we confirmed that administration of vanillin, an active component of GE, ameliorates TMT-induced seizures, which may be related to the reduced neuronal death and microglial activation. Therefore, this review encourages the identification of specific GE components for use in possible preventive or therapeutic strategies for various neurodegenerative disorders and may also be helpful for the development of new treatments for incurable disorders.


Neuropharmacological Potential of Gastrodia elata Blume and Its Components.

Jang JH, Son Y, Kang SS, Bae CS, Kim JC, Kim SH, Shin T, Moon C - Evid Based Complement Alternat Med (2015)

Schematic representation of the neuropharmacological effects of Gastrodia elata (GE). Multiple disease mechanisms, such as neurotransmitter imbalance, oxidative damage, and neuroinflammation, reportedly induce a variety of neurodegenerative disorders. GE has the potential to positively restore the neuronal cell damage in neurodegenerative diseases via the upregulation of inhibitory neurotransmitters and downregulation of oxidative stress and neuroinflammation. ASK-1: apoptosis signal-regulating kinase-1; CaMKII: Ca2+/calmodulin-dependent kinase II; COX-2: cyclooxygenase-2; GABA-T: gamma aminobutyric acid transaminase; GAD: glutamate decarboxylase; GE: Gastrodia elata; iNOS: inducible nitric oxide synthase; JNK: c-jun N-terminal kinases; MAPK: mitogen-activated protein kinase; NO: nitric oxide; SOD: superoxide dismutase; SSADH: succinic semialdehyde dehydrogenase.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4620291&req=5

fig5: Schematic representation of the neuropharmacological effects of Gastrodia elata (GE). Multiple disease mechanisms, such as neurotransmitter imbalance, oxidative damage, and neuroinflammation, reportedly induce a variety of neurodegenerative disorders. GE has the potential to positively restore the neuronal cell damage in neurodegenerative diseases via the upregulation of inhibitory neurotransmitters and downregulation of oxidative stress and neuroinflammation. ASK-1: apoptosis signal-regulating kinase-1; CaMKII: Ca2+/calmodulin-dependent kinase II; COX-2: cyclooxygenase-2; GABA-T: gamma aminobutyric acid transaminase; GAD: glutamate decarboxylase; GE: Gastrodia elata; iNOS: inducible nitric oxide synthase; JNK: c-jun N-terminal kinases; MAPK: mitogen-activated protein kinase; NO: nitric oxide; SOD: superoxide dismutase; SSADH: succinic semialdehyde dehydrogenase.
Mentions: Many patients suffer from incurable neurodegenerative disorders, but there are few therapeutic drugs for treating these diseases. The pathological mechanisms involved in neurodegenerative diseases are mediated by neurotransmitter imbalance, oxidative stress, and neuroinflammation; however, treatment efficacy is not satisfactory. Herbal decoctions including GE rhizome have been used in oriental medicine in East Asia to treat a variety of diseases. To reveal the active components within such herbal decoctions, numerous studies have investigated cellular and molecular mechanisms using GE and its components. In this review, we summarized the protective effects of GE against neurodegenerative disorders and proposed the underlying mechanisms of the neuropharmacological potential of GE and its components. These mechanisms may be related to the correction of neurotransmitter imbalance and inhibition of oxidative response and neuroinflammation (Figure 5). In addition, we confirmed that administration of vanillin, an active component of GE, ameliorates TMT-induced seizures, which may be related to the reduced neuronal death and microglial activation. Therefore, this review encourages the identification of specific GE components for use in possible preventive or therapeutic strategies for various neurodegenerative disorders and may also be helpful for the development of new treatments for incurable disorders.

Bottom Line: Several neurodegenerative models are characterized by oxidative stress and inflammation in the brain, which lead to cell death via multiple extracellular and intracellular signaling pathways.The blockade of certain signaling cascades may represent a compensatory therapy for injured brain tissue.Specifically, GE rhizome extract and its components have been shown to protect neuronal cells and recover brain function in various preclinical brain injury models by inhibiting oxidative stress and inflammatory responses.

View Article: PubMed Central - PubMed

Affiliation: College of Veterinary Medicine and Animal Medical Institute, Chonnam National University, Gwangju 500-757, Republic of Korea ; Cheongju Hamsoa Oriental Clinic, Cheongju 361-814, Republic of Korea.

ABSTRACT
Research has been conducted in various fields in an attempt to develop new therapeutic agents for incurable neurodegenerative diseases. Gastrodia elata Blume (GE), a traditional herbal medicine, has been used in neurological disorders as an anticonvulsant, analgesic, and sedative medication. Several neurodegenerative models are characterized by oxidative stress and inflammation in the brain, which lead to cell death via multiple extracellular and intracellular signaling pathways. The blockade of certain signaling cascades may represent a compensatory therapy for injured brain tissue. Antioxidative and anti-inflammatory compounds isolated from natural resources have been investigated, as have various synthetic chemicals. Specifically, GE rhizome extract and its components have been shown to protect neuronal cells and recover brain function in various preclinical brain injury models by inhibiting oxidative stress and inflammatory responses. The present review discusses the neuroprotective potential of GE and its components and the related mechanisms; we also provide possible preventive and therapeutic strategies for neurodegenerative disorders using herbal resources.

No MeSH data available.


Related in: MedlinePlus