Antioxidant Activities of <i>Dracocephalum tanguticum</i> Maxim Extract and Its Up-Regulation on the Expression of Neurotrophic Factors in a Rat Model of Permanent Focal Cerebral Ischemia

Xu, Jianrong; Mi, Yang; Deng, Kejun; Zhou, Hong

doi:10.1142/s0192415x11008658

Cited by 13 publications

(8 citation statements)

References 38 publications

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“…In addition, there is consistent report that a catechol group is related to antioxidant capacity (Cai et al, 2006). There are some reports showing antioxidant effects via antioxidant enzymes (Chiang et al, 2006; Sahin et al, 2010; Xu et al, 2011). In our previous report, baicalein induced Mn SOD via the activation of Nrf2 transcription factor; this resulted in the protection of mitochondria against oxidative stress (Lee et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Baicalein inhibits oxidative stress-induced cellular damage via antioxidant effects

et al. 2011

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Baicalein (5,6,7-trihydroxyflavone) is a phenolic flavonoid compound derived mainly from the root of Scutellaria baicalensis Georgi, a medicinal plant traditionally used in oriental medicine. In our previous study, baicalein attenuated mitochondrial oxidative stress by scavenging reactive oxygen species (ROS) and by induction of nuclear factor erythroid 2-related factor 2 transcription factor-mediated manganese superoxide dismutase. In the present study, the protective effects of baicalein against oxidative stress-induced damage, especially cellular components including DNA, lipid, and protein, were studied. The results of this study showed that baicalein scavenged intracellular ROS. Baicalein inhibited the H₂O₂-induced DNA damage that was demonstrated by decreased phospho-H2A.X expression and DNA tail formation. In addition, it prevented the lipid peroxidation shown by the fluorescence intensity of diphenyl-1-pyrenylphosphine and the formation of thiobarbituric acid reactive substances. Moreover, baicalein inhibited protein oxidation demonstrated by protein carbonyl formation. Furthermore, baicalein protected cells via the inhibition of apoptosis induced by H₂O₂. The findings of this study suggest that baicalein provides protection for cellular components against oxidative damage via scavenging ROS and inhibiting apoptosis.

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Section: Discussionmentioning

confidence: 99%

Baicalein inhibits oxidative stress-induced cellular damage via antioxidant effects

et al. 2011

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“…In this regard, animal studies have demonstrated neuroprotective effects of: (1) infusion of BDNF into the brain (Beck et al, 1994; Novikova et al, 2000; Nomura et al, 2005); (2) viral vector-mediated delivery of the BDNF gene into neurons (Bemelmans et al, 2006; Nosheny et al, 2007; Nagahara et al, 2009); (3) transplantation of cells genetically engineered to overexpress BDNF (Frim et al, 1994; Liu et al, 1999; Nomura et al, 2005); (4) administration of chemicals that stimulate neurons to produce BDNF (Hou et al, 2010; Xu et al, 2011; Fass et al, 2012); and (5) treatment with chemicals that activate trkB (Lee and Chao, 2001; Massa et al, 2010; Devi and Ohno, 2012; Schmid et al, 2012). Drugs in one class of widely prescribed anti-depressants, the serotonin- and norepinephrine reuptake inhibitors, are believed to exert their clinical benefit by up-regulating BDNF production (Xu et al, 2003, 2006; De Foubert et al, 2004; Russo-Neustadt et al, 2004; Yoshimura et al, 2007).…”

Section: Potential Therapeutic Interventions To Sustain Restore and mentioning

confidence: 99%

Activity-dependent, stress-responsive BDNF signaling and the quest for optimal brain health and resilience throughout the lifespan

2013

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During development of the nervous system, the formation of connections (synapses) between neurons is dependent upon electrical activity in those neurons, and neurotrophic factors produced by target cells play a pivotal role in such activity-dependent sculpting of the neural networks. A similar interplay between neurotransmitter and neurotrophic factor signaling pathways mediates adaptive responses of neural networks to environmental demands in adult mammals, with the excitatory neurotransmitter glutamate and brain-derived neurotrophic factor (BDNF) being particularly prominent regulators of synaptic plasticity throughout the central nervous system. Optimal brain health throughout the lifespan is promoted by intermittent challenges such as exercise, cognitive stimulation and dietary energy restriction, that subject neurons to activity-related metabolic stress. At the molecular level, such challenges to neurons result in the production of proteins involved in neurogenesis, learning and memory and neuronal survival; examples include proteins that regulate mitochondrial biogenesis, protein quality control, and resistance of cells to oxidative, metabolic and proteotoxic stress. BDNF signaling mediates up-regulation of several such proteins including the protein chaperone GRP-78, antioxidant enzymes, the cell survival protein Bcl-2, and the DNA repair enzyme APE1. Insufficient exposure to such challenges, genetic factors may conspire to impair BDNF production and/or signaling resulting in the vulnerability of the brain to injury and neurodegenerative disorders including Alzheimer’s, Parkinson’s and Huntington’s diseases. Further, BDNF signaling is negatively regulated by glucocorticoids. Glucocorticoids impair synaptic plasticity in the brain by negatively regulating spine density, neurogenesis and long-term potentiation, effects that are potentially linked to glucocorticoid regulation of BDNF. Findings suggest that BDNF signaling in specific brain regions mediates some of the beneficial effects of exercise and energy restriction on peripheral energy metabolism and the cardiovascular system. Collectively, the findings described in this article suggest the possibility of developing prescriptions for optimal brain health based on activity-dependent BDNF signaling.

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“…It has been shown that developmental exposure to toluene,(Win-Shwe et al ., 2010) lead,(Chao et al ., 2007) and infectious agents (Pang et al ., 2010) increased biomarkers of oxidative stress and neuroinflammation that were associated with decreased expression of neurotrophins in regions of the brain including the hippocampus. Along this line, NGF has been shown to upregulate glutathione synthesis in mice,(Arsenijevic et al ., 2007) and antioxidant therapy increased the expression of BDNF in hippocampus (Xu et al ., 2011; Moriya et al ., 2011; Liu et al ., 2009). In disorders of the CNS such as autism, oxidative stress appears inextricably linked to the loss of neurotrophic support (Sajdel-Sulkowska et al ., 2009; Sajdel-Sulkowska et al ., 2011a).…”

Section: Introductionmentioning

confidence: 99%

Postnatal exposure to trichloroethylene alters glutathione redox homeostasis, methylation potential, and neurotrophin expression in the mouse hippocampus

et al. 2012

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Previous studies have shown that continuous exposure throughout gestation until the juvenile period to environmentally-relevant doses of trichloroethylene (TCE) in the drinking water of MRL+/+ mice promoted adverse behavior associated with glutathione depletion in the cerebellum indicating increased sensitivity to oxidative stress. The purpose of this study was to extend our findings and further characterize the impact of TCE exposure on redox homeostasis and biomarkers of oxidative stress in the hippocampus, a brain region prone to oxidative stress. Instead of a continuous exposure, the mice were exposed to water only or two environmentally relevant doses of TCE in the drinking water postnatally from birth until 6 weeks of age. Biomarkers of plasma metabolites in the transsulfuration pathway and the transmethylation pathway of the methionine cycle were also examined. Gene expression of neurotrophins was examined to investigate a possible relationship between oxidative stress, redox imbalance and neurotrophic factor expression with TCE exposure. Our results show that hippocampi isolated from male mice exposed to TCE showed altered glutathione redox homeostasis indicating a more oxidized state. Also observed was a significant, dose dependent increase in glutathione precursors. Plasma from the TCE treated mice showed alterations in metabolites in the transsulfuration and transmethylation pathways indicating redox imbalance and altered methylation capacity. 3-Nitrotyrosine, a biomarker of protein oxidative stress, was also significantly higher in plasma and hippocampus of TCE-exposed mice compared to controls. In contrast, expression of key neurotrophic factors in the hippocampus (BDNF, NGF, and NT-3) was significantly reduced compared to controls. Our results demonstrate that low-level postnatal and early life TCE exposure modulates neurotrophin gene expression in the mouse hippocampus and may provide a mechanism for TCE-mediated neurotoxicity.

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Antioxidant Activities of Dracocephalum tanguticum Maxim Extract and Its Up-Regulation on the Expression of Neurotrophic Factors in a Rat Model of Permanent Focal Cerebral Ischemia

Cited by 13 publications

References 38 publications

Baicalein inhibits oxidative stress-induced cellular damage via antioxidant effects

Baicalein inhibits oxidative stress-induced cellular damage via antioxidant effects

Activity-dependent, stress-responsive BDNF signaling and the quest for optimal brain health and resilience throughout the lifespan

Postnatal exposure to trichloroethylene alters glutathione redox homeostasis, methylation potential, and neurotrophin expression in the mouse hippocampus

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