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== Effects on ALS ==
 
== Effects on ALS ==
  
Potential HSP-70 inducer: ''Treatment of cells with paeoniflorin but not glycyrrhizin resulted in enhanced phosphorylation and acquisition of the deoxyribonucleic acid–binding ability of heat shock transcription factor 1 (HSF1), as well as the formation of characteristic HSF1 granules in the nucleus, suggesting that the induction of HSPs by paeoniflorin is mediated by the activation of HSF1.'' {{#pmid:15633296|yan2004}}
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Potential HSP-70 inducer: ''Treatment of cells with paeoniflorin but not glycyrrhizin resulted in enhanced phosphorylation and acquisition of the deoxyribonucleic acid–binding ability of heat shock transcription factor 1 (HSF1), as well as the formation of characteristic HSF1 granules in the nucleus, suggesting that the induction of HSPs by paeoniflorin is mediated by the activation of HSF1.'' [1]
  
''Furthermore, PF decreased the release of IL-1β, IL-6 and TNF-α as well as inhibited the mRNA expression of IL-1β, IL-6 and TNF-α in the hippocampus of VD rats (P<0.05 or P<0.01). PF also could decrease the protein expressions of inducible nitric oxide synthase and cyclooxygenase-2 in the hippocampus of VD rats (P<0.05 orP<0.01). In addition, PF significantly inhibited the nuclear factor κB (NF-κB) pathway in the hippocampus of VD rats.'' {{#pmid:26577108|yang2015}}
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''Furthermore, PF decreased the release of IL-1β, IL-6 and TNF-α as well as inhibited the mRNA expression of IL-1β, IL-6 and TNF-α in the hippocampus of VD rats (P<0.05 or P<0.01). PF also could decrease the protein expressions of inducible nitric oxide synthase and cyclooxygenase-2 in the hippocampus of VD rats (P<0.05 orP<0.01). In addition, PF significantly inhibited the nuclear factor κB (NF-κB) pathway in the hippocampus of VD rats.'' [2]
  
 
''Here, we have examined the efficacy of PF in the repression of inflammation-induced neurotoxicity and microglial inflammatory response. In organotypic hippocampal slice cultures, PF significantly blocked lipopolysaccharide (LPS)-induced hippocampal cell death and productions of nitric oxide (NO) and interleukin (IL)-1β. PF also inhibited the LPS-stimulated productions of NO, tumor necrosis factor-α, and IL-1β from primary microglial cells. These results suggest that PF possesses neuroprotective activity by reducing the production of proinflammatory factors from activated microglial cells.'' {{#pmid:23559368|nam2013}}
 
''Here, we have examined the efficacy of PF in the repression of inflammation-induced neurotoxicity and microglial inflammatory response. In organotypic hippocampal slice cultures, PF significantly blocked lipopolysaccharide (LPS)-induced hippocampal cell death and productions of nitric oxide (NO) and interleukin (IL)-1β. PF also inhibited the LPS-stimulated productions of NO, tumor necrosis factor-α, and IL-1β from primary microglial cells. These results suggest that PF possesses neuroprotective activity by reducing the production of proinflammatory factors from activated microglial cells.'' {{#pmid:23559368|nam2013}}
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== References ==
 
== References ==
  
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[1]
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<bibtex>
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@article{Yan2004,
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abstract = {Heat shock proteins (HSPs) are induced by various physical, chemical, and biological stresses. HSPs are known to function as molecular chaperones, and they not only regulate various processes of protein biogenesis but also function as lifeguards against proteotoxic stresses. Because it is very useful to discover nontoxic chaperone-inducing compounds, we searched for them in herbal medicines. Some herbal medicines had positive effects on the induction of HSPs (Hsp70, Hsp40, and Hsp27) in cultured mammalian cells. We next examined 2 major constituents of these herbal medicines, glycyrrhizin and paeoniflorin, with previously defined chemical structures. Glycyrrhizin had an enhancing effect on the HSP induction by heat shock but could not induce HSPs by itself. In contrast, paeoniflorin had not only an enhancing effect but also an inducing effect by itself on HSP expression. Thus, paeoniflorin might be termed a chaperone inducer and glycyrrhizin a chaperone coinducer. Treatment of cells with paeoniflorin but not glycyrrhizin resulted in enhanced phosphorylation and acquisition of the deoxyribonucleic acid-binding ability of heat shock transcription factor 1 (HSF1), as well as the formation of characteristic HSF1 granules in the nucleus, suggesting that the induction of HSPs by paeoniflorin is mediated by the activation of HSF1. Also, thermotolerance was induced by treatment with paeoniflorin but not glycyrrhizin. Paeoniflorin had no toxic effect at concentrations as high as 80 microg/ mL (166.4 microM). To our knowledge, this is the first report on the induction of HSPs by herbal medicines.},
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author = {Yan, Dai and Saito, Kiyoto and Ohmi, Yuri and Fujie, Noriyo and Ohtsuka, Kenzo},
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file = {:C$\backslash$:/Users/riku/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Yan et al. - 2004 - Paeoniflorin, a novel heat shock protein-inducing compound.pdf:pdf},
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issn = {1355-8145},
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journal = {Cell stress \& chaperones},
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keywords = {Animals,Anti-Infective Agents,Anti-Infective Agents: pharmacology,Benzoates,Benzoates: metabolism,Bridged Compounds,Bridged Compounds: metabolism,DNA-Binding Proteins,DNA-Binding Proteins: drug effects,DNA-Binding Proteins: metabolism,Electrophoretic Mobility Shift Assay,Glucosides,Glucosides: genetics,Glucosides: metabolism,Glycyrrhizic Acid,Glycyrrhizic Acid: pharmacology,HeLa Cells,Heat-Shock Proteins,Heat-Shock Proteins: drug effects,Heat-Shock Proteins: metabolism,Herbal Medicine,Hot Temperature,Humans,Monoterpenes,Paeonia,Paeonia: metabolism,Phytotherapy,Rats,Transcription Factors},
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mendeley-groups = {peony},
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month = jan,
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number = {4},
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pages = {378--89},
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pmid = {15633296},
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title = {{Paeoniflorin, a novel heat shock protein-inducing compound.}},
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url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1065277\&tool=pmcentrez\&rendertype=abstract},
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volume = {9},
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year = {2004}
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}
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</bibtex>
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[2]
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<bibtex>
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@article{Zhang2015,
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abstract = {OBJECTIVE: To explore the delayed neuroprotection induced by paeoniflorin (PF), the principal component of Paeoniae radix prescribed in Chinese medicine, and its underlying mechanisms in rats subjected to vascular dementia (VD).
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METHODS: A rat model of VD was induced by bilateral common carotid arteries occlusion (BCCAO). Low-dose or high-dose PF (20 or 40 mg/kg once per day) was administrated for 28 days after VD. The behavioral analysis of rat was measured by water morris. Regional cerebral blood volume (rCBV), regional cerebral blood flow (rCBF) and mean transit time (MTT) were measured in the bilateral hippocampus by perfusion-weighted imaging (PWI). The levels of interleukin-1$\beta$ (IL-1$\beta$), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-$\alpha$) were measured by commercially available enzyme-linked immunosorbent assay kits. Protein levels were evaluated by western blot analysis. mRNA levels were evaluated by real time-polymerase chain reaction. Western blotting was used to estimate p65 translocation.
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RESULTS: The behavioral analysis showed that PF could decrease the escape latency time (P<0.05), and increase the residence time of the original platform quadrant and the across platform frequency in water maze in VD rats (P<0.05). Likewise, PF remarkably promoted the rCBV (P<0.05), rCBF and decreased per minute MTT (P<0.05) in hippocampus of VD rats. Furthermore, PF decreased the release of IL-1$\beta$, IL-6 and TNF-$\alpha$ as well as inhibited the mRNA expression of IL-1$\beta$, IL-6 and TNF-$\alpha$ in the hippocampus of VD rats (P<0.05 or P<0.01). PF also could decrease the protein expressions of inducible nitric oxide synthase and cyclooxygenase-2 in the hippocampus of VD rats (P<0.05 orP<0.01). In addition, PF significantly inhibited the nuclear factor $\kappa$B (NF-$\kappa$B) pathway in the hippocampus of VD rats.
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CONCLUSIONS: PF significantly attenuates cognitive impairment, improves hippocampus perfusion and inhibits inflammatory response in VD rats. In addition, the anti-inflammatory effects of PF might be due to inhibiting the NF-$\kappa$B pathway. PF may be a potential clinical application in improving VD.},
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author = {Zhang, Li-Gong and Wang, Li-Jun and Shen, Qing-Qing and Wang, Hao-Feng and Zhang, Ying and Shi, Cui-Ge and Zhang, Shu-Cheng and Zhang, Meng-Yuan},
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doi = {10.1007/s11655-015-2124-3},
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issn = {1672-0415},
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journal = {Chinese journal of integrative medicine},
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mendeley-groups = {peony},
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month = nov,
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pmid = {26577108},
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title = {{Paeoniflorin improves regional cerebral blood flow and suppresses inflammatory factors in the hippocampus of rats with vascular dementia.}},
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url = {http://www.ncbi.nlm.nih.gov/pubmed/26577108},
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year = {2015}
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}
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</bibtex>
  
 
[[Category:Supplement data pages]]
 
[[Category:Supplement data pages]]
 
[[Category:Anti-inflammatory supplements]]
 
[[Category:Anti-inflammatory supplements]]

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