FAQ/Help |
Calendar |
Search |
Today's Posts |
01-18-2014, 11:16 AM | #1 | |||
|
||||
In Remembrance
|
Nobiletin is an extract from citrus peel - Has anyone tried it or know more?
1. Neuroscience. 2013 Dec 4;259C:126-141. doi: 10.1016/j.neuroscience.2013.11.051. [Epub ahead of print] Nobiletin treatment improves motor and cognitive deficits seen in MPTP-induced Parkinson model mice. Yabuki Y(1), Ohizumi Y(2), Yokosuka A(3), Mimaki Y(3), Fukunaga K(4). Author information: (1)Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan. (2)School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan; Department of Anti-dementia Functional Food Development, Graduate School of Engineering, Tohoku University, Sendai, Japan; Laboratory of Kampo Medicines, Yokohama College of Pharmacy, Yokohama, Japan; Kasei Fukushi Research Center, Tohoku Fukushi University, Sendai, Japan. (3)Laboratory of Medicinal Plant Science, School of Pharmacy, Tokyo University of Pharmacy and Life Science, Tokyo, Japan. (4)Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan. Electronic address: kfukunaga@m.tohoku.ac.jp. Nobiletin, a polymethoxylated flavonoid found in citrus fruit peel, reportedly improves memory impairment in rodent models. Here we report its effect on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced motor and cognitive deficits. Nobiletin administration (50mg/kg i.p.) for 2 consecutive weeks improved motor deficits seen in MPTP-induced Parkinson model mice by 2weeks, an effect that continued until 2weeks after drug withdrawal. Drug treatment promoted similar rescue of MPTP-induced cognitive impairment at equivalent time points. Nonetheless, nobiletin treatment did not block loss of dopaminergic neurons seen in the MPTP-treated mouse midbrain, nor did it rescue decreased tyrosine hydroxylase (TH) protein levels seen in the striatum or hippocampal CA1 region of these mice. Interestingly, nobiletin administration (50mg/kg i.p.) rescued reduced levels of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) autophosphorylation and phosphorylation at Thr-34 of dopamine- and cAMP-regulated phosphoprotein-32 (DARPP-32) in striatum and hippocampal CA1 to levels seen in sham-operated mice. Likewise, CaMKII- and cAMP kinase-dependent TH phosphorylation was significantly restored by nobiletin treatment. MPTP-induced reduction of dopamine contents in the striatum and hippocampal CA1 region was improved by nobiletin administration (50mg/kg i.p.). Acute intraperitoneal administration of nobiletin also enhanced dopamine release in striatum and hippocampal CA1, an effect partially inhibited by treatment with nifedipine (a L-type Ca(2+) channel inhibitor) or NNC 55-0396 (a T-type Ca(2+) channel inhibitor) and completely abolished by combined treatment with both. Overall, our study describes a novel nobiletin activity in brain and suggests that nobiletin rescues motor and cognitive dysfunction in MPTP-induced Parkinson model mice, in part by enhancing dopamine release. Copyright © 2013 IBRO. Published by Elsevier Ltd. All rights reserved. PMID: 24316474 [PubMed - as supplied by publisher]
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
|||
Reply With Quote |
01-18-2014, 11:36 AM | #2 | |||
|
||||
In Remembrance
|
1. Curr Opin Lipidol. 2013 Feb;24(1):34-40. doi: 10.1097/MOL.0b013e32835c07fd.
Citrus flavonoids and lipid metabolism. Assini JM, Mulvihill EE, Huff MW. Author information: Department of Biochemistry, Department of Medicine, The University of Western Ontario, London, Ontario, Canada. PURPOSE OF REVIEW: Citrus flavonoids are polyphenolic compounds with powerful biological properties. This review aims to summarize recent advances towards understanding the ability of citrus flavonoids to regulate lipid metabolism and other metabolic parameters relevant to the metabolic syndrome, type 2 diabetes and cardiovascular disease. RECENT FINDINGS: Citrus flavonoids, including naringenin, hesperidin, nobiletin and tangeretin, have emerged as promising therapeutic agents for the treatment of metabolic dysregulation. Epidemiological studies report that intake of citrus flavonoid-containing foods attenuates cardiovascular diseases. Experimental and a limited number of clinical studies reveal lipid-lowering, insulin-sensitizing, antihypertensive and anti-inflammatory properties. In animal models, citrus flavonoid supplements prevent hepatic steatosis, dyslipidemia and insulin sensitivity primarily through inhibition of hepatic fatty acid synthesis and increased fatty acid oxidation. Citrus flavonoids blunt the inflammatory response in metabolically important tissues including liver, adipose tissue, kidney and the aorta. The mechanisms underlying flavonoid-induced metabolic regulation have not been completely established. In mouse models, citrus flavonoids show marked suppression of atherogenesis through improved metabolic parameters and also through direct impact on the vessel wall. SUMMARY: These recent studies suggest an important role of citrus flavonoids in the treatment of dyslipidemia, insulin resistance, hepatic steatosis, obesity and atherosclerosis. The favorable outcomes are achieved through multiple mechanisms. Human studies focussed on dose, bioavailability, efficacy and safety are required to propel the use of these promising therapeutic agents into the clinical arena. PMID: 23254473 [PubMed - indexed for MEDLINE]
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
|||
Reply With Quote |
"Thanks for this!" says: | RLSmi (01-20-2014) |
01-18-2014, 12:04 PM | #3 | |||
|
||||
In Remembrance
|
Some familiar names-
1. Biol Pharm Bull. 2010;33(11):1814-21. Anti-neuroinflammatory activity of nobiletin on suppression of microglial activation. Cui Y, Wu J, Jung SC, Park DB, Maeng YH, Hong JY, Kim SJ, Lee SR, Kim SJ, Kim SJ, Eun SY. Author information: Institute of Medical Science, Jeju National University School of Medicine, 66 Jejudaehakno, Jeju-si, Jeju-do 690–756, Republic of Korea. A growing body of evidence suggests that nobiletin (5,6,7,8,3',4'-hexamethoxy flavone) from the peel of citrus fruits, enhances the damaged cognitive function in disease animal models. However, the neuroprotective mechanism has not been clearly elucidated. Since nobiletin has shown anti-inflammatory effects in several tissues, we investigated whether nobiletin suppresses excessive microglial activation implicated in neurotoxicity in lipopolysaccharide (LPS)-stimulated BV-2 microglia cell culture models. Release of nitric oxide (NO), the major inflammatory mediator in microglia, was markedly suppressed in a dose-dependent manner following nobiletin treatment (1-50 µM) in LPS-stimulated BV-2 microglia cells. The inhibitory effect of nobiletin was similar to that of minocycline, a well-known microglial inactivator. Nobiletin significantly inhibited the release of the pro-inflammatory cytokine tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β). LPS-induced phosphorylations of extracellular signal-regulated kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), and p38 mitogen-activated protein kinases (MAPKs) were also significantly inhibited by nobiletin treatment. In addition, nobiletin markedly inhibited the LPS-induced pro-inflammatory transcription factor nuclear factor κB (NF-κB) signaling pathway by suppressing nuclear NF-κB translocation from the cytoplasm and subsequent expression of NF-κB in the nucleus. Taken together, these results may contribute to further exploration of the therapeutic potential and molecular mechanism of nobiletin in relation to neuroinflammation and neurodegenerative diseases. PMID: 21048305 [PubMed - indexed for MEDLINE]
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
|||
Reply With Quote |
"Thanks for this!" says: | Floridagal (01-22-2014), RLSmi (01-20-2014) |
Reply |
|
|