Ferulic Acid

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- Ferulic Acid -

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Observations:

Ferulic Acid: therapeutic potential through its antioxidant property.
J Clin Biochem Nutr. 2007 Mar;40(2):92-100.
Srinivasan M, Sudheer AR, Menon VP.

Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar - 608 002, Tamil Nadu, India.
Abstract

There has been considerable public and scientific interest in the use of phytochemicals derived from dietary components to combat human diseases. They are naturally occurring substances found in plants. Ferulic acid (FA) is a phytochemical commonly found in fruits and vegetables such as tomatoes, sweet corn and rice bran. It arises from metabolism of phenylalanine and tyrosine by Shikimate pathway in plants. It exhibits a wide range of therapeutic effects against various diseases like cancer, diabetes, cardiovascular and neurodegenerative. A wide spectrum of beneficial activity for human health has been advocated for this phenolic compound, at least in part, because of its strong antioxidant activity. FA, a phenolic compound is a strong membrane antioxidant and known to positively affect human health. FA is an effective scavenger of free radicals and it has been approved in certain countries as food additive to prevent lipid peroxidation. It effectively scavenges superoxide anion radical and inhibits the lipid peroxidation. It possesses antioxidant property by virtue of its phenolic hydroxyl group in its structure. The hydroxy and phenoxy groups of FA donate electrons to quench the free radicals. The phenolic radical in turn forms a quinone methide intermediate, which is excreted via the bile. The past few decades have been devoted to intense research on antioxidant property of FA. So, the present review deals with the mechanism of antioxidant property of FA and its possible role in therapeutic usage against various diseases.

PMID: 18188410 [PubMed]PMCID: PMC2127228
http://www.ncbi.nlm.nih.gov/pubmed/18188410
Free full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2127228/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2127228/pdf/jcbn2007013.pdf

Ferulic Acid benefit as antioxidant supplement
by Ray Sahelian, M.D.
Ferulic acid is an antioxidant found naturally in plant cell walls, leaves and seeds. A good amount of ferulic acid is found in oats, brown rice, whole wheat, peanuts, apples, and pineapples... Ferulic acid is similar to curcumin in chemical structure. Ferulic acid is a derivative of trans-cinnamic acid and a precursor to vanillin... Coffee is particularly rich in bound phenolic acids, such as caffeic acid, ferulic acid...
http://www.raysahelian.com/ferulicacid.html

Inhibitory effects of long-term administration of ferulic acid on microglial activation induced by intracerebroventricular injection of beta-amyloid peptide (1-42) in mice.
Biol Pharm Bull. 2004 Jan;27(1):120-1.
Pharmaceutical Society of Japan
Vol. 27, No. 1
Kim HS, Cho JY, Kim DH, Yan JJ, Lee HK, Suh HW, Song DK.

Department of Pharmacology, College of Medicine, Institute of Natural Medicine, Hallym University, Chunchon 200-702, Republic of Korea.
Abstract

Flavonoids and monophenolic compounds have been well described in recent years as antioxidants and scavengers of reactive oxygen and nitrogen species. In the present study, we aimed to characterize the effects of long-term administration of ferulic acid on the centrally administered beta-amyloid peptide (Abeta)(1-42)-induced activation of microglial cells in mice. Abeta(1-42) increased the immunoreactivity of OX-42, a microglial marker, and interferon-gamma in the hippocampus at 8 h after the intracerebroventricular injection. The effects were suppressed by long-term (4-week) pretreatment with ferulic acid. This inhibition of microglial cell activation may underlie the beneficial effects of long-term administration of ferulic acid on Abeta(1-42)-induced toxicity in vivo.

PMID: 14709913 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/14709913
Free PDF full text article: http://bpb.pharm.or.jp/bpb/200401/b01_0120.pdf

Protection against amyloid beta-peptide (1-42)-induced loss of phospholipid asymmetry in synaptosomal membranes by tricyclodecan-9-xanthogenate (D609) and ferulic acid ethyl ester: implications for Alzheimer's disease.
Biochim Biophys Acta. 2005 Jun 30;1741(1-2):140-8. Epub 2004 Dec 25.
Mohmmad Abdul H, Butterfield DA.

Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA.
Abstract

Amyloid-beta (1-42) [Abeta (1-42)] deposition in the brain is a hallmark of Alzheimer's disease (AD) and has been shown to induce apoptosis and disrupt cellular ion homeostasis. Abeta (1-42) induces membrane lipid peroxidation, and 4-hydroxynonenal (HNE) and 2-propenal (acrolein) are the two reactive products of lipid peroxidation, which structurally modify proteins by covalent interaction and inhibit enzyme function. Phosphatidylserine (PS), an aminophospholipid, is sequestered in the inner leaflet of the plasma membrane in nonstimulated cells. An early signal of synaptosomal apoptosis is the loss of phospholipid asymmetry and the appearance of phosphatidylserine in the outer leaflet of the membrane. The ATP-requiring enzyme, flippase, maintains phospholipid asymmetry of PS. Here, we have investigated the inactivation of the transmembrane enzyme aminophospholipid-translocase (or flippase) by Abeta (1-42). Flippase activity depends on a critical cysteine residue, a putative site of covalent modification by the Abeta (1-42)-induced lipid peroxidation products, HNE or acrolein. The present study is aimed to investigate the protective effects of tricyclodecan-9-xanthogenate (D609) and ferulic acid ethyl ester (FAEE) on Abeta (1-42) induced modulation in phospholipid asymmetry in the synaptosomal membranes. Pretreatment of synaptosomes with D609 and FAEE significantly protected Abeta (1-42)-induced loss of phospholipid asymmetry in synaptosomal membranes. Our results suggest that D609 and FAEE exert protective effects against Abeta (1-42) induced apoptosis. The increase in intracellular Ca(2+) might not be the sole cause for the loss of flippase activity. Rather, other mechanisms that could modulate the function of flippase might be important in the modulation of phospholipid asymmetry. The results of this study are discussed with relevance to neuronal loss in the AD brain.

PMID: 15955457 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/15955457
Full text: http://www.chem.uky.edu/research/butterfield/dab_pdfs/Abdul -Mohmmad Abdul and Butterfield 2005 Biochim Biophys Acta 1741 140-148.pdf

What is Ferulic acid?
Pure ferulic acid is a yellowish powder. Ferulic acid belong to the family of hydroxycinnamic acid. The chemical structure of ferulic acid is very similar to that of curcumin...
http://www.phytochemicals.info/phytochemicals/ferulic-acid.php

Ferulic Acid Protects Against Alzheimer’s
Ferulic Acid is found in our old friend the blueberry and other foods...
http://www.antioxidants-anti-aging-super-foods.com/ferulic-acid.html

Protection against beta-amyloid peptide toxicity in vivo with long-term administration of ferulic acid.
Br J Pharmacol. 2001 May;133(1):89-96.
Yan JJ, Cho JY, Kim HS, Kim KL, Jung JS, Huh SO, Suh HW, Kim YH, Song DK.

Department of Pharmacology, College of Medicine, Institute of Natural Medicine, Hallym University, Chunchon, 200-702, S. Korea.
Abstract

1. beta-Amyloid peptide (A beta), a 39 -- 43 amino acid peptide, is believed to induce oxidative stress and inflammation in the brain, which are postulated to play important roles in the pathogenesis of Alzheimer's disease. Ferulic acid is an antioxidant and anti-inflammatory agent derived from plants; therefore, the potential protective activity of ferulic acid against A beta toxicity in vivo was examined. 2. Mice were allowed free access to drinking water (control) or water containing ferulic acid (0.006%). After 4 weeks, A beta 1-42 (410 pmol) was administered via intracerebroventricular injection. 3. Injection of control mice with A beta 1-42 impaired performance on the passive avoidance test (35% decrease in step-through latency), the Y-maze test (19% decrease in alternation behaviour), and the water maze test (32% decrease in percentage time in platform-quadrant). In contrast, mice treated with ferulic acid prior to A beta 1-42 administration were protected from these changes (9% decrease in step-through latency; no decrease in alternation behaviour; 14% decrease in percentage time in platform-quadrant). A beta 1-42 induced 31% decrease in acetylcholine level in the cortex, which was tended to be ameliorated by ferulic acid. 4. In addition, A beta 1-42 increased immunoreactivities of the astrocyte marker glial fibrillary acidic protein (GFAP) and interleukin-1 beta (IL-1 beta) in the hippocampus, effects also suppressed by pretreatment with ferulic acid. 5. Administration of ferulic acid per se unexpectedly induced a transient and slight increase in GFAP and IL-1 beta immunoreactivity in the hippocampus on day 14, which returned to basal levels on day 28. A slight (8%) decrease in alternation behaviour was observed on day 14. 6. These results demonstrate that long-term administration of ferulic acid induces resistance to A beta 1-42 toxicity in the brain, and suggest that ferulic acid may be a useful chemopreventive agent against Alzheimer's disease.

PMID: 11325798 [PubMed]PMCID: PMC1572763
http://www.ncbi.nlm.nih.gov/pubmed/11325798

Ferulic Acid: an intriguing new supplement with some unusual antioxidant properties
The Delano Report

* Anti-aging
* Diabetes
* Cardiovascular disease
* Cancer
* Neuroprotection (Alzheimer’s, cognitive decline, macular degeneration)
* Bone degeneration (osteoporosis)
* Immunity
* Athletic performance
* Safety and dosage: A commonly recommended dose is 250 mg twice per day
http://delano.com/blog/?p=154

EFFECT OF ANM176TM CONTAINING FERULIC ACID AND GARDEN ANGELICA EXTRACT ON ALZHEIMER´S DISEASE

S. Nakamura, K. Sasaki
Rakuwakai Otowa Hospital, Neurology, Kyoto, Japan, 2Kinoko Espoir Hospital, Psychiary, Kasoka, Japan

Background: Ferulic acid has been shown to prevent amyloid β (Aβ) induced neurotoxiciy in rat hippocampus and also to protect rats against the impairment of inhibitory avoidance caused by Aβ, scopolamine or cycloheximide.
Methods: We administered ANM176TM containing ferulic acid and garden angelica extract to 143 Alzheimer disease (AD) patients for 9 months. Their cognitive function was measured by Japanese version of Alzheimer's disease assessment scale-cognitive subscale (ADAS-Jcog) or mini-mental scale examination (MMSE). ANM176TM was supplied by the courtesy of Scigenic Co., Korea.
Findings: The change of ADAS-Jcog score in patients treated with ANM176TM for 9 months lessened, when compared with the previously reported change of ADAS-Jcog score in the natural course of AD. The decline of cognitive function was suppressed significantly more remarkably after 9 months in AD patients with ADAS-Jcog score < 20 at onset than those with score ≥30, or in those with MMSE score ≥24 at onset than those with score ≤10. AD cases with early-onset (< 65 years old) after 6 months exhibited significantly greater worsening than those with late-onset (≥65 years old) after 9 months when measured with ADAS-Jcog. ANM176TM attenuated worsening in ADAS-Jcog score after 6 months more effectively when administered alone, compared with those accompanied with donepezil treatment. ANM176TM was well tolerated without any noticeable side effect.
Interpretation: Present results suggest ANM176TM could be recommended for relatively mild AD patients with late-onset without donepezil treatment.
http://www.kenes.com/adpd2009/posters/Abstract1138.htm
PDF of paper: http://www.kenes.com/adpd2009/cd/pdf/316.pdf

Effect of ferulic acid and Angelica archangelica extract on behavioral and psychological symptoms of dementia in frontotemporal lobar degeneration and dementia with Lewy bodies
Takemi Kimura1,*, Hideki Hayashida2, Masako Murata1, Junichi Takamatsu1
Article first published online: 28 JAN 2011
Japan Geriatrics Society

Angelica archangelica;behavioral and psychological symptoms of dementia;dementia with Lewy bodies;ferulic acid;frontotemporal lobar degeneration
Aim: The behavioral and psychological symptoms of dementia place a heavy burden on caregivers. Antipsychotic drugs, though used to reduce the symptoms, frequently decrease patients' activities of daily living and reduce their quality of life. Recently, it was suggested that ferulic acid is an effective treatment for behavioral and psychological symptoms. We have also reported several patients with dementia with Lewy bodies showing good responses to ferulic acid and Angelica archangelica extract (Feru-guard). The present study investigated the efficacy of Feru-guard in the treatment of behavioral and psychological symptoms in frontotemporal lobar degeneration and dementia with Lewy bodies.

Methods: We designed a prospective, open-label trial of daily Feru-guard (3.0 g/day) lasting 4 weeks in 20 patients with frontotemporal lobar degeneration or dementia with Lewy bodies. Behavioral and psychological symptoms of dementia were assessed at baseline and 4 weeks after the start of treatment, using the Neuropsychiatric Inventory. The Neuropsychiatric Inventory scores were analyzed using the Wilcoxon rank sum test.

Results: Treatment with Feru-guard led to decreased scores on the Neuropsychiatric Inventory in 19 of 20 patients and significantly decreased the score overall. The treatment also led to significantly reduced subscale scores on the Neuropsychiatric Inventory (“delusions”, “hallucinations”, “agitation/aggression”, “anxiety”, “apathy/indifference”, “irritability/lability” and “aberrant behavior”). There were no adverse effects or significant changes in physical findings or laboratory data.

Conclusion: Feru-guard may be effective and valuable for treating the behavioral and psychological symptoms of dementia in frontotemporal lobar degeneration and dementia with Lewy bodies. Geriatr Gerontol Int 2011; 11

DOI: 10.1111/j.1447-0594.2010.00687.x
http://onlinelibrary.wiley.com/doi/10.1111/j.1447-0594.2010.00687.x/abstract

Protective effect of Z-ligustilide against amyloid beta-induced neurotoxicity is associated with decreased pro-inflammatory markers in rat brains.
Pharmacol Biochem Behav. 2009 Jun;92(4):635-41. Epub 2009 Mar 24.
Kuang X, Du JR, Chen YS, Wang J, Wang YN.

State Key Laboratory of Biotherapy, West China Medical School, Sichuan University, Chengdu 610041, China.
Abstract

Neuroinflammatory responses induced by accumulation and aggregation of beta-amyloid (Abeta) peptide are mainly involved in Alzheimer's disease (AD) pathogenesis. Z-ligustilide (LIG), a novel neuroprotectant against ischemic stroke, was reported to have significant anti-inflammatory effects via inhibition of TNF-alpha production and bioactivity. The present study investigated the effect of LIG on AD-like cognitive impairment and neuropathological and neuroinflammatory changes induced by bilateral intracerebroventricular injections of Abeta(25-35) at a dose of 50 nmol/rat. Rats received oral administration of 40 mg/kg LIG or volume-matched vehicle 1 h before Abeta(25-35) treatment then once daily for 15 days. Morris water maze was used to detect the cognitive dysfunction induced by Abeta(25-35). Compared to the sham-operated rats, Abeta(25-35) injection significantly prolonged the mean escape latency in vehicle-treated rats in the Morris water maze test (p < 0.01) and increased both AD-related neuropathological signs (i.e., Abeta, amyloid precursor protein, and phosphorylated Tau immunoreactivity) and pro-inflammatory mediators (i.e., TNF-alpha and activated NF-kappaB) in the prefrontal cortex and CA1 subregion of the hippocampus. And these neurotoxic effects of Abeta(25-35) were significantly ameliorated with LIG treatment (p < 0.01 vs. vehicle-treated group). The present data suggest that LIG modulates TNF-alpha-activated NF-kappaB signaling pathway with respect to its protective effect against Abeta(25-35)-induced neurotoxicity. LIG would be a potential candidate for further preclinical study aimed at the prevention and treatment of cognitive deficits in AD.

PMID: 19324070 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/19324070

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