Although the carrot plant is primarily grown with the aim of obtaining roots, Carrot Seeds are produced when the flowering process is induced; and the plant turns from the vegetative phase to the reproductive phase thus producing a rod or floral tassel at the end of it and umbels which carry the seeds.
The seeds are used as a flavoring agent in many food products and cosmetics in addition to its utilization as medicinal purposes. Carrot seeds oil not only has antioxidant effect but also possesses counteractive role for several disease such as cancer, diabetes and inflammation.[1:1]
- Carotol is one of the compounds found in carrot seed oil.[1:2]
- Methanol extract of carrot seeds exhibited high radical-scavenging activity more than α-tocopherol.[1:3]
- Carrot seeds oil possesses an antifungal effect; attributed to its carotol content.[1:4]
Ethanol extract of carrot seeds has demonstrated the ability to prevent damage to the liver; against the impact of toxins such as thioacetamide and carbon tetrachloride.[1:5]
Carrot seeds ethanol extract had the most promising effect on preventing brain aging.[1:6]
Oral administration of carrot seed extract could reverse the negative effects of D-galactose including the reduction in catalase and the elevation in malondialdehyde (MDA) either in brain or in plasma and the elevation in plasma Tumor necrosis factor alpha (TNF-α), Butyrylcholinesterase (BChE) as well as the liver and kidney functions. On this basis, it was concluded that the studied extracts have promising protective effect against the accelerated brain aging.[1:7]
- This may be attributed to the presence of oleic acid as monounsaturated fatty acid.
- Fatty acids stimulate gene expression and neuronal activity, boost synaptogenesis and neurogenesis, and prevent neuro-inflammation and apoptosis. By doing so, they promote brain development, ameliorate cognitive function, serve as anti-depressants and anticonvulsants, bestow protection against traumatic insults, and enhance repairing processes.[1:8]
- The oral administration of carrot seed extract can contribute to an elevation in acetyl cholinesterase activity which has been shown to help reverse memory deficits.[1:9]
Disease / Symptom Treatment
Impaired insulin signaling is a major contributor in the development of Alzheimer’s dementia (AD).
[The] D-galactose model of aging results in a diminishing of learning and memory function by producing a state of impaired insulin signaling that causes a cascade of deleterious events like oxidative stress, inflammation, and tau hyper-phosphorylation.[2:1]
- Carrot seeds extract may have a beneficial effect in treating Alzheimer’s dementia due to the superiority of carrot seeds ethanol extracts in the protection against the negative effect of D-galactose.[1:10]
- This ability might be due to the high content of phenolic compounds and flavonoids as found in carrot seed extract.[1:11]
Study Type: Animal Study, Review
Title: Protective effect of kumquat fruits and carrot seeds extracts against brain aging in rats
Author(s): Doha Abdou Mohamed, Karem Fouda, Ibrahim Mohamed Hamed, Sherein S. Abdelgayed
Institution(s): Nutrition and Food Sciences Department, National Research Centre, Dokki, Cairo, Egypt; Pathology Department, Faculty of Veterinary Medicine, Cairo University, Cairo, Egypt
Publication: Journal of Herbmed Pharmacology
Date: July 2019
Abstract: Introduction: Protection of brain against accelerated aging helps avoiding the occurrence of neurodegenerative diseases. So, the current work was conducted to evaluate the rescuing role of kumquat fruits crude ethanol extract, carrot seeds ethanol and petroleum ether extracts against the brain aging induced by D-galactose in rats. Methods: Forty male Sprague Dawley rats were divided equally into five groups. Group I was served as normal control, rats of group II were daily injected intraperitoneally (i.p.) with 150 mg/kg BW of D-galactose. Rats of group III, IV and V were daily injected i.p. with the same dose of D-galactose and administered orally with 250 mg/kg BW/day of kumquat fruits crude ethanol extract, carrot seeds ethanol extract and carrot seeds petroleum ether extract, respectively. After 6 weeks the rats were scarified, brain tissues were analyzed for malondialdehyde (MDA), catalase (CAT) as well as histological examination. Also, the plasma was analyzed for MDA, tumor necrosis factor-α (TNF-α), creatinine and urea levels, as well as CAT, butyrylcholinesterase (BChE), aspartate transaminase (AST) and alanine transaminase (ALT) activities. Results: From the results, it was elucidated that the tested extracts suppressed both the reduction in CAT and the elevation in MDA either in brain or plasma and the increase in plasma TNF-α, BChE as well as liver and kidney parameters. Conclusion: The tested extracts can be served as potent protective agents against the accelerated aging parameters which may be due to anti-oxidant and anti-inflammatory activities.
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Study Type: Animal Study
Title: Involvement of insulin resistance in D-galactose-induced age-related dementia in rats: Protective role of metformin and saxagliptin
Author(s): Sara Kenawy, Rehab Hegazy, Azza Hassan, Siham El-Shenawy, Nawal Gomaa, Hala Zaki, and Amina Attia
Institution(s): Pharmacology Department, Medical division, National Research Centre, Giza, Egypt; Pathology Department, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt; Pharmacology and Toxicology Department, Faculty of Pharmacy, Cairo University, Cairo, Egypt; Nathan S Kline Institute, UNITED STATES
Publication: PLoS One
Date: August 2017
Abstract: Age-related dementia is one of the most devastating disorders affecting the elderly. Recently, emerging data suggest that impaired insulin signaling is the major contributor in the development of Alzheimer’s dementia (AD), which is the most common type of senile dementia. In the present study, we investigated the potential therapeutic effects of metformin (Met) and saxagliptin (Saxa), as insulin sensitizing agents, in a rat model of brain aging and AD using D-galactose (D-gal, 150 mg/kg/day, s.c. for 90 successive days). Six groups of adult male Wistar rats were used: normal, D-gal, Met (500 mg/kg/day, p.o), and Saxa (1 mg/kg/day, p.o) control groups, as well as D-gal/Met and D-gal/Sax treated groups. Impaired learning and memory function was observed in rats treated with D-gal using Morris water maze test. Biochemical and histopathological findings also revealed some characteristic changes of AD in the brain that include the increased content of acetylcholine, glutamate, and phosphorelated tau, as well as deposition of amyloid plaques and neurofibrillary tangles. Induction of insulin resistance in experimentally aged rats was evidenced by increased blood glycated hemoglobin, brain contents of insulin and receptors for advanced glycated end-products, as well as decreased brain insulin receptor level. Elevation of oxidative stress markers and TNF-α brain content was also demonstrated. Met and Saxa, with a preference to Met, restored the normal memory and learning functions in rats, improved D-gal-induced state of insulin resistance, oxidative stress and inflammation, and ameliorated the AD biochemical and histopathological alterations in brain tissues. Our findings suggest that D-gal model of aging results in a diminishing of learning and memory function by producing a state of impaired insulin signaling that causes a cascade of deleterious events like oxidative stress, inflammation, and tau hyper-phosphorylation. Reversing of these harmful effects by the use of insulin-sensitizing drugs like Met and Saxa suggests their involvement in alleviation insulin resistance as the underlying pathology of AD and hence their potential use as anti-dementia drugs.
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