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2024-12-20 at 5:28 pm #61634
Celery seed is a potent and delicious spice, used in recipes ranging from curries to salad dressings. The benefits of this fine herbal seed may likely go beyond its culinary use, however: many studies have indicated that celery seeds provide powerful medicinal effects, and may be safe alternatives to conventional medicines. Celery seeds can relieve and prevent many conditions, from gout to hypertension.
Chemical constituents of Celery seed Extract powder
Celery seed contains coumarins (aprigravin, celerin, osthenol) and coumarin glycosides, including bergapten, apiumoside, apiumetin, vellein, celereoin, nodakenin, and celereoside; also, pthalide glycosides (celephtalides A–C), sesquiterpenoid glucosides (celeriosides A–E), phthalides (senkyunolide-J and -N), 3′-methoxy apiin, tryptophan, and others.
Benefits of taking Celery seed Extract powder supplements:
Antihypertensive effect
>Antihypertensive effect of celery seed on rat blood pressure in chronic administration.
(Source-Pharmaceutical Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.)
Abstract
This study investigated the effects of different celery (Apium graveolens) seed extracts on blood pressure (BP) in normotensive and deoxycorticosterone acetate-induced hypertensive rats. The hexanic, methanolic, and aqueous-ethanolic extracts were administered intraperitoneally and their effects on BP and heart rate (HR) were evaluated in comparison with spirnolactone as a diuretic and positive control. Also, the amount of n-butylphthalide (NBP), as an antihypertensive constituent, in each extract was determined by HPLC. The results indicated that all extracts decreased BP and increased the HR in hypertensive rats, but had no effect on normotensive rats. The data showed that administration of 300 mg/kg of hexanic, methanolic, and aqueous-ethanolic (20/80, v/v) extracts of the celery seed caused 38, 24, and 23 mmHg reduction in BP and 60, 25, and 27 beats per minute increase in the HR, respectively. Also, the HPLC analysis data revealed that the content of NBP in the hexanic extract was 3.7 and 4 times greater than methanolic and aqueous-ethanolic extracts. It can be concluded that celery seed extracts have antihypertensive properties, which appears to be attributable to the actions of its active hydrophobic constitutes such as NBP and can be considered as an antihypertensive agent in chronic treatment of elevated BP.
>Arabinogalactan present in the mountain celery seed extract potentiated hypolipidemic bioactivity of coexisting polyphenols in hamsters.
(Source-Department of Food and Nutrition, Research Institute of Biotechnology, Hungkuang University, Taichung Hsien, Taiwan 43302.)
Abstract
CONTEXT:
Previously, we showed the essential oils (EO) of the mountain celery [Cryptotaenia japonica Hass (Umbelliferae)] seeds (MCS) to be a prominent hypolipidemic agent.
OBJECTIVE:
We hypothesized the aqueous extract (AE) of its seeds could also exhibit a comparable nutritional effect.
MATERIALS AND METHODS:
Experiments were carried out for compositional analysis, antioxidant assay, and hypolipidaemic assay with AE in hamsters.
RESULTS:
AE contained soluble arabinogalactan (AGal) with molecular weight (MW) 878 kDa. AE also was enriched in polyphenolics and flavonoids, reaching 30.4 and 2.20 mg/100 g, respectively. AGal consisted of eight monosaccharides (in mols %), galactose (28.75), arabinose (24.84), glucose (17.91), mannose (6.93), ribose (6.03), fucose (5.83), xylose (5.30), and rhamnose (4.41), with average MW 878 kDa. In vitro, AE showed potent ferrous chelating and DPPH scavenging effects but only moderate H₂O₂ scavenging capability. In hamsters, AE exhibited promising hypolipidemic bioactivity, in particular, the HDL-C and hepatic unsaturated fatty acid (UFA) biosynthesis regarding oleic, linoleic, and arachidonic acids.
DISCUSSION AND CONCLUSION:
The presence of AGal enhanced the hypolipidemic and antioxidative bioactivity of MCS. MCS is feasibly beneficial to the hepatic de novo UFA synthesis and the hypolipidemics as evidenced by hamster model.
Stomach cancer
>Molecular mechanisms of celery seed extract induced apoptosis via s phase cell cycle arrest in the BGC-823 human stomach cancer cell line.
(Source-Department of Pathology and Pathophysiology, Taishan Medical University, Taian, China.
Abstract)
BACKGROUND:
Mechanisms of apoptosis in tumor cells is an important field of tumor therapy and cancer molecular biology. Loss of cell cycle control, leading to uncontrolled proliferation, is common in cancer. Therefore, the identification of potent and selective cyclin dependent kinase inhibitors is a priority for anti-cancer drug discovery. There are at least two major apoptotic pathways, initiated by caspase-8 and caspase-9, respectively, which can activate caspase cascades. Apoptosis triggered by activation of the mitochondrial-dependent caspase pathway represents the main programmed cell death mechanism. This is activated by various intracellular stresses that induce permeabilization of the mitochondrial membrane. Anti-tumor effects of celery seed extract (CSE) and related mechanisms regarding apoptosis were here investigated in human gastric cancer BGC-823 cells.
METHODS:
CSE was produced by supercritical fluid extraction. Cell viability was analyzed by 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyl-tetrazolium bromide (MTT) assay and apoptosis by flow cytometry using Annexin/PI staining and DAPI staining and a laser scanning confocal microscope (LSCM). Cell cycling was evaluated using PI staining with flow cytometry and expression of cell cycle and apoptosis-related proteins cyclin A, CDK2, bcl-2 and bax was assessed by immunohistochemical staining.
RESULTS:
CSE had an anti-proliferation effect on human gastric cancer BGC-823 cells in a dose- and time-dependent manner. After treatment, the apoptotic rate significantly increased, with morphological changes typical of apoptosis observed with LSCM by DAPI staining. Cell cycle and apoptosis related proteins, such as cyclin A, CDK2 and bcl-2 were all down-regulated, whereas bax was up-regulated.
CONCLUSIONS:
The molecular determinants of inhibition of cell proliferation as well as apoptosis of CSE may be associated with cycle arrest in the S phase.
Celery seed and Alzheimer's
>L-3-n-butylphthalide reduces tau phosphorylation and improves cognitive deficits in AβPP/PS1-Alzheimer's transgenic mice.
(Source-State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.)
Abstract
L-3-n-butylphthalide (L-NBP), an extract from seeds of Apium graveolens Linn (Chinese celery), has been shown to have neuroprotective effects on cerebral ischemic, vascular dementia and amyloid-β (Aβ)-induced animal models by inhibiting oxidative injury, neuronal apoptosis and glial activation, regulating amyloid-β protein precursor (AβPP) processing and reducing Aβ generation. The aim of the present study was to examine the effect of L-NBP on learning and memory in AβPP and presenilin 1 (PS1) double-transgenic AD mouse model (AβPP/PS1) and the mechanisms of L-NBP in reducing Aβ accumulation and tau phosphorylation. Twelve-month old AβPP/PS1 mice were given 15 mg/kg L-NBP by oral gavage for 3 months. L-NBP treatment significantly improved the spatial learning and memory deficits compared to the vehicle-treated AβPP/PS1 mice, whereas L-NBP treatment had no effect on cerebral Aβ plaque deposition and Aβ levels in brain homogenates. However, we found an L-NBP-induced reduction of tau hyperphosphorylation at Ser199, Thr205, Ser396, and Ser404 sites in AβPP/PS1 mice. Additionally, the expressions of cyclin-dependent kinase and glycogen synthase kinase 3β, the most important kinases involved in tau phosphorylation, were markedly decreased by L-NBP treatment. The effects of L-NBP on decreasing tau phosphorylation and kinases activations were further confirmed in neuroblastoma SK-N-SH cells overexpressing wild-type human AβPP695 (SK-N-SH AβPPwt). L-NBP shows promising candidate of multi-target neuronal protective agent for the treatment of Alzheimer's disease.
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