Scientific Research on Celery seed extract
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Apium graveolens (of the family Apiaceae) is a vegetable commonly referred to as 'Celery', which has apparently been cultivated for over 3000 years mostly in Egypt. The term 'celeriac' refers to a variant of this species known as apium graveolens var. rapaceum. Despite the stem being the most commonly ingested portion of the plant as a common vegetable, the seeds of celery appears to have been used for medicinal purposes (Egypt and China) to treat; bronchitis, asthma, liver and spleen diseases and with hepatoprotective activity against many hepatotoxins. It has also been reported to be diluted in beverages and drunk with wine to cool a hot temper.
The difference between the 'vegetable' or 'stem' (edible portion of celery commonly seen in grocery stores) and the seeds or seed oil (common component of supplement) should be emphazied. The information below may not apply to vegetable consumption if using the seed oil
Celery seed oil is comprised of both the oil component (fatty acids) and the volatile component (small molecular weight molecules); the fatty acids in celery seed oil include:
Sedanolide (aka. 3-butyltetrahydrophthalide; 24%)
4,7-dimethoxy-5-(prop-2-enyl)benzo-1,3-dioxolan or apiole (23%)
β-pinene (19.4%) and α-pinene (1.3%)
γ-himachalene (10.3% in portuguese volatiles, 0.3% in italian)
For the most part, the volatile oil of celery is comprised of limonene and a large amount of monoterpenoid volatiles and a large phthalide content. The phthalide content is what is unique to celery as a supplement/food, and the phthalide known as Sedanolide is the main bioactive in celery seed oil. There appears to be a large degree of variability as to the amount of volatiles in a source of celery seed oil
With trace (0.1% or less) amounts of cumene, nonane, α-Thujene, carveol, and Terpinen-4-ol. The volatile oil is a large percentage of monoterpene hydrocarbons (46%) and a high source of phthalide compounds (42.3%). The aerial parts of celery also contain phthalides, but are more variable (1-39.5% of total volatiles) than the seeds with the vegetable stem containing 28.1% of total volatiles as the celery aromatic sedalonide.
The aerial parts (water extract) contain irioids and coumarins, whereas the methanolic seed extract does not.
The ethanolic extract of celery leaves has been found to inhibit the MAO-A enzyme with an IC50 of 5μg/mL, being slightly less effective than fenugreek (4μg/mL). The water extract was less effective, and all extracts of celery failed to significantly influence citalopram-binding to the serotonin receptor (suggesting no affinity).
Ligustilide has been noted to activate TRPA1 channels (EC50 of 44μM for activation; IC50 for inhibition at 1,456μM) and aromatization of ligustilide to dehydroligustilide (occurs via exposure to the air or celery aging) reversed this action (EC50 of 539μM yet an IC40 of 23μM); it appears to act via its electrophilic properties via alkylation of cysteine residues on TRPA1 (antagonism from dehydroligustilide appears to be independent).
Celery oil (50µl/kg orally) for 6 weeks has shown protective effects in an animal model of DHEP toxicity (a phthalate alongside Bisphenol A that targets PPARα and confers antiandrogenic properties given alongside the celery oil for 6 weeks) was able to attenuate the increase in relative liver weight and lipids as well as serum lipids and liver enzymes.
The methanolic extract of the seeds has shown protective effects against thioacetamide and paracetamol (assessed by liver enzymes in serum and histological examination).
In an ulcer test, 300mg/kg of the methanolic and water extracts of celery seeds in a gastric ulcer test (induced by alcohol) was able to inhibit 91% and 95% of the ulceration, respectively; a similar potency to the active control omeprazole (94%). Lower doses (100-200mg/kg) of water extracts of the aerial parts of celery were not significantly effective, and this anti-ulcer effect against ethanol has been noted elsewhere.
200mg/kg celery oil to rats also given the testicular toxic phthalate (DHEP) was able to exert protective effects when coingested.
In human cancer BGC-823 cells, celery seed oil is able to induce apoptosis in a concentration and time dependent manner with 300µg/mL for 72 hours reaching near 70% apoptosis which was characterized by a decrease in cells in G0/G1 phase (58.38% to 38.72%) and increase in S phase (30.51 to 61.54%) and decreased expression of CDK2 and Cyclin A.
In mammalian systems, one study using acute doses of sedanolide or other phthalides from celery noted reductions in tumor size and multiplicity (tumors induced by benzo(a)pyrene) which was thought to be secondary to inducing the antioxidant enzyme glutathione S-transferase (GST).pyrene-induced forestomach cancer in mice by natural phthalides from celery seed oil|published=1993|authors=Zheng GQ, Kenney PM, Zhang J, Lam LK|journal=Nutr Cancer]
At least one study using Sedanolide from celery oil in vitro failed to find a significant protective effect of this molecule against H2O2 or tert-butyl hydroperoxide induced DNA damage.
Up to 5,000mg/kg of celery seed extract for 28 days in rats failed to result in any clinically significant side effects (a small rise in the liver weight of female rats, but was without pathological changes; a small increase in serum globulin and phosphorus in males that was small enough to be deemed not relevant).
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