apigenin has been researched along with Skin-Neoplasms* in 3 studies
3 other study(ies) available for apigenin and Skin-Neoplasms
Article | Year |
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Cancer chemopreventive agents (antitumor-promoters) from Ajuga decumbens.
Sixteen compounds (1-16) isolated from the flowering whole plant of Ajuga decumbens have been tested for their inhibitory effects on Epstein-Barr virus early antigen (EBV-EA) induction by the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), as a primary screening test for antitumor-promoters (potential cancer chemopreventive agents). Five compounds (6, 9, and 12-14) showed strong inhibitory effects on EBV-EA induction. Of these active compounds, two major constituents of this plant, cyasterone (6) and 8-acetylharpagide (13), showed potent antitumor-promoting activities on a mouse-skin in vivo two-stage carcinogenesis procedure, using 7, 12-dimethylbenz[a]anthracene as initiator and TPA as promoter. Further, compound 13 also exhibited potent chemopreventive activity in a mouse pulmonary tumor model. Topics: 4-Nitroquinoline-1-oxide; Animals; Antineoplastic Agents, Phytogenic; Antiviral Agents; Carcinogens; Female; Glycerol; Herpesvirus 4, Human; Lung Neoplasms; Mice; Mice, Inbred ICR; Papilloma; Plants, Medicinal; Skin Neoplasms; Tetradecanoylphorbol Acetate; Tumor Cells, Cultured | 1999 |
Influence of vehicle, distant topical delivery, and biotransformation on the chemopreventive activity of apigenin, a plant flavonoid, in mouse skin.
This study was designed to (a) establish a short-term in vivo system to evaluate topical formulations of apigenin, (b) determine whether apigenin should be topically delivered to the local skin tissue or systemic circulation, (c) investigate if biotransformation was involved in apigenin's chemopreventive activity.. The effect of topical applied apigenin in acetone/DMSO (A/D, 9:1) on the promotion of skin tumorigenesis was studied. The influence of apigenin in DMSO, A/D (4:1), and propylene glycol/DMSO (PG/D, 4:1) on 12-O-tetradecanoylphorbol-13 acetate (TPA) induced ornithine decarboxylase (ODC) activity was compared. Distant topical delivery of apigenin was conducted on abdominal skin and ODC activity was monitored in dorsal skin. Potential glucuronidation/sulfation of apigenin in intact skin was assessed by measuring isolated apigenin before and after enzyme hydrolysis with glucuronidase/sulfatase. The epidermal extracts from apigenin-treated SENCAR mice were analyzed for metabolites by HPLC.. Apigenin (5 mumol) in A/D did not significantly reduce skin tumor incidence in contrast to previous data with DMSO. Inhibition of TPA-induced ODC by apigenin in three vehicles was in the order of DMSO > A/D > PG/D. TPA-induced ODC in dorsal skin was not inhibited by apigenin delivered from abdominal skin. The quantity of apigenin recovered from epidermal extract was not different before and after beta-glucuronidase/sulfatase treatment. Metabolites were not observed in the HPLC profiles of epidermal extracts from apigenin treated mice.. (a) The short-term TPA-induced ODC was validated for evaluating topical formulations of apigenin. (b) Topical delivery of apigenin should target the local skin tissue. (c) Glucuronidation/sulfation appeared not to be involved in apigenin's chemopreventive activity. Topics: 9,10-Dimethyl-1,2-benzanthracene; Acetone; Administration, Topical; Animals; Anticarcinogenic Agents; Biotransformation; Carcinogens; Chamomile; Dimethyl Sulfoxide; Drug Interactions; Enzyme Induction; Female; Flavonoids; Mice; Mice, Inbred SENCAR; Oils, Volatile; Ornithine Decarboxylase; Pharmaceutical Vehicles; Plants, Medicinal; Propylene Glycol; Propylene Glycols; Skin; Skin Neoplasms; Tetradecanoylphorbol Acetate | 1996 |
Inhibitory effect of apigenin, a plant flavonoid, on epidermal ornithine decarboxylase and skin tumor promotion in mice.
This investigation studied the effect of topical application of apigenin on skin tumorigenesis initiated by 7,12-dimethylbenz(a)anthracene (DMBA) and promoted by 12-O-tetradecanoylphorbol-13-acetate (TPA) in SENCAR mice. Apigenin was a potent inhibitor of epidermal ornithine decarboxylase induction by TPA in a dose-dependent manner from 1 to 20 mumol. Two tumorigenesis studies were conducted. In the first study, 20 mumol of apigenin was applied topically and no effect on body weight was observed. By week 33 after DMBA initiation, 48% of DMBA/TPA-treated mice developed carcinomas, while none occurred in DMBA/apigenin/TPA-treated groups. In the second study, doses of 5 and 20 mumol of apigenin were used. The papilloma incidence for 0, 5, and 20 mumol apigenin at 26 weeks after DMBA was 93.3, 58, and 39.3%, and papilloma numbers per mouse were 7.5, 2.5, and 1.8, respectively. Apigenin prolonged by 3 weeks the latency period of tumor appearance. In addition, apigenin significantly inhibited the incidence of carcinoma and the numbers of carcinomas. The incidence of carcinomas per tumor-bearing animal and the ratio of carcinomas/papillomas in two apigenin-treated groups decreased although there were no significant differences between the three groups. These data indicate that apigenin inhibited skin papillomas and showed the tendency to decrease conversion of papillomas to carcinomas. Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; Chamomile; Cocarcinogenesis; Dose-Response Relationship, Drug; Enzyme Induction; Epidermis; Flavonoids; Mice; Oils, Volatile; Ornithine Decarboxylase; Papilloma; Plants, Medicinal; Skin Neoplasms; Tetradecanoylphorbol Acetate | 1990 |