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![Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA](/_next/image?url=https%3A%2F%2Fcloudfront.jove.com%2FCDNSource%2Fteasers%2F60445.jpg&w=3840&q=50)
Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA
Published on: December 19, 2019
Bryostatin 1 causes attenuation of TPA‑mediated tumor promotion in mouse skin
Ning Zeng1, Yi Xu1, Yiping Wu1
1Department of Plastics and Aesthetic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Abstract:
The present study was designed to investigate the tumor inhibitory potential of bryostatin 1 in a 12‑O‑tetradecanoylphorbol‑13‑acetate (TPA)‑induced mouse model of skin cancer. The radical inhibition potential of various doses of bryostatin 1 was investigated against 2,2‑diphenyl‑1‑picrylhydrazyl (DPPH) bleach in vitro. The DPPH radical potential was observed compared with treatment with 5, 10, 15, 20, 25 and 30 µM doses of bryostatin 1. In vivo, bryostatin 1 prevented the TPA‑mediated increase in the level of H2O2 and myeloperoxidase in mouse epidermal tissue. Pretreatment of the mice with bryostatin 1 (30 µM) followed by administration of TPA reduced the edema, as demonstrated via punched‑out mouse ear tissue, to 7.2 mg, compared with 14 mg in the TPA‑treated group. Treatment with bryostatin 1 prior to TPA administration markedly prevented the inflammation of the skin by inhibiting hyperplasia in the epidermal layer and the aggregation of inflammatory cells. The results demonstrated that treatment of mice with bryostatin 1 at a 30 µM dose prior to TPA administration significantly (P<0.005) inhibited the TPA‑mediated increase in the level of COX‑2. The activity of ornithine decarboxylase, increased by TPA, was additionally inhibited following pretreatment of the mice with bryostatin 1. In the mice treated with bryostatin 1 at 30 µM doses prior to the administration of TPA, the appearance of papillomas was 20%, compared with 100% in the TPA group. Mice pretreated with bryostatin 1 at 30 µM doses prior to TPA administration exhibited the appearance of 0.4 mean papillomas in each animal, compared with 5.2 in the TPA group. Therefore, the results of the present study demonstrated that bryostatin 1 inhibited the development and progression of tumors of skin in the mice, through the prevention of inflammation‑inducing processes and the quenching of radicals. Therefore, bryostatin 1 maybe considered to be adrug of importance in the treatment of skin tumor.
Insights
Bryostatin 1 effectively inhibited skin tumor development in a mouse model by reducing inflammation and oxidative stress. This compound shows promise as a potential therapeutic agent for skin tumors.
Area of Science:
- Oncology
- Dermatology
- Pharmacology
Background:
- Skin cancer is a significant health concern, with chemical carcinogens like 12-O-tetradecanoylphorbol-13-acetate (TPA) used to induce tumors in research models.
- Understanding the mechanisms of tumor initiation and progression is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the tumor inhibitory potential of bryostatin 1 in a TPA-induced mouse model of skin cancer.
- To evaluate the in vitro radical scavenging activity of bryostatin 1.
- To assess the effects of bryostatin 1 on inflammation-related markers and tumor development in vivo.
Main Methods:
- In vitro antioxidant activity assay using 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical.
- In vivo study using TPA-induced mouse skin carcinogenesis model.
- Measurement of hydrogen peroxide (H2O2), myeloperoxidase, edema, epidermal hyperplasia, inflammatory cell aggregation, COX-2, and ornithine decarboxylase activity.
- Assessment of papilloma incidence and multiplicity.
Main Results:
- Bryostatin 1 demonstrated significant free radical scavenging activity in vitro.
- In vivo, bryostatin 1 (30 µM) pretreatment prevented TPA-induced increases in H2O2 and myeloperoxidase.
- Bryostatin 1 significantly reduced TPA-mediated edema, epidermal hyperplasia, inflammatory cell infiltration, COX-2, and ornithine decarboxylase activity.
- Papilloma incidence was reduced from 100% to 20%, and multiplicity from 5.2 to 0.4 mean papillomas per animal in bryostatin 1 pretreated mice.
Conclusions:
- Bryostatin 1 exhibits potent anti-inflammatory and antioxidant properties.
- Bryostatin 1 effectively inhibits skin tumor development and progression in a TPA-induced mouse model.
- Bryostatin 1 holds potential as a therapeutic agent for skin tumors due to its ability to counteract inflammation and oxidative stress.
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