Hypocrellin B

Int J Radiat Biol. 2014 Jul;90(7):575-9.

Effect of photodynamic therapy with hypocrellin B on apoptosis, adhesion, and migration of cancer cells.[Pubmed: 24661233]

In the present study, we investigated effects of photodynamic therapy with Hypocrellin B on apoptosis, adhesion, and migration of cancer cells in vitro.
METHODS AND RESULTS:
Human ovarian cancer HO-8910 cell as a cancer model cell was incubated with Hypocrellin B at a concentration of 2.5 μM for 5 h and irradiated by light from a light-emitting diodes (LED) source. Cell apoptosis was analyzed by flow cytometry with annexin V/propidium iodide (PI) staining and nuclear staining 6 h after Hypocrellin B photoirradiation. Cell adhesion was assessed using the 3-(4, 5-dimthylthiazol-2-yl)-2, 5 diphenyl-tetrazolium bromide (MTT) assay 4 h after photodynamic treatment. Cell migration was measured 48 h after photodynamic treatment. Flow cytometry with annexin V/PI staining showed that early apoptotic and late apoptotic (necrotic) rates following photodynamic therapy with Hypocrellin B markedly increased to 16.40% and 24.67%, respectively. Nuclear staining found nuclear condensation and typical apoptotic body in the treated cells. The number of cell migration was significantly decreased to 183 ± 28 after photodynamic therapy with Hypocrellin B (p < 0.01). Light irradiation alone and Hypocrellin B alone had no significant effect on cell migration. The cell adhesion inhibitory rate due to photodynamic action of Hypocrellin B was 53.2 ± 1.8%, significantly higher than 2.7 ± 2.1% of light treatment alone and 1.0 ± 0.4% of Hypocrellin B treatment alone (p < 0.01).
CONCLUSIONS:
The findings demonstrated that photodynamic therapy with Hypocrellin B remarkably induced apoptosis and inhibited adhesion and migration of cancer cells in vitro.

Ultrasonics. 2012 Apr;52(4):543-6.

Hypocrellin B-mediated sonodynamic action induces apoptosis of hepatocellular carcinoma cells.[Pubmed: 22172458]

The present study aims to investigate apoptosis of hepatocellular carcinoma cells induced by Hypocrellin B-mediated sonodynamic action.
METHODS AND RESULTS:
The Hypocrellin B concentration was kept constant at 2.5 μM and cells from the hepatocellular carcinoma HepG2 cell line were exposed to ultrasound with an intensity of 0.46 W/cm(2) for 8s. Cell cytotoxicity was quantified using an MTT assay 24 h after sonodynamic therapy (SDT) of Hypocrellin B. Apoptosis was investigated using a flow cytometry with Annexin V-FITC and propidium iodine staining. Intracellular reactive oxygen species (ROS) levels were detected using a flow cytometry with 2,7-dichlorodihydrofluorecein diacetate (DCFH-DA) staining. The cytotoxicity of Hypocrellin B-mediated sonodynamic action on HepG2 cells was significantly higher than those of other treatments including ultrasound alone, Hypocrellin B alone and sham treatment. Flow cytometry showed that Hypocrellin B-induced sonodynamic action markedly enhanced the apoptotic rate of HepG2 cells. Increased ROS was observed in HepG2 cells after being treated with Hypocrellin B-mediated sonodynamic action.
CONCLUSIONS:
Our data demonstrated that Hypocrellin B-mediated sonodynamic action remarkably induced apoptosis of HepG2 cells, suggesting that apoptosis is an important mechanism of cell death induced by Hypocrellin B-mediated SDT.

Int J Radiat Biol. 2015 May;91(5):399-406.

Hypocrellin B in hepatocellular carcinoma cells: Subcellular localization and sonodynamic damage.[Pubmed: 25565557]

To study subcellular localization of Hypocrellin B in hepatocellular carcinoma cells, and Hypocrellin B-mediated sonodynamic action-induced cell damage.
METHODS AND RESULTS:
After incubation with 2.5 μM of Hypocrellin B, human hepatocellular carcinoma HepG2 cells were exposed to ultrasound waves for 8 sec at an intensity of 0.46 W/cm(2). Additionally, subcellular localization of Hypocrellin B in HepG2 cells with organelle probe staining was also observed using CLSM. R. The colony forming units of HepG2 cells decreased substantially after sonodynamic treatment. The results of TEM showed microvilli disappearance, apoptotic body formation, swollen mitochondria with loss of cristae and mitochondrial myelin-like features (or membrane whorls). Collapse of MMP was found in the treated cells. Hypocrellin B was distributed in mitochondria and lysosomes as well as in endoplasmic reticulum and Golgi apparatus.
CONCLUSIONS:
The findings demonstrated that sonodynamic action of Hypocrellin B induced mitochondrial damage, survival inhibition, and apoptosis of HepG2 cells. Additionally, other subcellular organelles such as endoplasmic reticulum, Golgi apparatus and lysosomes were also the targets of Hypocrellin B-mediated sonodynamic action as well as mitochondria.

Photodiagnosis Photodyn Ther. 2012 Dec;9(4):337-43.

Apoptosis of breast cancer cells induced by hypocrellin B under light-emitting diode irradiation.[Pubmed: 23200015]

Hypocrellin B was used in the present study to investigate apoptosis induction in breast cancer MDA-MB-231 cells.
METHODS AND RESULTS:
Photocytotoxicity was investigated 24h after photodynamic treatment of Hypocrellin B using MTT reduction assay and light microscopy. Hypocrellin B-induced photocytotoxicity in MDA-MB-231 cells exhibited a dose-dependent manner. The amount of MDA-MB-231 cells attached to the bottom of well decreased significantly after photodynamic treatment of Hypocrellin B. Flow cytometry showed that the early and late apoptotic rate of MDA-MB-231 cells increased remarkably up to 17.46% and 32.80%, respectively, after treatment of LED-activated Hypocrellin B. In addition, nuclear condensation, fragmentation and chromatin margination, and topical apoptotic body in the treated cells were observed by nuclear staining and TEM.
CONCLUSIONS:
Photodynamic action of Hypocrellin B irradiated by light-emitting diodes could significantly kill breast cancer cells and induce apoptotic cell death, which suggests LED-activated Hypocrellin B is a promising strategy for combating breast cancer.