Mechanism of photodynamic therapy against human esophageal carcinoma xenografts in nude mice.
- Author:
Xiao-Hua CHEN
1
;
Rong-Cheng LUO
;
Li-Bo LI
;
Xue-Mei DING
;
Cheng-Wei LV
;
Xiao-Ping ZHOU
;
Xiao YAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Line, Tumor; Esophageal Neoplasms; drug therapy; pathology; Female; Hematoporphyrin Derivative; therapeutic use; Humans; Male; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Transplantation; Photochemotherapy; Random Allocation
- From: Journal of Southern Medical University 2009;29(11):2222-2224
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism of photodynamic therapy (PDT) in nude mice bearing human esophageal cancer cell line Eca-109 xenografts.
METHODSA nude mouse model bearing human esophageal carcinoma was established by subcutaneous transplantation of Eca-109 cells. The mice were then randomized into 4 groups, namely hematoporphyrin derivative (HpD)-PDT group (given HpD and laser irradiation), exclusive laser irradiation group, exclusive HpD group and blank control group. In HpD-PDT group, the mice were exposed to irradiation at the light energy density of 120 Jsol;cm(2) delivered via a DIOMED 630 PDT system 24 h after intraperitoneal HpD injection, and the mice in exclusive laser irradiation group received only laser irradiation. Three days later, all the nude mice were sacrificed for determination of malondialdehyde (MDA) production, immunohistochemistry for caspase-3 protein and HE staining of the tumor tissue.
RESULTSThe MDA level was significantly higher in HpD-PDT group than in the other 3 groups (P<0.01), and comparable between the latter 3 groups. Expression of caspase-3 protein was similar between HpD-PDT group and the blank control group (P>0.05). Under light microscope, HE staining visualized massive tissue necrosis in HpD-PDT group with homogeneous red staining.
CONCLUSIONIn human esophageal carcinoma xenografts in nude mice, HpD-PDT generates singlet oxygen to result in direct tumor cell damage and cause MDA production. Caspase-3 may not be activated in the apoptotic pathway, suggesting that this pathway may not be caspase-3-dependent.