Figure 3.

rhES aggravated hypoxia and the inflammatory response in the tumor microenvironment.

Notes: (A) Photographs showing the CD31 immunohistochemistry in Lewis lung carcinoma (LLC) tumors at 7 and 14 days after the initiation of treatment (×200, scale bar =10 μm). (B) Levels of vascular endothelial growth factor (VEGF) in LLC tumors were detected by an enzyme-linked immunosorbent assay (ELISA). (C) Hypoxic areas in LLC tumors were visualized by immunolabeling for the hypoxia-specific marker pimonidazole. (D) After 14 days of rhES treatment, necrotic or apoptotic cells in LLC tumor tissues were visualized by hematoxylin and eosin or terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, respectively (×200, scale bar =10 μm). (E) Levels of IL-2, IL-4, IL-6, and IL-10 in LLC tumors were detected by an ELISA. (F) Levels of CCL2 in LLC tumors were analyzed by Western blot. Samples 1, 2, and 3 were taken from tumors in the normal saline (NS) group. Samples 4, 5, and 6 were taken from tumors in the recombinant human endostatin (rhES) group. Data are presented as mean ± SD. *P<0.05.

Abbreviations: IL, interleukin; SD, standard deviation; DAPI, 4′,6-diamidino-2-phenylindole; D, days.