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Fig. 1 | BMC Cancer

Fig. 1

From: Modulation the crosstalk between tumor-associated macrophages and non-small cell lung cancer to inhibit tumor migration and invasion by ginsenoside Rh2

Fig. 1

RAW264.7 cells polarization into M2 macrophage. a Morphology of the polarized RAW264.7 cells to M1or M2 subsets.RAW264.7 cells were treated with LPS (100 ng/mL) plus INF-γ (20 ng/mL) for 48 h to differentiate into M1. RAW264.7 cells were treated withIL-4 (20 ng/mL) for 48 h to differentiate into M2. The scale bars indicate 200 μM. b Identification of the macrophages derived from RAW264.7 cells with specific markers FITC CD16/32 and APC CD206 by FACS. c Quantitation of CD206positive cells derived from RAW264.7 cells after different combination treatment for 48 h.**P < 0.01, compared with M0. d Quantitation of CD16/32 positive cells derived from RAW264.7 cells after different combination treatment for 48 h. **P < 0.01, compared with M0. e RNA was extracted from M1 and M2 macrophages differentiated from RAW264.7 cells. RT-PCR was used to quantitate TNFα, ARG-1, and INOS. * P < 0.05, compared with M0 control. f Morphology of the polarized THP-1 cells to M1 or M2 subsets. THP-1 cells were treated with LPS (100 ng/mL) plus INF-γ (20 ng/mL) for 48 h to differentiate into M1. THP-1 cells were treated with IL-4 (20 ng/mL) for 48 h to differentiate into M2. The scale bars indicate 200 μM. g Identification of the macrophages derived from THP-1 with specific markers FITC CD16/32 and APC CD206 by FACS. h Quantitation of CD206 positive cells differentiated from THP-1 cells after different combination treatment for 48 h. *P < 0.05, compared with M0. i Quantitation of CD16/32 positive cells differentiated from THP-1 cells after different combination treatment for 48 h. **P < 0.01, compared with M0. j RNA was extracted from M1 and M2 macrophages differentiated from THP-1 cells. RT-PCR was used to quantitate TNFα, ARG-1, and INOS. * P < 0.05, compared with M0 control

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