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. 2017 Apr 29;18(5):942. doi: 10.3390/ijms18050942

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© 2017 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Figure A4 — CE treatment inhibits IR-induced apoptosis and DNA damage in HSPCs. Mice were daily treated with the vehicle or CE as described in the Materials and Methods. Early apoptosis (Annexin V⁺PI⁻) (A), late apoptosis (Annexin V⁺PI⁺) (B) and MFI of γH2AX (C) in c-kit positive cells were measured on the 14th day after exposure to TBI; (D) A representative FACS analysis of the percentage of apoptosis in c-kit positive cells; (E) A representative analysis of γH2AX expression in c-kit positive cells by flow cytometry; (F) Gating strategy for the analysis of LSK apoptosis. CE treatment significantly reduced the percentage of cell apoptosis, and decreased the MFI of γH2AX in irradiated c-kit positive cells. All data are presented as means ± SEM (n = 5).

Figure A4 — CE treatment inhibits IR-induced apoptosis and DNA damage in HSPCs. Mice were daily treated with the vehicle or CE as described in the Materials and Methods. Early apoptosis (Annexin V⁺PI⁻) (A), late apoptosis (Annexin V⁺PI⁺) (B) and MFI of γH2AX (C) in c-kit positive cells were measured on the 14th day after exposure to TBI; (D) A representative FACS analysis of the percentage of apoptosis in c-kit positive cells; (E) A representative analysis of γH2AX expression in c-kit positive cells by flow cytometry; (F) Gating strategy for the analysis of LSK apoptosis. CE treatment significantly reduced the percentage of cell apoptosis, and decreased the MFI of γH2AX in irradiated c-kit positive cells. All data are presented as means ± SEM (n = 5).