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A B 100
Bright⁃field Hoechst EdU Merge
80
Control （%） 60 ** △ * △△

EdU 40 **

20
OGD 0
Control 25 μmol/L EA
OGD
50 μmol/L EA
μmol/L EA
50 μmol/L EA
25 C Control OGD 25 μmol/L EA
μmol/L EA Cyclin D1 34 kDa
PCNA
29 kDa
50 β⁃actin 42 kDa
D E G
0.8 * △△ 400
Cyclin D1 protein expression 0.3 ** * * △ PCNA protein expression 0.4 ** Cell migration number 300 ** ** △ △△
0.4
0.6
200
0.2
0.2
0.1
100
0
OGD
50 μmol/L EA
OGD
Control 25 μmol/L EA 0 Control 25 μmol/L EA 0 Control 25 μmol/L EA
OGD
50 μmol/L EA
50 μmol/L EA
F Control OGD 25 μmol/L EA 50 μmol/L EA

I
500
400
Number of nodes 300 ** △
H Control OGD 25 μmol/L EA 50 μmol/L EA * △△

200
100 **
0
OGD
Control 25 μmol/L EA
50 μmol/L EA
J Control OGD 25 μmol/L EA 50 μmol/L EA

100 nm

A，B：Cell proliferation was detected by EdU assay（green）. Nuclei were counterstained with Hoechst（blue）（×200）. C-E：Western blot analysis of
PCNA and Cyclin D1 expression with β⁃actin as the loading control. F，G：Transwell migration assay：representative images（F，×200）and quantification
of migrated cells（G）. H，I：Tube formation assay on Matrigel：representative images（H，×100）and quantification of total junctions（I）. J：Mitochon⁃
**
*
drial ultrastructure observed by transmission electron microscopy（TEM）. Compared with the control group，P < 0.05，P < 0.01；compared with the OGD
△△
△
group，P < 0.05， P < 0.01（n=3）.
图2 EA恢复OGD损伤的RBMEC的血管新生功能并保护线粒体超微结构
Figure 2 EA restores angiogenic functions and preserves mitochondrial ultrastructure in OGD⁃injured RBMEC