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第46卷第10期 刘怡珂,李超凡,宋海燕,等. 鞣花酸靶向miR⁃18a/TSP⁃1轴减轻缺血性脑损伤[J].
2026年10月 南京医科大学学报(自然科学版),2026,46(10):1479-1491 ·1489 ·
A Bright⁃field Hoechst EdU Merge
B 100
Control 80
(%) 60 △△
EdU 40 ** ##
OGD 20
0
Control OGD Antagomir
NC
NC
Control OGD NC
C Antagomir
Cyclin D1 34 kDa
Antagomir β⁃actin 29 kDa
PCNA
42 kDa
D 0.8 △△ E 0.4 △△ G 400
PCNA protein expression 0.6 ** **## Cyclin D1 protein expression 0.3 ** **## Cell migration number 300 ** △△ **##
0.2
0.4
200
0.1
0.2
100
0
Control OGD NC 0 Control OGD NC Antagomir 0 Control OGD NC
Antagomir
Antagomir
F Control OGD NC Antagomir
I
400
Number of nodes 200 ** **##
H Control OGD NC Antagomir 300 * △△
100
0
Control OGD NC
Antagomir
J Control OGD NC Antagomir
100 nm
A,B:Representative fluorescence images of the EdU assay(A,×200)and quantification of EdU⁃positive cells(B). C-E:Western blot analysis of
PCNA and Cyclin D1 expression:representative bands(C)and quantification(D,E). F,G:Representative images of the Transwell migration assay
(F,×200)and quantification(G). H,I:Representative images of tube formation on Matrigel(H,×100)and quantification of total tube junctions(I).
*
**
J:Representative TEM images showing mitochondrial ultrastructure. Compared with the control group,P < 0.05,P < 0.01;compared with the OGD
△ △△ # ##
group,P < 0.05, P < 0.01;compared with the NC group,P < 0.05,P < 0.01(n=3).
图6 抑制miR⁃18a阻断了EA的促血管生成作用及线粒体保护效应
Figure 6 Inhibition of miR⁃18a abrogates the pro⁃angiogenic and mitochondrial protective effects of EA
叉预测与 Metascape 功能富集分析发现 miR⁃18a 的 作为强效内源性血管新生抑制因子,可通过直接抑
潜在靶基因主要富集于“生物过程调控”“发育过 制内皮细胞增殖、迁移及管形成能力,阻碍缺血后
程”“细胞过程”及“免疫/节律调控”等。其中,TSP⁃1 血管修复 [24] ,其编码基因Thbs1被预测为miR⁃18a的

