Page 75 - 《中国药科大学学报》2025年第5期

第 56 卷第 5 期 栾亚萁，等：医用臭氧对脓毒症肾损伤的治疗作用及其机制 607
A Kidney tissue B Kidney tissue C Kidney tissue

p-AMPK 62 kD SR-A1 50 kD IL-1β 22 kD
AMPK 60 kD β-actin 42 kD β-actin 42 kD
***
ns ** ** ns
1.0 1.5 1.5
* * ** **
0.8 1.0 1.0
Fold of control 0.6 Fold of control Fold of control
0.4
0.2 0.5 0.5
0 0 0
Comtrol LPS LPS+Ozone Ozone Comtrol LPS LPS+Ozone Ozone Comtrol LPS LPS+Ozone Ozone

D Kidney tissue E Kidney tissue F Kidney tissue
TNF-α 30 kD KIM-1 40 kD Bax 21 kD
β-actin 42 kD β-actin 42 kD β-actin 42 kD
ns ns
1.5 * * 1.0 ** ** 1.0 ns
** **
0.8 0.8
Fold of control Fold of control 0.6 Fold of control 0.6
1.0
0.4
0.4
0.5
0.2 0.2
0 0 0
Comtrol LPS LPS+Ozone Ozone Comtrol LPS LPS+Ozone Ozone Comtrol LPS LPS+Ozone Ozone

G Control LPS LPS+Ozone Ozone

Merge

KIM-1

DAPI

Figure 3 Ozone ameliorated kidney injury via upregulation of 5'-monophosphate-activated protein kinase (AMPK)/scavenger receptor
(SR)-A1 signaling ( x ± s, n=6)
A-F: Representative immunostaining and their quantification results for p-AMPK, SR-A1, IL-1β, TNF-α, kidney injury molecule (KIM)-1
and Bax in renal tissues; G: Representative confocal images of KIM-1 (Red)+tubules, scale bar=50 μm
*P<0.05, **P<0.01, ***P<0.001; ns: not significant
通过 Annexin V 标记循环系统中的微粒，检测 结果显示，模型小鼠循环 MPs 外膜 PS 的暴露水平