Page 99 - 《中国药科大学学报》2025年第5期

第 56 卷第 5 期 更 桑，等：基于网络药理学探究藏药佐汤卡擦丸治疗高血压的药理作用机制 631
A 0 week B 6 weeks C 12 weeks

200 **** **** **** **** 250 **** # 300 **** ###
Systolic pressure/mmHg 150 Systolic pressure/mmHg 150 Systolic pressure/mmHg 200
200

100
100
100
50
0 50 0 0
SHR+ZTKCW-M
SHR+ZTKCW-M
SHR+ZTKCW-M
SHR+ZTKCW-L SHR+ZTKCW-H SHR+ZTKCW-L SHR+ZTKCW-H SHR+ZTKCW-L SHR+ZTKCW-H
WKY SHR WKY SHR WKY SHR
D 0 week E 6 weeks F 12 weeks
150 **** **** **** **** 200 **** 200 ****
Diastolic pressure/mmHg 100 Diastolic pressure/mmHg 150 # Diastolic pressure/mmHg 150 ##

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0 0 0
SHR+ZTKCW-L SHR+ZTKCW-H SHR+ZTKCW-L SHR+ZTKCW-H SHR+ZTKCW-L SHR+ZTKCW-H
SHR+ZTKCW-M
SHR+ZTKCW-M
SHR+ZTKCW-M
WKY SHR WKY SHR WKY SHR
G 200 0 week H 200 **** 6 weeks ## I 200 **** 12 weeks ####
Mean arterial pressure/mmHg 150 **** **** **** **** Mean arterial pressure/mmHg 150 Mean arterial pressure/mmHg 150

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100
100
50
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0
SHR+ZTKCW-M
SHR+ZTKCW-M
SHR+ZTKCW-L SHR+ZTKCW-H SHR+ZTKCW-L SHR+ZTKCW-H SHR+ZTKCW-L SHR+ZTKCW-H
SHR+ZTKCW-M
WKY SHR 0 WKY SHR 0 WKY SHR
Figure 4 Therapeutic effects of ZTKCW on spontaneously hypertensive rats (SHR) ( x ± s, n=10)
A-C: Systolic pressure of Wistar Kyoto rats (WKY) group (control), SHR group, SHR+ZTKCW-L group (0.41 g/kg), SHR+ZTKCW-M group
(0.82 g/kg), and SHR+ZTKCW-H group (1.64 g/kg) before dosing (A), 6 weeks after dosing (B) and 12 weeks after dosing (C); D-F:
Diastolic pressure of WKY group (control), SHR group, SHR+ZTKCW-L group (0.41 g/kg), SHR+ZTKCW-M group (0.82 g/kg), and
SHR+ZTKCW-H group (1.64 g/kg) before dosing (D), 6 weeks after dosing (E) and 12 weeks after dosing (F); G-I: Mean arteria pressure
of WKY group (control), SHR group, SHR+ZTKCW-L group (0.41 g/kg), SHR+ZTKCW-M group (0.82 g/kg), and SHR+ZTKCW-H group
(1.64 g/kg) before dosing (G), 6 weeks after dosing (H) and 12 weeks after dosing (I)
###
##
#
****P<0.000 1 vs WKY group, P<0.05, P<0.01, P<0.001, #### P<0.000 1 vs SHR group
的高血压和细胞凋亡，减少 ROS 产生 。AngⅡ是 增加白细胞介素-6（interleukin-6，IL-6）的表达 ，而
[9]
[11]
一种缩血管活性成分，除了导致血压升高和细胞凋 IL-6 以 及 其 他 炎 症 因 子 ， 包 括 肿 瘤 坏 死 因 子
亡，也能够刺激 ROS 生成，从而抑制内皮一氧化氮 α（tumour necrosis factor-α，TNF-α）、白细胞介素-1
合酶（endothelial nitric oxide synthase，eNOS），减少 （interleukin-1，IL-1）等在血管中的堆积会进一步诱
一氧化氮（NO）生成，进一步阻碍血管舒张 。AngⅡ 发血管纤维化 。NO 是内皮源性舒张因子，NO 含
[10]
[12]
也参与血管重塑，通过激活 JAK2/STAT3 信号通路 量不足导致机体舒血管效应受损，而 NO 过多则会