Investigating the mechanism of <italic>Chaihu Sanshen Capsule</italic>(柴胡三参胶囊) in mitigating doxorubicin-induced cardiovascular toxicity

<sec> <title>目的</title> 探讨柴胡三参胶囊治疗阿霉素心血管毒性的可能作用机制。 </sec> <sec> <title>方法</title> 用胰蛋白酶和Ⅱ型胶原酶联合消化法分离出新生大鼠心室肌细胞(NRVM),用阿霉素诱导生成NRVM损伤模型,分为对照(NT)组,阿霉素处理(Model)组和柴胡三参胶囊预处理(CHSSC)组,采用CCK8法检测细胞活力,化学荧光检测ROS,试剂盒检测丙二醛(MDA)等氧化指标,TUNEL及流式细胞检测细胞凋亡,Western blot法检测c-Caspase3、p-p38MAPK、Bcl-2、Bax表达情况。 </sec> <sec> <title>结果</title> 与NT组比较,Model组以阿霉素剂量依赖性方式降低NRVM细胞活力,诱发细胞凋亡(<italic>P</italic>&lt;0.01);ROS荧光强度增强;MDA升高(<italic>P</italic>&gt;0.05),SOD降低(<italic>P</italic>&lt;0.05),GPX下降(<italic>P</italic>&gt;0.05);p-P38MAPK、c-Caspase3、Bax升高(<italic>P</italic>&lt;0.01),Bcl-2下降(<italic>P</italic>&lt;0.01)。与Model组比较,CHSSC组增加细胞活力,减轻细胞凋亡(<italic>P</italic>&lt;0.01);ROS荧光减弱(<italic>P</italic>&lt;0.05);MDA下降(<italic>P</italic>&gt;0.05),SOD、GPX升高(<italic>P</italic>&gt;0.05);p-P38MAPK、c-Caspase3、Bax降低(<italic>P</italic>&lt;0.01),Bcl-2增加(<italic>P</italic>&lt;0.01)。 </sec> <sec> <title>结论</title> 柴胡三参胶囊可能通过影响阿霉素诱导的ROS生成,调节MDA、GPX、SOD水平,调控c-Caspase3和p-P38MAPK、Bax、Bcl-2蛋白表达从而逆转阿霉素诱导的氧化应激和原代新生大鼠心室肌细胞的凋亡。 </sec>

Authors

Publication Details

Journal
Lishizhen medicine and materia medica research
Published
2025-05-01
DOI
https://doi.org/10.70976/j.1008-0805.szgygy-2025-1007
Primary Topic
Cancer Treatment and Pharmacology
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Investigating the mechanism of &lt;italic&gt;Chaihu Sanshen Capsule&lt;/italic&gt;(柴胡三参胶囊) in mitigating doxorubicin-induced cardiovascular toxicity

Jianhe LIU, Lihuai WANG, Christopher M. Tan, Zhihui Zhang et al.
Lishizhen medicine and materia medica research
Cancer Treatment and Pharmacology
article

Investigating the mechanism of &lt;italic&gt;Chaihu Sanshen Capsule&lt;/italic&gt;(柴胡三参胶囊) in mitigating doxorubicin-induced cardiovascular toxicity

Jianhe LIU, Lihuai WANG, Christopher M. Tan, Zhihui Zhang, Yang Xiao
article en

Abstract

<sec> <title>目的</title> 探讨柴胡三参胶囊治疗阿霉素心血管毒性的可能作用机制。 </sec> <sec> <title>方法</title> 用胰蛋白酶和Ⅱ型胶原酶联合消化法分离出新生大鼠心室肌细胞(NRVM),用阿霉素诱导生成NRVM损伤模型,分为对照(NT)组,阿霉素处理(Model)组和柴胡三参胶囊预处理(CHSSC)组,采用CCK8法检测细胞活力,化学荧光检测ROS,试剂盒检测丙二醛(MDA)等氧化指标,TUNEL及流式细胞检测细胞凋亡,Western blot法检测c-Caspase3、p-p38MAPK、Bcl-2、Bax表达情况。 </sec> <sec> <title>结果</title> 与NT组比较,Model组以阿霉素剂量依赖性方式降低NRVM细胞活力,诱发细胞凋亡(<italic>P</italic>&lt;0.01);ROS荧光强度增强;MDA升高(<italic>P</italic>&gt;0.05),SOD降低(<italic>P</italic>&lt;0.05),GPX下降(<italic>P</italic>&gt;0.05);p-P38MAPK、c-Caspase3、Bax升高(<italic>P</italic>&lt;0.01),Bcl-2下降(<italic>P</italic>&lt;0.01)。与Model组比较,CHSSC组增加细胞活力,减轻细胞凋亡(<italic>P</italic>&lt;0.01);ROS荧光减弱(<italic>P</italic>&lt;0.05);MDA下降(<italic>P</italic>&gt;0.05),SOD、GPX升高(<italic>P</italic>&gt;0.05);p-P38MAPK、c-Caspase3、Bax降低(<italic>P</italic>&lt;0.01),Bcl-2增加(<italic>P</italic>&lt;0.01)。 </sec> <sec> <title>结论</title> 柴胡三参胶囊可能通过影响阿霉素诱导的ROS生成,调节MDA、GPX、SOD水平,调控c-Caspase3和p-P38MAPK、Bax、Bcl-2蛋白表达从而逆转阿霉素诱导的氧化应激和原代新生大鼠心室肌细胞的凋亡。 </sec>

Lishizhen medicine and materia medica researchVol. 36(10)
Zero hunger
Openalex Percentile: Top 72%
Cancer Treatment and Pharmacology
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.