Material basis and molecular mechanisms of Chaihuang Qingyi Huoxue Granule in the treatment of acute pancreatitis based on network pharmacology and molecular docking-based strategy

PI3K/AKT/mTOR通路 AKT1型 信号转导 蛋白激酶B 小桶 免疫印迹 药理学 磷酸化 细胞凋亡 化学 生物 癌症研究 细胞生物学 生物化学 基因 基因表达 基因本体论
作者
Jia Yang,Yuhong Jiang,Xin Zhou,Jiaqi Yao,Yangyang Wang,Jian‐Qin Liu,Pengcheng Zhang,Wenfu Tang,Zhi Li
出处
期刊:Frontiers in Immunology [Frontiers Media SA]
卷期号:15
标识
DOI:10.3389/fimmu.2024.1353695
摘要

Objectives This study aimed to analyze active compounds and signaling pathways of CH applying network pharmacology methods, and to additionally verify the molecular mechanism of CH in treating AP. Materials and methods Network pharmacology and molecular docking were firstly used to identify the active components of CH and its potential targets in the treatment of AP. The pancreaticobiliary duct was retrogradely injected with sodium taurocholate (3.5%) to create an acute pancreatitis (AP) model in rats. Histological examination, enzyme-linked immunosorbent assay, Western blot and TUNEL staining were used to determine the pathway and mechanism of action of CH in AP. Results Network pharmacological analysis identified 168 active compounds and 276 target proteins. In addition, there were 2060 targets associated with AP, and CH had 177 targets in common with AP. These shared targets, including STAT3, IL6, MYC, CDKN1A, AKT1, MAPK1, MAPK3, MAPK14, HSP90AA1, HIF1A, ESR1, TP53, FOS, and RELA, were recognized as core targets. Furthermore, we filtered out 5252 entries from the Gene Ontology(GO) and 186 signaling pathways from the Kyoto Encyclopedia of Genes and Genomes(KEGG). Enrichment and network analyses of protein-protein interactions predicted that CH significantly affected the PI3K/AKT signaling pathway, which played a critical role in programmed cell death. The core components and key targets showed strong binding activity based on molecular docking results. Subsequently, experimental validation demonstrated that CH inhibited the phosphorylation of PI3K and AKT in pancreatic tissues, promoted the apoptosis of pancreatic acinar cells, and further alleviated inflammation and histopathological damage to the pancreas in AP rats. Conclusion Apoptosis of pancreatic acinar cells can be enhanced and the inflammatory response can be reduced through the modulation of the PI3K/AKT signaling pathway, resulting in the amelioration of pancreatic disease.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
orixero应助amber采纳,获得10
刚刚
科目三应助万刈采纳,获得10
1秒前
2秒前
Str0n发布了新的文献求助10
2秒前
QAQ发布了新的文献求助10
3秒前
领导范儿应助夜之樱花采纳,获得10
4秒前
4秒前
ssffzb2008完成签到,获得积分10
4秒前
SCINEXUS应助鱼鱼玉玉米采纳,获得30
5秒前
hhhhhhhhhh发布了新的文献求助30
5秒前
keepmoving_12完成签到 ,获得积分10
6秒前
6秒前
7秒前
sjsjjj完成签到,获得积分20
7秒前
laoxiaozi发布了新的文献求助30
7秒前
8秒前
8秒前
8秒前
共享精神应助aaa采纳,获得10
8秒前
orixero应助Alicer采纳,获得10
8秒前
打打应助狄语蕊采纳,获得10
8秒前
9秒前
9秒前
9秒前
11秒前
11秒前
11秒前
于听枫完成签到 ,获得积分10
11秒前
万能图书馆应助yy采纳,获得10
11秒前
12秒前
12秒前
阳佟初兰发布了新的文献求助10
12秒前
温柔难敌完成签到,获得积分10
13秒前
phero发布了新的文献求助10
13秒前
jsmmm完成签到,获得积分10
14秒前
借两颗星星关注了科研通微信公众号
14秒前
14秒前
Lucas应助嗯哼采纳,获得10
14秒前
jessica发布了新的文献求助30
14秒前
15秒前
高分求助中
Sustainability in Tides Chemistry 2000
The ACS Guide to Scholarly Communication 2000
Studien zur Ideengeschichte der Gesetzgebung 1000
TM 5-855-1(Fundamentals of protective design for conventional weapons) 1000
Threaded Harmony: A Sustainable Approach to Fashion 810
Pharmacogenomics: Applications to Patient Care, Third Edition 800
Gerard de Lairesse : an artist between stage and studio 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3075882
求助须知:如何正确求助?哪些是违规求助? 2728806
关于积分的说明 7506117
捐赠科研通 2377016
什么是DOI,文献DOI怎么找? 1260379
科研通“疑难数据库(出版商)”最低求助积分说明 610960
版权声明 597151