Evidence mapPaperPMID 39333622Full record

ArticleScientific reports2024

Integrating network pharmacology and experimental validation to decipher the pharmacological mechanism of DXXK in treating diabetic kidney injury.

Chenxu Zhang, Zhangxin Ji, Na Xu, Jingjing Yuan, Wen Zeng, Yadong Wang, Qing He, Jiaxing Dong, Xinyu Zhang, Dongmei Yang and 5 more

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Chenxu Zhang *Key Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, People's Republic of China.
Zhangxin Ji *Key Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, People's Republic of China.
Na XuState Key Laboratory of Tea Plant Biology and Utilization, School of Tea & Food Science and International Joint Laboratory On Tea Chemistry and Health Effects of Ministry of Education, Anhui Agricultural University, Hefei, 230036, Anhui, People's Republic of China.
Jingjing YuanKey Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, People's Republic of China.
Wen ZengResearch and Technology Center, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, People's Republic of China.
Yadong WangDepartment of Pathology, School of Integrative Medicine, Anhui University of Chinese Medicine, Hefei, 230012, Anhui, People's Republic of China.
Qing HeKey Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, People's Republic of China.
Jiaxing DongKey Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, People's Republic of China.
Xinyu ZhangKey Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, People's Republic of China.
Dongmei YangKey Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, People's Republic of China.
Wei JiangSchool of Nursing, Anhui Medical College, Furong Road Campus, Hefei, 230601, Anhui, People's Republic of China.
Yibo YanSecond Clinical Medical College, Anhui Medical University, Hefei, 230601, Anhui, People's Republic of China.
Wencui ShangSchool of Graduate, Anhui University of Chinese Medicine, Hefei, 230012, Anhui, People's Republic of China.
Jun ChuKey Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, People's Republic of China. chuj@ahtcm.edu.cn.
Quangen ChuKey Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, People's Republic of China. 286428483@qq.com.

Funding

Anhui Provincial Department of Education 2020 Key Project of Natural Science in University KJ2020A0383Open Fund of State Key Laboratory of Tea Plant Biology and Utilization SKLTOF20210101
6 · The paper itself

Abstract

Diabetes mellitus (DM) is a chronic metabolic disease that is highly susceptible to kidney injury. Di'ao XinXueKang capsules (DXXK) is a novel Chinese herbal medicine that has been used in clinical trials for the therapy of DM and kidney disease, but the underlying pharmacological mechanism remains unclear. This study aims to integrate network pharmacology, molecular docking and in vivo experiments to explore the potential mechanisms of DXXK in the treatment of diabetic kidney injury. The chemical constituents of DXXK were extracted from the ETCM and Batman-TCM databases, and then evaluated for their pharmacological activity via the Swiss ADME platform. Multiple disease databases were searched and integrated for DM-related targets. Overlapping targets were then collected to construct a protein-protein interaction (PPI) network. KEGG and GO enrichment analyses were performed based on the Metascape database, and molecular docking was performed using AutoDock Vina software. The main components in DXXK were analyzed by HPLC. The results of network pharmacology and molecular docking were validated in an animal model of DM induced by the combination of a high-fat diet (HFD) and streptozotocin (STZ). We screened and obtained 7 ingredients and identified dioscin, protodioscin, and pseudoprotodioscin as the major components of DXXK by HPLC. A total of 2,216 DM-related pathogenic genes were obtained from DrugBank, GeneCards, OMIM, and DisGeNET databases. KEGG and GO enrichment analyses indicated that the TGF-beta signaling pathway is a critical pathway associated with DM therapy. Molecular docking revealed that the ingredients in DXXK bind to the pivotal targets TGFβ1, Smad2, and Smad3. In diabetic mice, we found that DXXK alleviated diabetic symptoms, lowered blood glucose, improved insulin tolerance, and modulated lipid metabolism. Furthermore, DXXK attenuated renal lesions and fibrosis by downregulating TGFβ1, Smad2, and Smad3. Collectively, our results suggest that DXXK has the potential to regulate glucolipid metabolism in DM, and it may serve as a viable therapeutic option for renoprotection by inhibiting of the TGF-β1/Smad2/3 pathway.

Indexed as

Diabetes Mellitus, ExperimentalDiabetic NephropathiesDrugs, Chinese HerbalMolecular Docking SimulationNetwork PharmacologyAnimalsMaleMiceProtein Interaction MapsDrugs, Chinese Herbal

Identifiers

PMID39333622
PMCPMC11436795

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.