机构:[1]Department of Nephrology, Wuhan Hospital of Traditional Chinese and Western Medicine, Wuhan, China[2]State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China广东省中医院[3]Department of Respiratory, The Third Affiliated Hospital, Beijing University of Chinese Medicine, Beijing, China[4]Department of Nephrology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China大德路总院肾内科大德路总院肾内科广东省中医院
Background: Renal anemia occurs frequently in patients with chronic kidney disease (CKD) and is related to chronic inflammation. Danggui Buxue Decoction (DBD) can treat anemia and improve the chronic inflammation. However, whether DBD treatment attenuates anemia by regulating inflammation in CKD patients with renal anemia is unknown. Therefore, this study explored inflammation-related network targets of DBD in renal anemia therapy and verified the interaction between DBD active ingredients and inflammatory proteins by molecular docking. Methods: The main effective components and targets of DBD were screened using the Traditional Chinese Medicine System Pharmacology Database and Analysis Platform. Renal anemia-related biomolecules were searched in the GeneCards, OMIM, TTD, Pharmgkb, and DrugBank databases. Protein-protein interaction (PPI) data were downloaded from the STRING database and core targets were obtained. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses for core targets were performed. Finally, active ingredients and core biomolecules were determined using molecular docking. Results: Twenty-two active components and 158 targets for DBD treatment of renal anemia were screened, and an "ingredient-target" network was constructed. Twenty core target genes were screened from the PPI data. Vascular endothelial growth factor A, Signal Transducer and Activator of transcription 1, C-X-C motif chemokine ligand 8, post-transcriptional gene silencing 2, and interleukin (IL)-1 beta were identified as inflammatory proteins. GO items related to inflammation and DBD included lipopolysaccharide, cellular response to chemical stress, and oxidative stress-related reactions. KEGG enrichment analyses showed that core inflammatory pathways mainly involved the IL-17 signaling pathway, tumor necrosis factor signaling pathway, and phosphoinositide 3-kinase-protein kinase B signaling pathway. Molecular docking results indicated that the binding energy of quercetin, an active ingredient of DBD, to the 5 core proteins was less than -6 kcal center dot mol(-1). Conclusion: DBD might have protective effects against renal anemia by improving inflammation. Quercetin might modulate multiple inflammatory proteins and pathways.
基金:
Project of Science and Technology Department of Guangdong Province [2016A020226042]
第一作者机构:[1]Department of Nephrology, Wuhan Hospital of Traditional Chinese and Western Medicine, Wuhan, China[2]State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China
共同第一作者:
通讯作者:
通讯机构:[1]Department of Nephrology, Wuhan Hospital of Traditional Chinese and Western Medicine, Wuhan, China[*1]Department of Nephrology, Wuhan Hospital of Traditional Chinese and Western Medicine, No. 215 Zhongshan Avenue, Wuhan 430022, Hubei Province, China
推荐引用方式(GB/T 7714):
Tu Can,Huang Guirui,Li Chuang,et al.Exploring Mechanisms by Which Danggui Buxue Decoction Regulates Inflammation and Improves Renal Anemia Based on Network Pharmacology[J].NATURAL PRODUCT COMMUNICATIONS.2022,17(5):doi:10.1177/1934578X221093905.
APA:
Tu, Can,Huang, Guirui,Li, Chuang,Cheng, Li,Min, Yonglong...&Xiong, Fei.(2022).Exploring Mechanisms by Which Danggui Buxue Decoction Regulates Inflammation and Improves Renal Anemia Based on Network Pharmacology.NATURAL PRODUCT COMMUNICATIONS,17,(5)
MLA:
Tu, Can,et al."Exploring Mechanisms by Which Danggui Buxue Decoction Regulates Inflammation and Improves Renal Anemia Based on Network Pharmacology".NATURAL PRODUCT COMMUNICATIONS 17..5(2022)