Buyang huanwu decoction protects against cerebral ischemia-reperfusion injury by inhibiting complement and coagulation cascades: A proteomics and experimental study.

Phytomedicine

Key Laboratory of Hunan Provincial for Integrated Traditional Chinese and Western Medicine on Prevention and Treatment of Cardio-Cerebral Diseases, Hunan University of Chinese Medicine, Changsha, Hunan, 410208, China. Electronic address:

Published: August 2025


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Objective: Proteomics Approach to Investigate the Mechanism of Buyang Huanwu Decoction(BYHWD) in Ameliorating Cerebral Ischemia-Reperfusion Injury through Inhibition of Complement and Coagulation Cascade Activation.

Methods: A Rat Model of Qi Deficiency and Blood Stasis Induced Cerebral Ischemia-Reperfusion Injury Was Established Using Exhaustive Swimming Combined with Middle Cerebral Artery Occlusion Model(MCAO). The therapeutic effects were evaluated through neurological scoring, TTC staining, and HE staining. Proteomics analysis revealed that Buyang Huanwu Decoction alleviates brain tissue damage by inhibiting the activation of complement and coagulation cascade pathways.

Results: In vivo and in vitro experiments demonstrated that Buyang Huanwu Decoction significantly improves neurological function, reduces infarct size and brain edema, inhibits the activation of complement and coagulation cascades, increases the release of anti-inflammatory factors, suppresses the release of pro-inflammatory factors, improves the blood-brain barrier, and inhibits abnormal synaptic cleavage.

Conclusion: In summary, BYHWD can improve brain tissue injury in cerebral ischemia-reperfusion injury with Qi deficiency and blood stasis syndrome. The mechanism may involve the inhibition of complement and coagulation cascade activation by BYHWD, thereby suppressing the inflammatory response, alleviating blood-brain barrier damage, and abnormal synaptic pruning, ultimately improving brain tissue injury after cerebral ischemia.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.phymed.2025.157205DOI Listing

Publication Analysis

Top Keywords

complement coagulation
20
buyang huanwu
16
cerebral ischemia-reperfusion
16
ischemia-reperfusion injury
16
huanwu decoction
12
coagulation cascade
12
brain tissue
12
coagulation cascades
8
inhibition complement
8
deficiency blood
8

Similar Publications

Background: Colorectal cancer (CRC) is a complex, heterogeneous disease characterized by frequent relapses and metastasis. Previous studies have reported that the invasion and progression of CRC in several cases can be controlled by targeting fusion genes. This study aimed to screen for potent fusion transcripts as potential molecular biomarkers and therapeutic targets for metastatic CRC (mCRC) using an approach.

View Article and Find Full Text PDF

Purpose: Urosepsis, a condition caused by a urinary tract infection spreading to the bloodstream, has a complex epigenetic behavior in its cellular and molecular pathophysiology. The objective of this study was to identify relevant genes and signaling pathways in adult urosepsis through a bioinformatic analysis of differentially expressed genes (DEGs).

Materials And Methods: In this in-silico study, the GSE69528 dataset, containing 138 total RNA blood samples from patients with sepsis and uninfected controls, was obtained from the Gene Expression Omnibus (GEO) database.

View Article and Find Full Text PDF

Role of monocytes in the pathogenesis of antiphospholipid syndrome and potential therapeutic targets (Review).

Mol Med Rep

November 2025

Department of Rheumatology and Immunology, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi Zhuang Autonomous Region 530016, P.R. China.

Antiphospholipid syndrome (APS) is an autoimmune disorder characterized primarily by arterial and/or venous thrombosis, obstetric complications and persistent positivity for antiphospholipid antibodies (aPLs). It has been proposed that the pathogenesis of APS is closely associated with vascular endothelial cell activation, complement activation and platelet activation. Notably, APS may be key to understanding the relationship between innate immune cells, and thrombosis and obstetric complications.

View Article and Find Full Text PDF

Characterization of formaldehyde-induced hepatotoxicity based on proteometabolomic analysis.

Toxicol Lett

September 2025

College of Pharmacy, Kyungpook National University, Daegu 41566, Republic of Korea; School of Pharmacy, Sungkyunkwan University, Suwon 16419, Republic of Korea. Electronic address:

Formaldehyde (FA) is a well-known environmental toxicant used in various industries, including biomedical, agriculture, and textiles, but poses significant health risks. Despite extensive research, the exact hepatotoxic mechanism of FA remains unclear. This study investigated FA-induced liver toxicity through an integrative analysis of proteomics and metabolomics in rat models, identifying 84 differentially expressed proteins and 66 metabolites.

View Article and Find Full Text PDF

C1 inhibitor: from complement system to bradykinin angioedema.

Curr Opin Immunol

September 2025

Univ. Grenoble Alpes, CNRS, CEA, UMR5075, IBS, Laboratoire d'Immunologie, CHU Grenoble Alpes, 38000 Grenoble, France.

C1 Inhibitor (C1INH) is a crucial regulator of multiple plasmatic pathways, including complement, coagulation, kallikrein-kinin systems, and fibrinolysis. C1INH deficiency results in the downstream overproduction of the vasoactive peptide bradykinin (BK), the primary mediator of angioedema (AE), a rare disease characterized by unpredictable attacks of swelling in various locations of the body. C1INH deficiency can be hereditary (caused by a mutation in SERPING1 gene) or acquired (frequently underlying lymphoproliferative disease); C1INH level and functional assays are the golden standard for biological diagnosis of C1INH deficiency.

View Article and Find Full Text PDF