Evidence map›Paper›PMID 39380225›Full record

ArticleJournal of traditional Chinese medicine = Chung i tsa chih ying wen pan2024

Neuroprotective effect of Naochuxue prescription on intracerebral hemorrhage: inhibition of autophagy downregulating high mobility group box-1.

Jin Hong, Wang Xinna, Wang Ruonan, L I Jinjian, Y U Junchao, Zhao Dexi, Zhai Lu

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Article in Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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7 authors.

Jin HongCollege of Chinese medicine, Changchun University of Chinese Medicine, Changchun 13000, China.
Wang XinnaDepartment of Encephalopathy, the Affiliated Hospital of Changchun University of Chinese Medicine, Changchun 130000, China.
Wang RuonanCollege of nursing, Changchun University of Chinese Medicine, Changchun 13000, China.
L I JinjianDepartment of Encephalopathy, the Affiliated Hospital of Changchun University of Chinese Medicine, Changchun 130000, China.
Y U JunchaoDepartment of Encephalopathy, the Affiliated Hospital of Changchun University of Chinese Medicine, Changchun 130000, China.
Zhao DexiDepartment of Encephalopathy, the Affiliated Hospital of Changchun University of Chinese Medicine, Changchun 130000, China.
Zhai LuResearch Center of Traditional Chinese Medicine, the First Affiliated Hospital of Changchun University of Chinese Medicine, Changchun 13000, China.

Funding

Anti-inflammatory Mechanism of Naochuxue Prescription based on Toll-like Receptor 4/AKT/Forkhead Box O3 Pathway Regulation of Microglia Autophagy 2021JC070Study on the Mechanism of Cerebral Hematoma Resorption by Intervening Cerebral Hemorrhage Prescription based on the Method of Breaking Blood and Removing Blood Stasis 81774224
6 · The paper itself

Abstract

objectiveTo determine the molecular mechanisms underlying the neuroprotective effects of Naochuxue prescription (,NCXP) in rats with intracerebral hemorrhage (ICH).

methodsSprague-Dawley rats were injected with collagenase to generate ICH models, which were then randomly divided into six groups, including control, sham, model, and three intervention groups. The intervention groups received different doses of NCXP (0.13, 0.26, and 0.52 g/kg) daily for 10 d. High-performance liquid chromatography (HPLC) was used to analyze the chemical characteristics of NCXP. The neurobehavioral outcomes of the rats were evaluated using neurological deficit scores (Zea Longa 5) and the corner turn test. Pathomorphological changes in perihematomal tissues after ICH were observed using hematoxylin and eosin staining. Immunohistochemistry (IHC) was used to detect the inflammation expression of interleukin 6 (IL-6) and toll-like receptor 4 (TLR4). High mobility group box-1 (HMGB1), Beclin1, microtubule-associated protein 1 light chain 3 beta (LC3), and sequestosome 1 (p62) were detected using real-time quantitative polymerase chain reaction and Western blotting in perihematomal tissues.

resultsHPLC showed that the NCXP had good stability. Rats with ICH had severe neurological function deficits compared to the control group. IHC results showed that NCXP significantly downregulated the expression of the inflammatory proteins IL-6 and TLR4. ICH rats treated with NCXP showed less neurological injury than the model group, accompanied by a significantly decreased expression of HMGB1, Beclin1, and LC3 and an increased expression of p62.

conclusionsThe neuroprotective effect of NCXP alleviated inflammation and autophagy possibly by downregulating HMGB1 expression. However, further research on the signaling pathways is required to verify this hypothesis.

Indexed as

AutophagyCerebral HemorrhageDrugs, Chinese HerbalHMGB1 ProteinNeuroprotective AgentsRats, Sprague-DawleyAnimalsBeclin-1Down-RegulationHumansInterleukin-6MaleRatsToll-Like Receptor 4Beclin-1Drugs, Chinese HerbalHMGB1 ProteinInterleukin-6Neuroprotective AgentsToll-Like Receptor 4autophagyHMGB proteinsinflammationintracerebral hemorrhageNaochuxue prescription

Identifiers

PMID39380225
PMCPMC11462531

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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 OpenQuestion graph.