Cardiac protection of <i>Bauhinia championii</i> against reperfusion injury

Chen, Yunfang; Chen, Wei-Yu; Chung, Ching‐Hu; Kuo, Chao‐Lin; Lee, An‐Sheng

doi:10.1002/tox.22912

Cited by 7 publications

(4 citation statements)

References 28 publications

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“…Extraction of the herb was prepared according to previous protocols [ 29 ]. Briefly, the herb of Bauhinia championii was mixed with water at a solid-to-liquid ratio of 1:10 for conventional heating reflux extraction.…”

Section: Methodsmentioning

confidence: 99%

Bauhinia championii alleviates extracellular matrix degradation in IL-1β induced chondrocytes via miRNA-145-5p/TLR4/NF-κB axis

Lin,

Huang,

Lin

et al. 2023

Heliyon

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Section: Methodsmentioning

confidence: 99%

Bauhinia championii alleviates extracellular matrix degradation in IL-1β induced chondrocytes via miRNA-145-5p/TLR4/NF-κB axis

Lin,

Huang,

Lin

et al. 2023

Heliyon

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“…It could also block Na + channels to lessen action potential depolarization and lessen necroptosis, which prevented I/R-caused ventricular arrhythmias and cardiomyocyte death. BC may be a novel possibility for the treatment of myocardial infarction and ventricular arrhythmias because it also inhibits the oxidation of CaMK, which lowers I/R-induced necroptosis [99].…”

Section: Chinese Medicinementioning

confidence: 99%

Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia–Reperfusion Injury

Zhang

Zang

et al. 2023

JCDD

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Cardiovascular disease morbidity/mortality are increasing due to an aging population and the rising prevalence of diabetes and obesity. Therefore, innovative cardioprotective measures are required to reduce cardiovascular disease morbidity/mortality. The role of necroptosis in myocardial ischemia–reperfusion injury (MI–RI) is beyond doubt, but the molecular mechanisms of necroptosis remain incompletely elucidated. Growing evidence suggests that MI–RI frequently results from the superposition of multiple pathways, with autophagy, ferroptosis, and CypD-mediated mitochondrial damage, and necroptosis all contributing to MI–RI. Receptor-interacting protein kinases (RIPK1 and RIPK3) as well as mixed lineage kinase domain-like pseudokinase (MLKL) activation is accompanied by the activation of other signaling pathways, such as Ca2+/calmodulin-dependent protein kinase II (CaMKII), NF-κB, and JNK-Bnip3. These pathways participate in the pathological process of MI–RI. Recent studies have shown that inhibitors of necroptosis can reduce myocardial inflammation, infarct size, and restore cardiac function. In this review, we will summarize the molecular mechanisms of necroptosis, the links between necroptosis and other pathways, and current breakthroughs in pharmaceutical therapies for necroptosis.

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“…Myocardial ischemia-reperfusion injury (MIRI) is defined as tissue damage that occurs when early and rapid coronary flow returns to the heart after ischemia, frequently exacerbating the myocardial injury [ 2 ]. Four different forms of myocardial reperfusion injury are recognized: lethal arrhythmias, lethal myocardial reperfusion injury, myocardial stunning, and microvascular obstruction [ 3 ]. MIRI is a significant contributor to the morbidity and mortality of coronary artery disease [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

TMT-based quantitative proteomics analysis of the effects of Jiawei Danshen decoction myocardial ischemia-reperfusion injury

et al. 2022

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Background Every year, approximately 17 million people worldwide die due to coronary heart disease, with China ranking second in terms of the death toll. Myocardial ischemia-reperfusion injury (MIRI) significantly influences cardiac function and prognosis in cardiac surgery patients. Jiawei Danshen Decoction (JWDSD) is a traditional Chinese herbal prescription that has been used clinically for many years in China to treat MIRI. The underlying molecular mechanisms, however, remain unknown. To investigate the proteomic changes in myocardial tissue of rats given JWDSD for MIRI therapy-based proteomics. Methods MIRI rat model was created by ligating/releasing the left anterior descending coronary artery. For seven days, the drugs were administered twice daily. The model was created following the last drug administration. JWDSD's efficacy in improving MIRI was evaluated using biochemical markers and cardiac histology. Tandem mass tag-based quantitative proteomics (TMT) technology was also used to detect proteins in the extracted heart tissue. To analyze differentially expressed proteins (DEPs), bioinformatics analysis, including gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathways, were employed. Furthermore, western blotting confirmed the potential targets regulated by JWDSD. Results The histopathologic characteristics and biochemical data showed JWDSD's protective effects on MIRI rats. A total of 4549 proteins were identified with FDR (false discovery rate) ≤1%. Twenty overlapping were identified (162 DEPs and 45 DEPs in Model/Control or JWDSD/Model group, respectively). Of these DEPs, 16 were regulated by JWDSD. GO analysis provided a summary of the deregulated protein expression in the categories of biological process (BP), cell component (CC), and molecular function (MF). KEGG enrichment analysis revealed that the signaling pathways of neutrophil extracellular trap formation, RNA polymerase, serotonergic synapse, and linoleic acid metabolism are all closely related to JWDSD effects in MIRI rats. Furthermore, T-cell lymphoma invasion and metastasis 1 (TIAM1) was validated using western blotting, and the results were consistent with proteomics data. Conclusions Our study suggests that JWDSD may exert therapeutic effects through multi-pathways regulation in MIRI treatment. This work may provide proteomics clues for continuing research on JWDSD in treating MIRI.

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Cardiac protection of Bauhinia championii against reperfusion injury

Cited by 7 publications

References 28 publications

Bauhinia championii alleviates extracellular matrix degradation in IL-1β induced chondrocytes via miRNA-145-5p/TLR4/NF-κB axis

Bauhinia championii alleviates extracellular matrix degradation in IL-1β induced chondrocytes via miRNA-145-5p/TLR4/NF-κB axis

Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia–Reperfusion Injury

TMT-based quantitative proteomics analysis of the effects of Jiawei Danshen decoction myocardial ischemia-reperfusion injury

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