Calycosin decreases cerebral ischemia/reperfusion injury by suppressing ACSL4-dependent ferroptosis

Liu, Hui; Zhao, Zongbo; Yan, Manyun; Zhang, Qiu; Jiang, Tingwang; Xue, Jianzhong

doi:10.1016/j.abb.2022.109488

Cited by 25 publications

(14 citation statements)

References 41 publications

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“…35 Calycosin exerts neuroprotection effects against cerebral I/R injury by inhibiting ACSL4-dependent ferroptosis. 36 Consistent with these reports, in this study, sevoflurane was found to inhibit the occurrence of ferroptosis events in MCAO rat brain and OGD/R-treated HT22 cells, which were represented by reduced iron content, decreased expression of TFR1 and FHT1, and increased expression of ACSL4 and GPX4. However, previous studies have shown that sevoflurane has different effects on ferroptosis in different cells and conditions.…”

Section: Discussionsupporting

confidence: 91%

Sevoflurane Postconditioning Attenuates Cerebral Ischemia-Reperfusion Injury by Inhibiting SP1/ACSL4-Mediated Ferroptosis

Lyu

2023

Hum Exp Toxicol

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Sevoflurane is the most commonly used anesthetic in clinical practice and exerts a protective effect on cerebral ischemia-reperfusion (I/R) injury. This study aims to elucidate the molecular mechanism by which sevoflurane postconditioning protects against cerebral I/R injury. Oxygen-glucose deprivation/reperfusion (OGD/R) model in vitro and the middle cerebral artery occlusion (MCAO) model in vivo were established to simulate cerebral I/R injury. Sevoflurane postconditioning reduced neurological deficits, cerebral infarction, and ferroptosis after I/R injury. Interestingly, sevoflurane significantly inhibited specificity protein 1 (SP1) expression in MACO rats and HT22 cells exposed to OGD/R. SP1 overexpression attenuated the neuroprotective effects of sevoflurane on OGD/R-treated HT22 cells, evidenced by reduced cell viability, increased apoptosis, and cleaved caspase-3 expression. Furthermore, chromatin immunoprecipitation and luciferase experiments verified that SP1 bound directly to the ACSL4 promoter region to increase its expression. In addition, sevoflurane inhibited ferroptosis via SP1/ACSL4 axis. Generally, our study describes an anti-ferroptosis effect of sevoflurane against cerebral I/R injury via downregulating the SP1/ASCL4 axis. These findings suggest a novel sight for cerebral protection against cerebral I/R injury and indicate a potential therapeutic approach for a variety of cerebral diseases.

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Section: Discussionsupporting

confidence: 91%

Sevoflurane Postconditioning Attenuates Cerebral Ischemia-Reperfusion Injury by Inhibiting SP1/ACSL4-Mediated Ferroptosis

Lyu

2023

Hum Exp Toxicol

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“… 27 SLC7A11 and FTH1 are common inhibitors of ferroptosis, while ACSL4 and TFR1 act as positive regulators of ferroptosis and promote ferroptosis. 28 , 29 Interfering with SLC3A2 expression in BLCA cells significantly increased lipid ROS, lipid peroxidation, and Fe 2 + levels, upregulating the expression of pro-ferroptosis factor proteins and downregulating the expression of antiferroptosis proteins in BLCA cells. These results suggest that interfering with SLC3A2 promotes ferroptosis in BLCA cells, suggesting the involvement of ferroptosis in BLCA progression.…”

Section: Discussionmentioning

confidence: 93%

Study on the Role and Mechanism of SLC3A2 in Tumor-Associated Macrophage Polarization and Bladder Cancer Cells Growth

Wu,

Zhao,

Kong

et al. 2024

Technol Cancer Res Treat

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Background: Solute carrier family 3 member 2 (SLC3A2) is highly expressed in various types of cancers, including bladder cancer (BLCA). However, the role and mechanism of SLC3A2 in the onset and progression of BLCA are still unclear. Methods: The interfering plasmid for SLC3A2 was constructed and transfected into BLCA cells. Cell proliferation, invasion, and migration abilities were assessed to evaluate the impact of SLC3A2 silencing on BLCA cell growth. M1 and M2 macrophage polarization markers were detected to evaluate macrophage polarization. The levels of reactive oxygen species (ROS), lipid peroxidation, and Fe2+, as well as the expression of ferroptosis-related proteins, were measured to assess the occurrence of ferroptosis. Ferroptosis inhibitors were used to verify the mechanism. Results: The experimental results showed that SLC3A2 was highly expressed in BLCA cell lines. The proliferation, invasion, and migration of BLCA cells were reduced after interfering with SLC3A2. Interference with SLC3A2 led to increase the expression of M1 macrophage markers and decreased the expression of M2 macrophage markers in M0 macrophages co-cultured with tumor cells. Additionally, interference with SLC3A2 led to increased levels of ROS, lipid peroxidation, and Fe2+, downregulated the expression of solute carrier family 7 member11 (SLC7A11) and glutathione peroxidase 4 (GPX4), while upregulated the expression of acyl-coA synthetase long chain family member 4 (ACSL4) and transferrin receptor 1 (TFR1) in BLCA cells. However, the impact of SLC3A2 interference on cell proliferation and macrophage polarization was impeded by ferroptosis inhibitors. Conclusion: Interference with SLC3A2 inhibited the growth of BLCA cells and the polarization of tumor-associated macrophages by promoting ferroptosis in BLCA cells.

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“…LDH is highly sensitive for the early detection of cardiomyocyte damage in patients with chest pain (Rossello et al, 2016). MDA is a major metabolite of oxygen-free radicals, reflecting the degree of peroxidation in myocardial tissue (Liu et al, 2023). And SOD, as an important antioxidant enzyme, can ameliorate myocardial oxidative stress injury by scavenging oxygen-free radicals (Kondo f Duan, J.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Cistanche deserticola Ma in the Treatment of Myocardial Ischemia-Reperfusion (I/R) Injury Based on Network Pharmacology and in vitro Experiments

Yue,

Li,

Wang

et al. 2023

Pharmacognosy Magazine

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Objectives To investigate the mechanism of Cistanche deserticola Ma (CDA) in the treatment of myocardial ischemia-reperfusion (I/R) injury by network pharmacology and cell experiments. Materials and Methods The main active components of CDA were collected from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). I/R-related targets were identified from DisGeNET, OMIMD, and TTD; the I/R protein–protein interaction (PPI) network was constructed using the STRING input. The targets of CDA that inhibit I/R injury in Matescape and Microshengxin were subjected to Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Cell viability, levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA), and protein expression of phosphatidylinositol 3-kinase (PI3K) and serine/threonine kinase 1 (Akt1) were determined. Results A total of 236 targets were identified, with PI3K, Akt, epithelial growth factor receptor (EGFR), and another kinase being the major targets, and according to GO and KEGG analysis, CDA was most likely to inhibit I/R through the PI3K-Akt pathway. The optimal concentration of 10% medicated serum of CDA was determined to be the most effective concentration. The levels of LDH and MDA were significantly decreased in the CDA and BEZ23 groups, but the levels of SOD were significantly increased, thereby alleviating cell damage. In addition, the expression of PI3K, Akt, and p-AKT proteins was significantly reduced in the CDA group. Conclusion CDA alleviates I/R injury through antioxidation and inhibition of the PI3K/Akt signaling pathway.

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Calycosin decreases cerebral ischemia/reperfusion injury by suppressing ACSL4-dependent ferroptosis

Cited by 25 publications

References 41 publications

Sevoflurane Postconditioning Attenuates Cerebral Ischemia-Reperfusion Injury by Inhibiting SP1/ACSL4-Mediated Ferroptosis

Sevoflurane Postconditioning Attenuates Cerebral Ischemia-Reperfusion Injury by Inhibiting SP1/ACSL4-Mediated Ferroptosis

Study on the Role and Mechanism of SLC3A2 in Tumor-Associated Macrophage Polarization and Bladder Cancer Cells Growth

Mechanism of Cistanche deserticola Ma in the Treatment of Myocardial Ischemia-Reperfusion (I/R) Injury Based on Network Pharmacology and in vitro Experiments

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