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| Exploring the effects of arctigenin on Treg/Th17 balance and cardiac function in rats with myocardial infarction based on the PERK-ATF4-CHOP pathway |
| Hits 214 Download times 24 Received:November 25, 2025 |
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| DOI
10.11656/j.issn.1672-1519.2026.03.10 |
| Key Words
arctigenin;PERK-ATF4-CHOP pathway;myocardial infarction;Treg/Th17 balance;cardiac function |
| Author Name | Affiliation | E-mail | | LAI Xing | Ward 1, Department of Geriatrics, Hubei Hospital of Integrated Chinese and Western Medicine, Wuhan 430000, China | | | XIAO Rui | Ward 1, Department of Geriatrics, Hubei Hospital of Integrated Chinese and Western Medicine, Wuhan 430000, China | 4467889@163.com |
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| Abstract
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| [Objective] To explore whether arctigenin(ARC) can regulate the PKR-like endoplasmic reticulum kinase(PERK)-activated transcription factor 4(ATF4)-C/EBP homologous protein(CHOP) pathway to affect the Regulatory T cells(Treg)/Helper T cell 17(Th17) balance and cardiac function in rats with myocardial infarction(MI). [Methods] Rats were randomly separated into the control(Con) group,the MI group,the ARC low-dose(ARC-L) group,the ARC high-dose(ARC-H) group,and the ARC-H+CCT020312(PERK activator) group. The cardiac function of rats,the levels of serum Lactate dehydrogenase(LDH),interleukins(IL-10,IL-17A,IL-22),the levels of myocardial injury markers Creatine kinase isoenzyme MB(CK-Mb),cardiac troponin I(cTnI),and cardiac troponin T(cTnT),the proportions of Th17 and Treg cells in peripheral blood,and the percentage of myocardial infarction area were measured. The morphology of rat cardiac tissue was observed. The apoptosis of myocardial tissue cells and the expression levels of Cleaved Caspase-3 and PERK/ATF4/CHOP pathway proteins were measured. [Results] Compared with the Con group,the myocardial tissue of rats in the MI group was clearly damaged,the levels of LVESP,LVEF and LVFS,the level of IL-10,the proportion of Treg cells,and the value of Treg/Th17 were lower,while the level of LVEDP,the levels of LDH,IL-17A and IL-22,the levels of CK-Mb,cTnI and cTnT,proportion of Th17 cells,percentage of myocardial infarction area,apoptosis rate,the expression levels of p-PERK/PERK,p-eIF2α/eIF2α,ATF4,CHOP and Cleaved Caspase-3 proteins were higher(P<0.05). Compared with the MI group,the myocardial tissue morphology of rats in the ARC-L group and the ARC-H group was clearly improved,the levels of LVESP,LVEF and LVFS,the level of IL-10,the proportion of Treg cells,and the value of Treg/Th17 were higher,while the level of LVEDP,the levels of LDH,IL-17A and IL-22,the levels of CK-Mb,cTnI and cTnT,proportion of Th17 cells,percentage of myocardial infarction area,apoptosis rate,the expression levels of p-PERK/PERK,p-eIF2α/eIF2α,ATF4,CHOP and Cleaved Caspase-3 proteins were lower(P<0.05). CCT020312 was able to reduce the improvement effect of ARC on MI rats(P<0.05). [Conclusion] ARC may reduce inflammation,cardiomyocyte apoptosis and myocardial injury in MI rats,and ameliorate Treg/Th17 balance and cardiac function by inhibiting the PERK-ATF4-CHOP pathway. |
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