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Basado en la vía de señalización AMPK/PPARα y el cuerpo inflamatorio NLRP3, se estudia el mecanismo de acción de la decocción de Huangqi y Chifengtang en la lucha contra la aterosclerosis

  • role： First author第一作者
  • Affiliation：

    Heilongjiang University of Chinese Medicine，Harbin 150040，China

  • Email：K18089718076@163.com
  • Introduction：梁玉琴，在读博士，从事中药药性理论及药效物质基础研究，E-mail：K18089718076@163.com
LIANG Yuqin1,  
  • Affiliation：

    Heilongjiang University of Chinese Medicine，Harbin 150040，China

LIU Jie1,  
  • Affiliation：

    Heilongjiang University of Chinese Medicine，Harbin 150040，China

ZHANG Chi1,  
  • Affiliation：

    Institute of Traditional Chinese Medicine，Heilongjiang University of Chinese Medicine，Harbin 150040，China

CHEN Pingping2,  
  • Affiliation：

    Institute of Traditional Chinese Medicine，Heilongjiang University of Chinese Medicine，Harbin 150040，China

LU Fang2,  
  • role： Corresponding author通信作者
  • Affiliation：

    Institute of Traditional Chinese Medicine，Heilongjiang University of Chinese Medicine，Harbin 150040，China

  • Email：keji-liu@163.com
  • Introduction：刘树民，博士，教授，博士生导师，从事中药药性理论及药效物质基础研究，Tel：0451-87266827，E-mail：keji-liu@163.com
LIU Shumin2*

resumen

El objetivo es investigar el efecto de la decocción de Huangqi y Chifengtang (HCT) en la mejora de la aterosclerosis (AS), y explicar su mecanismo de acción con la activación de la kinasa activada por AMP (AMPK) / receptor activado por proliferador de peroxisoma alfa (PPARα) y la relación con el complejo proteico NOD-like (NLRP3) inflamatorio. Con el fin de establecer un modelo de AS, 32 ratones C57BL/6J ApoE-/- fueron divididos en grupo normal, grupo modelo, grupo de fármaco positivo (atorvastatina, 5 mg/kg/día) y grupos de HCT de dosis baja y alta (1,95, 3,90 g/kg/día) después de la alimentación de ratones ApoE-/- con alta dieta de lípidos y colesterol. Los diversos grupos recibieron dosis equivalentes durante 28 días, y el grupo control y el grupo modelo fueron alimentados con la misma cantidad de solución salina fisiológica. Las aortas y los hígados de los ratones fueron observados con tinción de hematoxilina-eosina (HE); las condiciones patológicas de las arterias aórticas y los hígados fueron observadas con ensayos bioquímicos y de inmunoensayo enzimático (ELISA) para detectar el colesterol total (TC), los triglicéridos (TG), las lipoproteínas de baja densidad (LDL-C), la alanina aminotransferasa (ALT), la aspartato aminotransferasa (AST), la proteína C reactiva (CRP), la interleucina (IL)-1β

palabra clave

Huangqi Chifengtang;atherosclerosis;adenosine monophosphate-activated protein kinase（AMPK）/peroxisome proliferator-activated receptor α（PPARα） signaling pathway;nucleotide-binding oligomerization domain（NOD）-like receptor thermal protein domain associated protein 3（NLRP3） inflammasome;lipid metabolism

References

  1. 1.
    TSAO C W，ADAY A W，ALMARZOOQ Z I，et al.Heart disease and stroke statistics-2022 update：A report from the American Heart Association［J］.Circulation，2022，145（8）：e153-e639.
  2. 2.
    WANG R，WANG M，YE J，et al.Mechanism overview and target mining of atherosclerosis：Endothelial cell injury in atherosclerosis is regulated by glycolysis（review）［J］.Int J Mol Med，2021，47（1）：65-76.
  3. 3.
    LIU L，SHI Z，JI X，et al.Adipokines，adiposity，and atherosclerosis［J］.Cell Mol Life Sci，2022，79（5）：272.
  4. 4.
    LIBBY P.The changing landscape of atherosclerosis［J］.Nature，2021，592（7855）：524-533.
  5. 5.
    WEBER C，NOELS H. Atherosclerosis：Current pathogenesis and therapeutic options［J］.Nat Med，2011，17（11）：1410-1422.
  6. 6.
    BOUTAGY N E，GAMEZ-MENDEZ A，FOWLER J W，et al.Dynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice［J］.J Clin Invest，2024，134（4）：e170453.
  7. 7.
    BELLOSTA S，CORSINI A.Statin drug interactions and related adverse reactions：An update［J］.Expert Opin Drμg Saf，2018，17（1）：25-37.
  8. 8.
    ZHAO P Z，YANG Z，CHEN X Y，et al.Traditional Chinese medicine intervenes in atherosclerosis by regulating TLR/NLRP3 pathway via TRPV1/TRPA1［J］.Chin J Exp Tradit Med Form，2023，29（20）：247-256.
  9. 9.
    LIANG Q Z，CHEN Z T，ZHOU R R，et al.Role of endoplasmic reticulum stress in atherosclerosis and its regulation by traditional Chinese medicine：A review［J］.Chin J Exp Tradit Med Form，2024，30（5）：226-235.
  10. 10.
    ZHANG L，SHE Z G，LI H，et al.Non-alcoholic fatty liver disease：A metabolic burden promoting atherosclerosis［J］.Clin Sci，2020，134（13）：1775-1799.
  11. 11.
    STOLS-GONçALVES D，HOVINGH G K，NIEUWDORP M，et al.NAFLD and atherosclerosis：Two sides of the same dysmetabolic coin？［J］.Trends Endocrinol Metab，2019，30（12）：891-902.
  12. 12.
    DINIZ T A，DE LIMA JUNIOR E A，TEIXEIRA A A，et al.Aerobic training improves NAFLD markers and insulin resistance through AMPK-PPAR-α signaling in obese mice［J］.Life Sci，2021，266：118868.
  13. 13.
    GREBE A，HOSS F，LATZ E.NLRP3 inflammasome and the IL-1 pathway in atherosclerosis［J］.Circ Res，2018，122（12）：1722-1740.
  14. 14.
    LIU S Y，WANG Q Y，LIU S M.Therapeutic effect of huangqi chifengtang on cerebral infarction rat model and its effect on expression of ZO-1，Claudin-5，P-gp and MRP1 protein in brain tissue［J］.Chin J Exp Tradit Med Form，2022，28（6）：26-33.
  15. 15.
    LIANG Y Q，FU J Q，SHI Y H，et al.Mechanism of Huangqi Chifengtang in treating atherosclerosis based on 16S rRNA sequencing and metabolomics［J］.Chin J Exp Tradit Med Form，2025，31（13）：94-103.
  16. 16.
    WANG Q Y，LIU S Y，LIU S M.Study on extraction technique of Huangqi Chifeng decoction［J］.West China J Pharm Sci，2022，37（3）：311-314.
  17. 17.
    IX J H，SHARMA K.Mechanisms linking obesity，chronic kidney disease，and fatty liver disease：The roles of fetuin-A，adiponectin，and AMPK［J］.J Am Soc Nephrol，2010，21（3）：406-412.
  18. 18.
    HERZIG S，SHAW R J.AMPK：Guardian of metabolism and mitochondrial homeostasis［J］.Nat Rev Mol Cell Biol，2018，19（2）：121-135.
  19. 19.
    TREFTS E，SHAW R J.AMPK：Restoring metabolic homeostasis over space and time［J］.Mol Cell，2021，81（18）：3677-3690.
  20. 20.
    AL-KURAISHY H M，SULAIMAN G M，MOHSIN M H，et al.Targeting of AMPK/MTOR signaling in the management of atherosclerosis：Outmost leveraging［J］.Int J Biol Macromol，2025，309（Pt 2）：142933.
  21. 21.
    MONTAIGNE D，BUTRUILLE L，STAELS B.PPAR control of metabolism and cardiovascular functions［J］.Nat Rev Cardiol，2021，18（12）：809-823.
  22. 22.
    QIU Y Y，ZHANG J，ZENG F Y，et al.Roles of the peroxisome proliferator-activated receptors（PPARs） in the pathogenesis of nonalcoholic fatty liver disease（NAFLD）［J］.Pharmacol Res，2023，192：106786.
  23. 23.
    LIU Y，COLBY J K，ZUO X，et al. The role of PPAR-δ in metabolism，inflammation，and cancer：Many characters of a critical transcription factor［J］.Int J Mol Sci，2018，19（11）：3339.
  24. 24.
    TANASE D M，GOSAV E M，COSTEA C F，et al.The intricate relationship between type 2 diabetes mellitus（T2DM），insulin resistance（IR），and nonalcoholic fatty liver disease（NAFLD）［J］.J Diabetes Res，2020，2020：3920196.
  25. 25.
    ZHANG Z，HUANG Q，ZHAO D，et al.The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications［J］.Front Endocrinol（Lausanne），2023，14：1112363.
  26. 26.
    GUAN G，CHEN Y，DONG Y.Unraveling the AMPK-SIRT1-FOXO pathway：The in-depth analysis and breakthrough prospects of oxidative stress-induced diseases［J］.Antioxidants（Basel），2025，14（1）：70.
  27. 27.
    TIAN J Y，QIN W Y，YANG J，et al.Mechanism of modified guishenwan in regulating AMPK/Akt/Nrf2 pathway to improve glucose and lipid metabolism oxidative stress in polycystic ovary syndrome rats［J］.Chin J Exp Tradit Med Form，2025，31（8）：1-8.
  28. 28.
    GUO X，YIN X，LIU Z，et al.Non-alcoholic fatty liver disease（NAFLD） pathogenesis and natural products for prevention and treatment［J］.Int J Mol Sci，2022，23（24）：15489.
  29. 29.
    HANEKLAUS M，O'NEILL L A.NLRP3 at the interface of metabolism and inflammation［J］.Immunol Rev，2015，265（1）：53-62.
  30. 30.
    YAN J，LI M，WANG X D，et al. Peperomin E（PepE） protects against high fat diet-induced atherosclerosis in Apolipoprotein E deficient（ApoE-/-） mice through reducing inflammation via the suppression of NLRP3 signaling pathway［J］.Biomed Pharmacother，2018，105：862-869.
  31. 31.
    BIAN F，YANG X，ZHOU F，et al.C-reactive protein promotes atherosclerosis by increasing LDL transcytosis across endothelial cells［J］.Br J Pharmacol，2014，171（10）：2671-2684.
  32. 32.
    DEHGHAN A，DUPUIS J，BARBALIC M，et al.Meta-analysis of genome-wide association studies in >80000 subjects identifies multiple loci for C-reactive protein levels［J］.Circulation，2011，123（7）：731-738.

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