Study on the role of berberine in doxorubicin induced myocardial cell injury

  • SU Rina ,
  • HAN Xuanmao
Expand
  • The First Department of Cardiology,the First Affiliated Hospital of Baotou Medical College,Inner Mongolia University of Science and Technology,Baotou 014040, China

Received date: 2024-04-15

  Online published: 2025-03-26

Abstract

Objective: To investigate the effect of berberine (BBR),a traditional Chinese medicine extract,on doxorubicin (DOX) induced myocardial cell damage at the cellular level,and explore the possible mechanisms involved in this process. Methods: H9C2 rat cardiomyocytes were cultured,and DOX was divided into different concentrations to determine the concentration of DOX.Then they were divided into normal control group,DOX model group and treatment group (low-dose BBR,medium-dose BBR,high-dose BBR) to treat H9C2 cells. The cell growth trend and cell morphology were observed by inverted microscope. The cell viability was determined by cell counting kit (CCK8) method. The apoptosis was detected by flow cytometry. The relative expression levels of apoptosis and autophagy related proteins Bax,Bcl-2,Beclin1 and P62 in different groups were determined by Western-blot. Results: Under the microscope,it was found that with the increase of DOX concentration,the degree of myocardial cell injury increased in turn. CCK8 method was used to select 1 μmol/L DOX as the optimal modeling concentration for myocardial injury,compared with the control group,different concentrations of BBR in the treatment group could increase the viability of DOX-induced myocardial injury cells. The expression of pro-apoptotic protein Bax and autophagy-related protein Beclin1 in the middle dose of the treatment group was significantly decreased,and the expression of anti-apoptotic protein Bcl-2 and autophagy-related protein P62 was increased (P<0.05). Conclusion: Berberine can protect DOX-induced cardiomyocyte injury by reducing apoptosis,and this protective mechanism is related to autophagy.

Cite this article

SU Rina , HAN Xuanmao . Study on the role of berberine in doxorubicin induced myocardial cell injury[J]. Journal of Baotou Medical College, 2025 , 41(3) : 36 -40 . DOI: 10.16833/j.cnki.jbmc.2025.03.007

References

[1] Bhagat A, Shrestha P, Kleinerman ES. The Innate Immune System in Cardiovascular Diseases and Its Role in Doxorubicin-Induced Cardiotoxicity [J]. Int J Mol Sci, 2022, 23(23): 14649.
[2] Al-Malky HS, Al Harthi SE, Osman AM. Major obstacles to doxorubicin therapy: Cardiotoxicity and drug resistance [J]. J Oncol Pharm Pract, 2020, 26(2): 434-444.
[3] Xia P, Chen J, Liu Y, et al. Doxorubicin induces cardiomyocyte apoptosis and atrophy through cyclin-dependent kinase 2-mediated activation of forkhead box O1 [J]. J Biol Chem, 2020, 295(13): 4265-4276.
[4] Bartlett JJ, Trivedi PC, Pulinilkunnil T. Autophagic dysregulation in doxorubicin cardiomyopathy [J]. J Mol Cell Cardiol, 2017, 104: 1-8.
[5] Bartlett JJ, Trivedi PC, Yeung P, et al. Doxorubicin impairs cardiomyocyte viability by suppressing transcription factor EB expression and disrupting autophagy [J]. Biochem J, 2016, 473(21): 3769-3789.
[6] Kitakata H, Endo J, Ikura H, et al. Therapeutic Targets for DOX-Induced Cardiomyopathy: Role of Apoptosis vs. Ferroptosis [J]. Int J Mol Sci, 2022, 23(3).
[7] Feng X, Sureda A, Jafari S, et al. Berberine in Cardiovascular and Metabolic Diseases: From Mechanisms to Therapeutics [J]. Theranostics, 2019, 9(7): 1923-1951.
[8] Han Y, Xiang Y, Shi Y, et al. Pharmacokinetics and Pharmacological Activities of Berberine in Diabetes Mellitus Treatment [J]. Evid Based Complement Alternat Med, 2021, 2021: 9987097.
[9] Cheng H, Liu J, Tan Y, et al. Interactions between gut microbiota and berberine, a necessary procedure to understand the mechanisms of berberine [J]. J Pharm Anal, 2022, 12(4): 541-55.
[10] Chen H, Liu Q, Liu X, et al. Berberine attenuates septic cardiomyopathy by inhibiting TLR4/NF-kappaB signalling in rats [J]. Pharm Biol, 2021, 59(1): 121-8.
[11] Mohammadinejad R, Ahmadi Z, Tavakol S, et al. Berberine as a potential autophagy modulator [J]. J Cell Physiol, 2019, 234(9): 14914-26.
[12] Sangweni NF, Gabuza K, Huisamen B, et al. Molecular insights into the pathophysiology of doxorubicin-induced cardiotoxicity: a graphical representation [J]. Arch Toxicol, 2022, 96(6): 1541-50.
[13] Prathumsap N, Shinlapawittayatorn K, Chattipakorn SC, et al. Effects of doxorubicin on the heart: From molecular mechanisms to intervention strategies [J]. Eur J Pharmacol, 2020, 866: 172818.
[14] Christidi E, Brunham LR. Regulated cell death pathways in doxorubicin-induced cardiotoxicity [J]. Cell Death Dis, 2021, 12(4): 339.
[15] Kou Y, Tong B, Wu W, et al. Berberine Improves Chemo-Sensitivity to Cisplatin by Enhancing Cell Apoptosis and Repressing PI3K/AKT/mTOR Signaling Pathway in Gastric Cancer [J]. Front Pharmacol, 2020, 11: 616251.
Outlines

/