Trends in Immunotherapy

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Traditional Mongolian medicine RuXian-1 suppress the breast hyperplasia by GRP78/PERK/CHOP pathway in rat model

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https://doi.org/10.24294/ti.v8.i2.5689
Zhao, S., Chimedtseren, C., Jamiyansuren, J., & Tugjamba, A. (2024). Traditional Mongolian medicine RuXian-1 suppress the breast hyperplasia by GRP78/PERK/CHOP pathway in rat model. Trends in Immunotherapy, 8(2). https://doi.org/10.24294/ti.v8.i2.5689
Volume 8 Issue 2 (2024)
Copyright (c) 2024 Shuangquan Zhao, Chimedragchaa Chimedtseren, Jambaldorj Jamiyansuren, Alimaa Tugjamba
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Authors

  • Shuangquan Zhao Mongolian National University of Medical Sciences, Ulaanbaatar 14201, Mongolia; Affiliated Hospital of Inner Mongolia Minzu University, Tongliao 028043, China
  • Chimedragchaa Chimedtseren Mongolian National University of Medical Sciences, Ulaanbaatar 14201, Mongolia
  • Jambaldorj Jamiyansuren Mongolian National University of Medical Sciences, Ulaanbaatar 14201, Mongolia
  • Alimaa Tugjamba
    Mongolian National University of Medical Sciences, Ulaanbaatar 14201, Mongolia

In this study we aimed to study the protective effect of RuXian-1, which is a traditional Mongolian medicine on hyperplasia of mammary glands in rats and to explore its possible mechanism. Methods: The rat model of breast hyperplasia was induced by intramuscular injection of estradiol benzoate. The rats were randomly divided into 4 groups: saline treatment group (negative control), estrogen treatment group (model group), RuXian-1 treatment group and raloxifene treatment group (positive control). RuXian-1 group and raloxifene group were given 3.0 g/kg of RuXian-1 and 1.8 mg/kg of raloxifene daily for 4 weeks, respectively. After treatment, the breast tissue of each group was harvested and confirmed the expressions levels of glucose-related protein 78 (GRP78), C/EBP homologous protein (CHOP), and protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) which were known that functions as an endoplasmic reticulum stress marker by Western blotting. Results: Compared with the normal group, the GRP78, PERK and CHOP protein levels in the breast tissue of the model group were significantly decreased. Compared with the model group, the expression of GRP78, PERK and CHOP in RuXian-1 group significantly increased, the expression of GRP78 and CHOP of raloxifene significantly increased (p < 0.05), and the expression of PERK did not change. Conclusion: The Mongolian medicine RuXian-1 has therapeutic effect on mammary hyperplasia in rats, and its therapeutic mechanism is related to activating the GRP78/PERK/CHOP signaling pathway and promoting mammary gland cell apoptosis.

Keywords:

mammary gland hyperplasia Mongolian medicine RuXian-1 GRP78/PERK/CHOP signaling pathway

References

  1. Wei Q, Zhou XF. Research progress of traditional Chinese and western medicine in the treatment of breast hyperplasia. Journal of Inner Mongolia Medical University. 2021; 43(04): 434-437.
  2. Chen Y. Overview of traditional Chinese medicine treatment of mammary hyperplasia. Health Must Read. 2012; 11(11): 80-81.
  3. Lu P, Chen XY, Xiao XY, et al. Clinical observation of mammary gland Ⅰ capsule in the treatment of 120 cases of breast hyperplasia. Chinese Journal of General Surgery. 2014; 23(11): 1598-1600.
  4. Wu XH, Qiu X, Li YL. Breast I treatment of 160 cases of breast hyperplasia. Chinese Traditional Medicine Science and Technology. 2011; 18(03): 255.
  5. Yin J, Ma JZ. Research status of the mechanism of Mongolian medicine M-Ⅰ in the treatment of mammary hyperplasia. Chinese Journal of Clinical Pharmacology. 2021; 37(17): 2373-2376.
  6. Wang ZC, Li H, Zhang B, et al. Effect of Mongolian medicine Mamma-I on proliferation and apoptosis of mammary tissue cells in rats with mammary hyperplasia. Chinese Journal of Biochemical Drugs. 2014; (1): 56-58, 61.
  7. Liu LT. Expression of apoptosis-related genes in rat mammary hyperplasia treated with Mongolian medicine mast-i. Clinical practice of integrated traditional Chinese and Western medicine in Inner Mongolia University for Nationalities; 2014.
  8. Luo L, Li Y, Shan H, et al. L‐glutamine protects mouse brain from ischemic injury via up‐regulating heat shock protein 70. CNS Neuroscience & Therapeutics. 2019; 25(9): 1030-1041. doi: 10.1111/cns.13184
  9. Pinzi L, Rastelli G. Molecular docking: shifting paradigms in drug discovery. International Journal of Molecular Sciences. 2019; 20(18): 4331. doi: 10.3390/ijms20184331
  10. Ma Y, Di Z, Cao Q, et al. Xanthatin induces glioma cell apoptosis and inhibits tumor growth via activating endoplasmic reticulum stress-dependent CHOP pathway. Acta Pharmacologica Sinica. 2019; 41(3): 404-414. doi: 10.1038/s41401-019-0318-5
  11. Hu W, Wang H, Shu Q, et al. Green tea polyphenols modulated cerebral SOD expression and endoplasmic reticulum stress in cardiac arrest/cardiopulmonary resuscitation rats. BioMedical Research International. 2020; 2020: 9. doi: 10.1155/2020/5080832.5080832
  12. Birkenmeier EH, Gwynn B, Howard S, et al. Tissue-specific expression, developmental regulation, and genetic mapping of the gene encoding CCAAT/enhancer binding protein. Genes & Development. 1989; 3(8): 1146-1156. doi: 10.1101/gad.3.8.1146
  13. Umek RM, Friedman AD, McKnight SL. CCAAT-Enhancer Binding Protein: A Component of a Differentiation Switch. Science. 1991; 251(4991): 288-292. doi: 10.1126/science.1987644
  14. Ubeda M, Wang XZ, Zinszner H, et al. Habener J, Ron D. Stress-Induced Binding of the Transcription Factor CHOP to a Novel DNA Control Element. Molecular and Cellular Biology. 1996; 16(4): 1479-1489. doi: 10.1128/mcb.16.4.1479
  15. Li Y, Guo Y, Tang J, et al. New insights into the roles of CHOP-induced apoptosis in ER stress. Acta Biochimica et Biophysica Sinica. 2014; 46(8): 629-640. doi: 10.1093/abbs/gmu048
  16. Li HZ, Lu PZ. Effects of endoplasmic reticulum stress on cetuximab resistance in triple-negative breast cancer cells. Guide to Chinese Medicine. 2013; 15(02): 334-335.