Vol 17 No 2 (2020)
Research Papers

Centella Asiatica (GOTU KOLA) TREATMENT ATTENUATES PRO-INFLAMMATORY MEDIATORS IN LIVER OF RATS WITH ELECTRICAL FOOT SHOCK STRESS MODEL

Mawaddah Ar Rochmah
Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada
Published November 18, 2020
Keywords
  • apoptotic, Centella asiatica, inflammatory cells, liver injury, stress
How to Cite
Sari, D. C. R., Setyaningsih, W. A. W., Mainichi, R. N., Dara, G. M., Kemalasari, R., Romi, M. M., Ar Rochmah, M., & Arfian, N. (2020). Centella Asiatica (GOTU KOLA) TREATMENT ATTENUATES PRO-INFLAMMATORY MEDIATORS IN LIVER OF RATS WITH ELECTRICAL FOOT SHOCK STRESS MODEL. African Journal of Traditional, Complementary and Alternative Medicines, 17(2), 1-7. https://doi.org/10.21010/ajtcam v17n2.1

Abstract

Background: Stress induces secretion of cathecolamines and glucocorticoids, which may produce liver injury. Followed by the production of inflammatory mediators, it causes apoptosis. Centella asiatica (CeA) has anti-inflammatory and hepatoprotective effects. The present study aims to determine the role of CeA in the attenuation of liver pro-inflammatory mediator expression in rats with electrical foot shock stress model.

Materials and Methods: Twenty-four Sprague-Dawley rats were randomized into four groups consisted of six rats each: (1) Control group, (2) CeA-treated group, (3) Stress group, and (4) CeA + stress group. Reverse transcriptase PCR of inflammatory and apoptosis markers as well as Real-Time PCR of β2-adrenergic receptor were performed from liver tissues.

Results: Electrical foot shock stress induced up-regulation of NFκB and TNF-α mRNA expressions as pro-inflammatory mediators, compared to control group. This alteration was followed by up-regulation of BAX and β2-adrenergic receptor, as well as the down-regulation of BCl2 compared to control. CeA treatment prevented enhancement of NFκB, TNF-α, TLR-4 and β-adrenergic receptor mRNA expressions, which was followed by down-regulation of BAX and up-regulation of BCl-2, compared to stress group.

Conclusion: CeA prevents secretion of pro-inflammatory chemokines and cytokines as well as apoptotic markers in liver cells through the activation of β2-adrenergic receptor.