Khat (Catha edulis) generates reactive oxygen species and promotes hepatic cell apoptosis via MAPK activation

  • Authors:
    • Morad Dirhem Naji Abid
    • Juan Chen
    • Min Xiang
    • Jie Zhou
    • Xiaoping Chen
    • Feili Gong
  • View Affiliations

  • Published online on: May 27, 2013     https://doi.org/10.3892/ijmm.2013.1394
  • Pages: 389-395
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

A number of studies have suggested an association between khat (Catha edulis) chewing and acute liver lesions or chronic liver disease. However, little is known about the effects of khat on hepatic cells. In the current study, we investigated the mechanism behind khat-induced apoptosis in the L02 human hepatic cell line. We used cell growth inhibition assay, flow cytometry and Hoechst 33258 staining to measure hepatocyte apoptosis induced by khat. Western blot analysis was used to detect the expression levels of caspase-8 and -9, as well as those of Bax and Bcl-2. We also measured reactive oxygen species production. The results indicated that khat induced significant hepatocyte apoptosis in L02 cells. We found that khat activated caspase-8 and -9, upregulated Bax protein expression and downregulated Bcl-2 expression levels, which resulted in the coordination of apoptotic signals. Khat-induced hepatocyte apoptosis is primarily regulated through the sustained activation of the c-Jun NH2-terminal kinase (JNK) pathway and only partially via the extracellular signal-regulated kinase (ERK) cascade. Furthermore, the khat-induced reactive oxygen species (ROS) production and the activation of the ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the khat-induced activation of JNK and ERK. Our results demonstrate that khat triggers the generation of intracellular ROS and sequentially induces the sustainable activation of JNK, which in turn results in a decrease in cell viability and an increase in cell apoptosis.
View Figures
View References

Related Articles

Journal Cover

August 2013
Volume 32 Issue 2

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Abid MD, Chen J, Xiang M, Zhou J, Chen X and Gong F: Khat (Catha edulis) generates reactive oxygen species and promotes hepatic cell apoptosis via MAPK activation. Int J Mol Med 32: 389-395, 2013.
APA
Abid, M.D., Chen, J., Xiang, M., Zhou, J., Chen, X., & Gong, F. (2013). Khat (Catha edulis) generates reactive oxygen species and promotes hepatic cell apoptosis via MAPK activation. International Journal of Molecular Medicine, 32, 389-395. https://doi.org/10.3892/ijmm.2013.1394
MLA
Abid, M. D., Chen, J., Xiang, M., Zhou, J., Chen, X., Gong, F."Khat (Catha edulis) generates reactive oxygen species and promotes hepatic cell apoptosis via MAPK activation". International Journal of Molecular Medicine 32.2 (2013): 389-395.
Chicago
Abid, M. D., Chen, J., Xiang, M., Zhou, J., Chen, X., Gong, F."Khat (Catha edulis) generates reactive oxygen species and promotes hepatic cell apoptosis via MAPK activation". International Journal of Molecular Medicine 32, no. 2 (2013): 389-395. https://doi.org/10.3892/ijmm.2013.1394