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Triterpenoid pristimerin induced HepG2 cells apoptosis through ROS-mediated mitochondrial dysfunction.
J BUON. 2013 Apr-Jun; 18(2):477-85.JB

Abstract

PURPOSE

To investigate the anticancer properties implicated in a natural triterpenoid (pristimerin)-induced apoptosis and inhibited proliferation in human hepatocellular carcinoma (HCC) HepG2 cell line.

METHODS

The cytotoxic activity of pristimerin in HepG2 cells was determined by MTT assay. Apoptotic morphology was observed by fluorescence microscope with Hoechst 33258 staining and percent apoptosis was measured by annexin V/PI double staining. DiOC6 for mitochondrial potential (ΔΨm) and DCFH-DA for reactive oxygen species (ROS) were determined by flow cytometry. Changes of apoptotic- related proteins were analysed by Western blot.

RESULTS

Pristimerin exerted a potent cytotoxic effect on HepG2 cells. After HepG2 cells were treated with pristimerin, typical apoptotic bodies, increasing the proportion of apoptotic annexin V-positive cells and activation of caspase-3 were detected in a dose-dependent manner. It was intriguing that pristimerin increased the generation of ROS with a collapse of the mitochondrial membrane potential in the cells. In addition, there was significant change in other mitochondrial membrane proteins triggered by pristimerin, such as Bcl-2 and Bax. Pristimerin also effectively induced subsequent release of cytochrome C from mitochondria into the cytosol, downregulated EGFR protein expression and inhibited downstream signaling pathways in HepG2 cells. Pretreatment with N-acetylcysteine (NAC) blocked ROS generation and resulted in loss of mitochondrial membrane potential, release of cytochrome C and apoptosis induced by pristimerin.

CONCLUSION

These data indicate that ROS play an essential role in the induction of apoptosis by pristimerin in HepG2 cells.

Authors+Show Affiliations

Wuhai Municipal People's Hospital, Wuhai, Inner Mongolia, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23818365

Citation

Guo, Yan, et al. "Triterpenoid Pristimerin Induced HepG2 Cells Apoptosis Through ROS-mediated Mitochondrial Dysfunction." Journal of B.U.ON. : Official Journal of the Balkan Union of Oncology, vol. 18, no. 2, 2013, pp. 477-85.
Guo Y, Zhang W, Yan YY, et al. Triterpenoid pristimerin induced HepG2 cells apoptosis through ROS-mediated mitochondrial dysfunction. J BUON. 2013;18(2):477-85.
Guo, Y., Zhang, W., Yan, Y. Y., Ma, C. G., Wang, X., Wang, C., & Zhao, J. L. (2013). Triterpenoid pristimerin induced HepG2 cells apoptosis through ROS-mediated mitochondrial dysfunction. Journal of B.U.ON. : Official Journal of the Balkan Union of Oncology, 18(2), 477-85.
Guo Y, et al. Triterpenoid Pristimerin Induced HepG2 Cells Apoptosis Through ROS-mediated Mitochondrial Dysfunction. J BUON. 2013 Apr-Jun;18(2):477-85. PubMed PMID: 23818365.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Triterpenoid pristimerin induced HepG2 cells apoptosis through ROS-mediated mitochondrial dysfunction. AU - Guo,Yan, AU - Zhang,Wei, AU - Yan,Yan-Yan, AU - Ma,Cun-Gen, AU - Wang,Xia, AU - Wang,Chen, AU - Zhao,Jia-Li, PY - 2013/7/3/entrez PY - 2013/7/3/pubmed PY - 2013/11/20/medline SP - 477 EP - 85 JF - Journal of B.U.ON. : official journal of the Balkan Union of Oncology JO - J BUON VL - 18 IS - 2 N2 - PURPOSE: To investigate the anticancer properties implicated in a natural triterpenoid (pristimerin)-induced apoptosis and inhibited proliferation in human hepatocellular carcinoma (HCC) HepG2 cell line. METHODS: The cytotoxic activity of pristimerin in HepG2 cells was determined by MTT assay. Apoptotic morphology was observed by fluorescence microscope with Hoechst 33258 staining and percent apoptosis was measured by annexin V/PI double staining. DiOC6 for mitochondrial potential (ΔΨm) and DCFH-DA for reactive oxygen species (ROS) were determined by flow cytometry. Changes of apoptotic- related proteins were analysed by Western blot. RESULTS: Pristimerin exerted a potent cytotoxic effect on HepG2 cells. After HepG2 cells were treated with pristimerin, typical apoptotic bodies, increasing the proportion of apoptotic annexin V-positive cells and activation of caspase-3 were detected in a dose-dependent manner. It was intriguing that pristimerin increased the generation of ROS with a collapse of the mitochondrial membrane potential in the cells. In addition, there was significant change in other mitochondrial membrane proteins triggered by pristimerin, such as Bcl-2 and Bax. Pristimerin also effectively induced subsequent release of cytochrome C from mitochondria into the cytosol, downregulated EGFR protein expression and inhibited downstream signaling pathways in HepG2 cells. Pretreatment with N-acetylcysteine (NAC) blocked ROS generation and resulted in loss of mitochondrial membrane potential, release of cytochrome C and apoptosis induced by pristimerin. CONCLUSION: These data indicate that ROS play an essential role in the induction of apoptosis by pristimerin in HepG2 cells. SN - 1107-0625 UR - https://www.unboundmedicine.com/medline/citation/23818365/Triterpenoid_pristimerin_induced_HepG2_cells_apoptosis_through_ROS_mediated_mitochondrial_dysfunction_ L2 - https://www.jbuon.com/archive/18-2-477.pdf DB - PRIME DP - Unbound Medicine ER -