CHENG Qi-lai, LI Hong-liang, HUANG Zhi-qin. Study on Apoptosis of HepG2 Cell Induced by Celosin A from Celosia Semen and its Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(23): 200-204.
DOI:
CHENG Qi-lai, LI Hong-liang, HUANG Zhi-qin. Study on Apoptosis of HepG2 Cell Induced by Celosin A from Celosia Semen and its Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(23): 200-204. DOI: 10.11653/syfj2013230200.
Study on Apoptosis of HepG2 Cell Induced by Celosin A from Celosia Semen and its Mechanism
Objective: To investigate the apoptosis in human hepatic cancer HepG2 cell strain induced by celosin A(CA) from Celosia Semen and its mechanism. Method: The viability of HepG2 cells was detected by the method cell counting kit-8 (CCK-8).The activity of lactic dehydrogenase (LDH) was measured by thiazolyl blue(MTT)assay.Immune colorimetry was used to test the proliferation of HepG2 cells.The change of morphoiogy of apoptosis HepG2 cells was observed by 4
6-2 amidine base-2-phenyl indole(DAPI) fluorescence staining.Western blot was used to detect the expressions of Caspase-3/7 and nuclear factor kappa B(NF-κB) proteins of HepG2 cells. Result: After HepG2 cells were treated by CA of different concentration
the leakage of LDH increased in a dosage and time dependent manner.In the process of determination of BrdU and CCK-8
the inhibitory effect of CA to HepG2 cell was stronger than standard drugs
and showed clear inhibitory effect on the HepG2 cell proliferation with the increase of concentration and the acting time.By using the DAPI fluorescence dyes
the HepG2 cell cytoplasm concentrating
nucleolus dispersion and chromatin aglomeration were observed.The Western blot analysis showed that the expression of Caspase-3/7 was significantly enhanced and the expression of NF-κB proteins was down-regulated. Conclusion: Celosin A could induce the apoptosis of HepG2 cells and its mechanism related to activating the activity of Caspase-3/7 and down-regulating the expression of NF-κB protein.