Authors

Tingting Gu, Xin Rui, Huafeng Pan, Li Wang, Zhongliang Cheng* 

Departments

Ningbo Huamei Hospital, University of Chinese Academy of Sciences, Ningbo 315000, PR China

Abstract

Objective: The role of nuclear factor kappa B (NF-κB) in proliferation, apoptosis, anti-apoptosis and autophagy in BPH1 cells was explored in this paper. 

Methods: BPH1 cells were cultured in vitro and randomly divided into the control group (normal complete medium), NF-κB inhibitor group (100 μmol/L PDTC reagent complete medium) or NF-κB activator group (100 μg/L PMA reagent complete medium). The CCK-8 method was used to detect cell proliferation and the apoptosis rate was detected using flow cytometry. The expression of NF-κB p65, apoptosis protein Bcl-2, caspase-3 and autophagy protein LC-3Ⅱ were detected using the western blot method. 

Results: While the proliferation rate of the NF-κB inhibitor group was significantly lower, the apoptosis rate of the NF-κB inhibitor group was significantly higher than both the control group and the NF-κB activator group (P<0.05). The expression of NF-κB p65 protein in the NF-κB inhibitor group was significantly lower than the control group at 8h, 12h and 24h (P<0.05). The expression of NF-κB p65 protein in the NF-κB activator group was significantly higher than the control group at 4h, 8h, 12h and 24h (P<0.05). The expression of Bcl-2 protein in the NF-κB inhibitor group was significantly lower, while the expression of the caspase-3 protein was significantly higher than the control group and the NF-κB activator group (P<0.05). The expression of LC-3 Ⅱ protein in the NF-κB activator group was significantly lower than in the control group (P<0.05). 

Conclusion: NF-κB can significantly inhibit the proliferation and apoptosis of BPH cells and inhibit the autophagy level. The results of the present study represent a new research direction for prostate proliferation related target gene therapy and drug therapy.

Keywords

NF-κB, prostatic hyperplasia cells, proliferation, apoptosis, anti-apoptosis, autophagy.

DOI:

10.19193/0393-6384_2021_4_353