Protective Effect of Modified Human Acidic Fibroblast Growth Factor against Actinomycin D-Induced NRK52E Cells Apoptotic Death 

Hua XU^{1 *}, Hong XU², Guang-fan HAI³, Qing HE¹, Chang-e ZHANG^4*

¹Jinan University College of Pharmacy, Guangzhou, Guangzhou 510632, ²United Front Work Department, Guangxi Medical University, Nanning, 530021, ³Department of Pharmacology, Xin-xiang Medical College, Xin-xiang 450031, ⁴Department of Pathophysiology, Guangzhou Medical College, Guangzhou 510182, China. 

*For correspondence: Email: huax_mail@126.com  

Received:  17 July 2012                                                                    Revised accepted: 10 April 2013

Tropical Journal of Pharmaceutical Research, June 2013; 12(3): 343-349

Purpose: To investigate whether modified acidic fibroblast growth factor (MaFGF) can protect NRK52E cell against apoptotic death induced by actinomycin D (Act D) and the effect of MaFGF on PI3K/Akt signaling pathway.

Methods: NRK52E cell apoptotic death was measured by several methods including cell morphologic observation, Hoechst 33342 staining and flow cytometry. In addition, the levels of phosphorylated-Akt protein were analyzed by Western blotting method.

Results: The results showed that 0.75 mg/L Act D-treated NRK52E cell for 20 h was the optimal conditions for establishing NRK52E cell apoptotic model. Different doses of MaFGF (0.01, 0.03, 0.1, 0.3 and 1.0 mg/L) decreased apoptotic rate but enhanced the expression of phosphorylated Akt protein. However, MaFGF’s protection against Act D-induced apoptosis was significantly (p < 0.05) prevented when NRK52E cells were exposed to wortmannin.

Conclusion: These results reveal that MaFGF can reduce the level of ActD-induced apoptotic cell death in 20 h, and the protective mechanism of MaFGF may be associated with the activation of PI3K/Akt signaling pathway by up-regulation of expression of phosphorylated Akt protein.