[Effects of overexpression of heat shock protein 70 on the damage induced by formaldehyde in vitro].

Objective: To investigate the protective role of inducible heat shock protein 70 (Hsp70) against damage induced by formaldehyde.

Methods: Human bronchial epithelium (HBE) cells were transfected with plasmid harboring hsp70 gene to increase the protein expression level. HBE cells transfected with pcDNA3.1 plasmid were used as transfection control and HBE cells cultured at normal condition served as control. Three groups were marked as HBE/hsp70, HBE/pcDNA and HBE. Hsp70 expression levels of 3 groups were detected. The cells of HBE/hsp70 and HBE groups were exposed to different concentrations of formaldehyde (0,0.39,1.56,6.25 mmol/L) for 4 h. The contents of GSH and MDA were measured, and KCl-SDS method was applied to measure DNA-protein crosslink (DPC).

Results: Hsp70 level in HBE/hsp70 group increased by 80% compared with HBE group. GSH contents in HBE/hsp70 group significantly increased and were 141.0, 119.6 mg/gpro at 0.39, 1.56 mmol/L, respectively (P<0.01), as compared with HBE group. However, it decreased when formaldehyde concentration increased to 6.25 mmol/L. While GSH content in HBE group remained decreasing. MDA contents in HBE/hsp70 and HBE group increased with formaldehyde. MDA content in HBE/hsp70 was 0.088 micromol/gpro and significantly lower than that (0.138 micromol/gpro) in HBE group (P<0.05) when formaldehyde concentration was 1.56 mmol/L, At the formaldehyde dose of 6.25 mmol/L MDA content in HBE/hsp70 was 0.140 micromol/gpro which was significantly lower than that (0.289 micromol/gpro) in HBE group (P<0.01). DPC% in two groups increased with formaldehyde. At the formaldehyde dose of 0.39 mmol/L, DPC% in HBE/hsp70 group was 3.94% which was significantly lower than that (6.25%) in HBE group (P< 0.01). At the formaldehyde dose of 1.56 mmol/L, DPC% in HBE/hsp70 group was 11.86% which was significantly lower than that (20.89%) in HBE group (P<0.05).

Conclusion: Hsp70 can reduce formaldehyde-induced damages in human bronchial epithelium cells in vitro.