BACKGROUND: Hydrophobic bile acids lead to the generation of oxygen free radicals in mitochondria. Accordingly, this study is to investigate if gene delivery of superoxide dismutase (SOD) will reduce hepatocyte injury...BACKGROUND: Hydrophobic bile acids lead to the generation of oxygen free radicals in mitochondria. Accordingly, this study is to investigate if gene delivery of superoxide dismutase (SOD) will reduce hepatocyte injury caused by experimental cholestasis. METHODS: The recombinant of pLNCX-SOD gene packaged with lipofection of AMINE was transfected into hepatocytes in vitro, which stably expressed the SOD gene. RESULTS: After transfection, hepatocytes enhanced the protective effect against injury to bile and the toxicity of serum in obstructive jaundice. The inhibition of bile at the concentration of 2% (v: v, bile: DMEM 1: 50) decreased obviously from (78.80 +/- 12.35)% to (43.35 +/- 9.69)% in 12 hours, from (82.55 +/- 11.27)% to (-26.64 +/- 7.66)% in 24 hours, and from (83.83 +/- 18.69)% to (-19.27 +/- 14.38)% in 48 hours, compared with that of the untransfected cells (P < 0.01). The inhibition of serum at the obstructive jaudice concentration of 2.5% was obviously decreased from (89.72 +/- 1.52)% to (14.68 +/- 14.33)% in 12 hours, from (92.2 +/- 11.27)% to (41.39 +/- 7.66)% in 24 hours, and from (94.25 +/- 8.96)% to (22.71 +/- 4.38)% in 48 hours (P < 0.01). CONCLUSION: Hepatocytes transfected with the pLNCX-SOD gene could obviously be resistant to the toxicity of bile and serum from rat with obstructive jaundice.展开更多
基金This study was supported by a grant from Science Foundation of Educational Department of Liaoning Province,China(No.202203257).
文摘BACKGROUND: Hydrophobic bile acids lead to the generation of oxygen free radicals in mitochondria. Accordingly, this study is to investigate if gene delivery of superoxide dismutase (SOD) will reduce hepatocyte injury caused by experimental cholestasis. METHODS: The recombinant of pLNCX-SOD gene packaged with lipofection of AMINE was transfected into hepatocytes in vitro, which stably expressed the SOD gene. RESULTS: After transfection, hepatocytes enhanced the protective effect against injury to bile and the toxicity of serum in obstructive jaundice. The inhibition of bile at the concentration of 2% (v: v, bile: DMEM 1: 50) decreased obviously from (78.80 +/- 12.35)% to (43.35 +/- 9.69)% in 12 hours, from (82.55 +/- 11.27)% to (-26.64 +/- 7.66)% in 24 hours, and from (83.83 +/- 18.69)% to (-19.27 +/- 14.38)% in 48 hours, compared with that of the untransfected cells (P < 0.01). The inhibition of serum at the obstructive jaudice concentration of 2.5% was obviously decreased from (89.72 +/- 1.52)% to (14.68 +/- 14.33)% in 12 hours, from (92.2 +/- 11.27)% to (41.39 +/- 7.66)% in 24 hours, and from (94.25 +/- 8.96)% to (22.71 +/- 4.38)% in 48 hours (P < 0.01). CONCLUSION: Hepatocytes transfected with the pLNCX-SOD gene could obviously be resistant to the toxicity of bile and serum from rat with obstructive jaundice.
