AIM:Liver regeneration is associated with apoptosis ofhepatocytes,which is mediated via tumor necrosis factorreceptor 1(TNFR1).The shedding of TNFR1 in liverregeneration and its mechanism to regulate this sheddingwere investigated.METHODS:The shedding of TNFR1 in liver regenerationand changes of TNF-α,PMA and plasma membrane purifiedfrom hepatocytes on this shedding process were measuredwith Western blot.Then,the relationship between TNFRishedding and apoptosis of hepatocytes induced by TNFαwas studied by detecting apoptotic index.RESULTS:The shedding of TNFR1 began at 4 hours andterminated before 2 months after partial hepatectomy.Inculture system,serum from rats at 36 h after partialhepatectomy could also promote this shedding process.Withthe stimulation of TNFα,PMA or purified plasma membranefrom hepatocytes at 36 h after partial hepatectomy or fromhepatooltes treated with TNF α for 2 h,membranous TNFR1was also shed.With the stimulation of both TNF α and plasmamembrane from hepatocytes affected with TNF α for 2 h orfrom hepatocytes at 36 h after partial hepatectomy,apoptoticindex of hepatocytes decreased from 21% to 7.52 % and8.45 %,respectively.PMA could also reduce apoptotic indexto 13.67 %.This descent occurred in hepatocytes culturedin serum from rats at 36 h after partial hepatectomy too,but not in serum from rats at 2 months after partialhepatectomy and sham-operated rats.CONCLUSION:Shedding of TNFR1 may help reduceapoptosis of hepatocytes induced by TNF α.Membrane-anchored metalloprotases could play a role in sheddingmembranous TNFR1.At the same time,PKC may take partin regulation of this shedding process. AIM: Liver regeneration is associated with apoptosis of hepatocytes, which is mediated via tumor necrosis factor receptor 1 (TNFR1). The shedding of TNFR1 in liver regeneration and its mechanism to regulate this shedding were investigated. METHODS: The shedding of TNFR1 in liver regeneration and changes of TNF- α, PMA and plasma membrane purified from hepatocytes on this shedding process were measured with Western blot. Chen, the relationship between TNFRished and apoptosis of hepatocytes induced by TNFαwas studied by Proboscio. apoptotic index .RESULTS: The shedding of TNFR1 began at 4 hours andterminated before 2 months after partial hepatectomy. In culture system, serum from rats at 36 h after partial hpatectomy could also promote this shedding process. Whether the stimulation of TNFα, PMA or purified plasma membranefrom hepatocytes at 36 h after partial hepatectomy or from hepatoolt treated with TNFα for 2 h, membranous TNFR1was also shed.With the stimulation of both TNFα and plasma membrane from hep atocytes affected with TNFα for 2 h orfrom hepatocytes at 36 h after partial hepatectomy, apoptotic index of hepatocytes decreased from 21% to 7.52% and 8.45% respectively. PMA could also reduce apoptotic index to 13.67%. This descent occurred in hepatocytes cultured in serum from rats at 36 h after partial hepatectomy too, but not in serum from rats at 2 months after partial hepatectomy and sham-operated rats. CONCLUSION: Shedding of TNFR1 may help reduceapoptosis of hepatocytes induced by TNFα. Membrane-anchored metalloprotases could play a role in sheddingmembranous TNFR1.At the same time, PKC may take partin regulation of this shedding process.