Objective To lay the foundation for analyzing the mechanism of liver cell injury caused by mtDNA deletion and mutation in patients with obstructive jaundice. Methods 30 patients were randomly selected as obstructive jaundice group (case group) and 10 patients as control group according to the strict condition. Author makes use of the methods of PCR amplification of the entire human mitochondrial genome in 17 mismatch-specific overlapping fragments and gene sequencing results to Preliminary estimate the localizathion of hepatocyte mtDNA damage in patients with obstructive jaundice. Result Deletions and length of partial liver cells were 8429-9591 of about 1. 1 kb, 16024-60 of about 0. 6 kb, 1889-3031 of about 1. 1 kb and 4977bps common deletion and the high mutation rate of some bases in D-loop region. Conclusion There are multiple mtDNA deletions and multiple point mutations in patients with obstructive jaundice

Objective To study the role of bone marrow mesenchymalstem cells in recovery process of hepatocyteinjury and to explore the possible mechanism. Methods BMSCs and primary generation of hepatocytes were cultured and identified. A model of hepatocyte injure was established. Liver cell proliferation at different conditionswas detected by MTT method. Hepatocytes were added with BMSCs,baxinhibitor and mixture of BMSCs and baxinhibitor for co?cultured.Expressions of TGF?β1,bcl?2,and baxwere detected by Westernblot and real?time PCR. Results BMSCs and primary generation of hepatocyte were successfully cultured and identified, and a model of hepatocyte injury was successfully established. MTT tests revealed that the OD value of the mixture wassignificant higher in BMSCs and HGF co?culture group than in BMSCs co?culture group or HGF co?culture group;there was no significant difference between BMSCs co?culture group and HGF co?culture group,while both groups were significant higher than control group. The MTT tests also revealed that the OD value of the mixture of BMSCs and Baxinhibitor co?culture group had no significant difference as compared with BMSCs co?culture group or Baxinhibitor co?culture group. There was no significant difference between BMSCs co?culture group and Baxinhibitor co?culture group,while the OD value was significant higher in both groups than in the control group. Westernb lot and real?time PCR results revealed that the value of TGF?β1 and bax in the mixture of BMSCs and Baxinhibitor co?culture group had no significant difference as compared with BMSCs co?culture group or Baxinhibitor co?culture group. There was no significant difference between BMSCs co?culture group and Baxinhibitor co?culture group,while both groups had a significant higher value than the control group. The value of Bcl?2 in the mixture of BMSCs and Baxinhibitor co?culture group had no significant difference as compared with BMSCs co?culture group or Baxinhibitor co?culture group. There was no significant difference between BMSCs co?culture group and Baxinhibitor co?culture group,while both groups had a significant lower value than the control group. Conclusions BMSCs can promote hepatocyte proliferation during the recovery process of hepatocyte injury,BMSCs and HGF promote liver cell proliferation have synergy effect,the effect of BMSCs probably through regulate TGF?β1/bcl?2(bax)correlation pathway.