AIM: To investigate the effect of ischemic preconditioning(IPC) on expression of nitric oxide synthase(NOS) in rat smallfor-size liver graft and its significance.METHODS: Sixty SD rats were randomly divided into 3 groups(n=10 pairs/group): nonwarm ischemia group(NWI);warm ischemic group(WI);and ischemic preconditioning group(IPC).The models of rat small-for-size liver transplantation were set up by two-cuff technique.Expression of eNOS mRNA and iNOS mRNA in hepatic tissue were detected by fluorescence-quantitating-PCR.RESULTS: Heptic expression of eNOS mRNA post-IPC was higher than that pre-IPC(P0.05).It was higher in IPC group than that in NWI and WI group(P

Objective To investigate the expression and genetic alterations of KLF6 in hepatocellular carcinoma (HCC) and explore their functional mechanisms in the oncogenesis and development of HCC. Methods Real-time quantitative-PCR, direct sequencing and LOH approaches were used to detect KLF6 genetic abnormalities in HCC. The experiment had 2 groups, an experimental group and a control group. In the experimental group, the transfected plasmid pcDNA3.0 was recombined with KLF6 and tranfected into HCC HepG2 cells. MTT, flow cytometry and Western blotting were used to observe the effect of anti-oncogene wild type KLF6 on HepG2 cells by transgenic method for 48 h.Results Expression levels of KLF6 were significantly downregulated in HCCs(P＜0. 01), as detected by qRT-PCR. LOH occurred in 11 (52%) of the 21 tumors, and all the samples with LOH showed KLF6 down-regulation. The mutational frequency was 29%, and sequence changes located in activation domain of KLF6. Meanwhile, MTT assay showed a significant antiproliferative effect of the transfected wtKLF6 on HepG2 cells(42.7%, P＜0.05). Fluorescence-activated cell sorting analysis revealed that KLF6 induced apoptosis. Conclusion The deregulation of KLF6 together with genetic abnormalities of allelic imbalance and mutations may play an important role in HCC pathogenesis.