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Keap1 -Nrf2/ARE pathway plays a wide role of cell protection function in anti-tumor,antistress,anti-apoptosis,anti-inflammatory response.It has become a focus of the neuroprotective effects in nervous system.We will review on the latest research of Keap1-Nrf2/ARE pathways in cerebral ischemia.It will provide a basis for the prevention and treatment of central nervous system.
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Objective To investigate the effects of SAHA on the differentiation of human hepatocellular carcinoma(HCC)SMMC-7721 cells.Methods Cell morphology was examined by light microscopy;Cell viability was determined by MTT assay;The expression of Alpha-fetoprotein(AFP)and proliferating cell nuclear antigen(PCNA)was analyzed with immunocytochemistry;Flow cytometry(FCM)was used to investigate the cell cycle;The expression of p21 WAF1 mRNA was detected by semi-quantitative RT-PCR.Results Light microscopy showed that SMMC-7721 cells induced by SAHA underwent restorational alterations in morphology which were different from those of nontreated cells but were similar to those of normal cells;MTT assay showed that SAHA inhibited the proliferation of SMMC-7721 cells in a dose-dependent and time-dependent way;Immunocytochemistry assay showed that the expression of AFP and PCNA decreased significantly;FCM analysis showed SAHA could arrest SMMC-7721 cells at G0/G1 phase,with an accumulation of the cells at G0/G1 phase while a decrease of cells at S phase;Semi-quantitative RT-PCR detection revealed that the expression of p21 WAF1mRNA was upregulated remarkably in the cells treated with SAHA.Conclusion SAHA could induce differentiation of human HCC SMMC-7721 cells inhibiting enzymatic activity of HDAC,upregulating the expression of p21 WAFlmRNA as well as causing arrest of HCC cells at G0/G1 phase.
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Objective To detect the induction of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in immunostimulated retinal pigment epithelial (RPE) cells to seek for the supplying of the arginine, a substrate for NOS; as well as the effects of produced NO on the tight junction of RPE-J cells. Methods Rat′s RPE-J cells were treated with interferon-?(INF-?), tumor necrosis factor-?(TNF-?) and lipopolysaccharide (LPS), and Northern and Western blotting were applied to analyze the expression of the citrulline-NO cycle enzymes and related enzymes and the effect of dexamethasone and cyclic adenosine monophosphate (camp) on the expression of iNOS. Immunocytochemistry reaction and Western blotting were used to evaluate the effect of produced NO on the tight junctions of RPE-J cells. Results iNOS and argininosuccinate synthetase (AS) were highly induced at both mRNA and protection levels in immunostimulated RPE cells while arginiosuccinate lyase (AL) was not induced. NO was produced by cells after stimulation with TNF?, IFN? and LPS. The induction of iNOS mRNA and the production of NO by these immunostimulated cells was further enhanced by cAMP. NO was produced from citrulline as well as from arginine. And the produced NO impaired the tight junction of RPE-J cells, decreased the production of tight junction related protein ZO-1. Conclusion In activated RPE-J cells, citrulline-arginine recycling is important for NO production, and the produced NO weakened the function of tight junction of RPE-J cells.