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Objective: By observing the effects of electroacupuncture (EA) on the apoptosis of conjunctival cells of rabbits with dry eye syndrome (DES) and the expressions of apoptosis-related proteins Caspase-3, Fas and Bcl-2, to discuss the mechanism of EA in the treatment of DES from the perspective of cell apoptosis. Methods: Male New Zealand rabbits were randomly divided into a normal group (NG), a model group (MG), an EA group (EAG) and a sham EA group (SEAG). DES rabbit model was developed by eye drop of 0.1％ benzalkonium chloride. The rabbit tear secretion and tear film break-up time (BUT) were measured; terminal deoxynucleotidyl transferase- mediated dUTP nick end labeling (TUNEL) assay was used to detect the apoptosis of conjunctival cells; the expressions of Caspase-3, Fas and Bcl-2 proteins in conjunctival cells were detected by immunohistochemistry. Results: Compared with the NG, the rabbit tear secretion decreased and the BUT was shortened in the MG (both P<0.01); compared with the MG and the SEAG, the rabbit tear secretion increased and the BUT was prolonged in the EAG (all P<0.05). Compared with the NG, the apoptosis of rabbit conjunctival cells increased (P<0.01), the expressions of Caspase-3 and Fas proteins increased (both P<0.05), and the expression of Bcl-2 protein decreased (P<0.01) in the MG; compared with the MG and the SEAG, the apoptosis of rabbit conjunctival cells decreased (both P<0.01), the expressions of Caspase-3 and Fas proteins decreased (all P<0.05), and the expression of Bcl-2 protein increased (both P<0.01) in the EAG. Conclusion: EA can inhibit the apoptosis of rabbit conjunctival cells, down-regulate the expressions of apoptosis-related proteins Caspase-3 and Fas, and up-regulate the expression of Bcl-2 protein, which may be one of the mechanisms of EA in treatment of DES.
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Objective To study the possible mechanisms by which repetitive transcranial magnetic stimulation (rTMS) pretreatment antagonizes seizures induced by lithium chloride-pilocarpine and any correlation with antiapoptosis in hippocampal CA1 neurons.Methods Thirty rats were randomly divided into a control group, a sham stimulation group and an rTMS pretreatment group. The rTMS pretreatment group was pretreated on 7 consecutive days with low-frequency rTMS (0.5 Hz, 75％ of threshold intensity, 20 times/bundle, and 5 bundles/d), while the sham-stimulation group was sham-stimulated with a similar sound. Lithium chloride-pilocarpine ( LPC ) was used to induce a model epileptic state.Epileptic stroke latency and severity were recorded ; neuronal morphology was observed using hematoxylin and eosin (HE) staining; mean positive-reactive cell number and mean optical density and absorbance of B cell lymphoma/leukemia gene-2 (Bcl-2) were recorded, and Fas and Caspase-3 protein in the hippocampal CA1 region were observed with immunohistochemistry.Results Compared with the sham stimulation group, epileptic latency in the rTMS pretreatment group was significantly longer. Seizures in the rTMS pretreatment group were less severe, and a number of degenerated neurons were observed to be apoptotic. Bcl-2 protein expression increased at each time point, but Fas and Caspase-3 protein expression decreased.Conclusions rTMS pretreatment has an anti-epilepsy effect. The possible neuronal protection might be produced by regulating the expression of Bcl-2, Fas and Caspase-3 protein in the hippocampus.
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Systemic lupus erythematosus is a prototypical autoimmune disease characterized by the deregulation of T and B cells, tissue infiltration by mononuclear cells, tissue damage and the production of autoantibodies. There is a consensus that accelerated apoptosis of circulating lymphocytes and/or impaired clearance of apoptotic bodies may increase the amount of nuclear antigens presented to T lymphocytes. This process is accompanied by autoimmune responses that can lead to the development of lupus. The dysfunction of apoptosis may be a direct consequence of alterations in proteins/genes such as Fas, Bcl-2 and C1q. Increased expression of Fas antigen could intensify the exposure of hidden antigens. The overexpression of Bcl-2 protein might inhibit the removal of auto-reactive cells, and the lack of C1q could impair the clearance of self-antigens. The complete knowledge of the role of apoptosis components in the etiopathogenesis of lupus could lead to the development of new therapies targeting the apoptotic threshold, which could result in a more specific and effective disease response compared to global immunosuppression. This review summarizes the role of each component of the apoptotic process in the pathogenesis of lupus.
Subject(s)
Humans , Apoptosis/immunology , Complement C1q/immunology , Fas Ligand Protein/immunology , Lupus Erythematosus, Systemic/etiology , /immunology , Complement C1q/deficiency , Fas Ligand Protein/metabolism , Lupus Erythematosus, Systemic/immunology , /metabolismABSTRACT
Objective To explore the molecular mechanism of bilirubin in the hippocampus of the newborn rats with hyperbilirubinemia. Methods Hyperbilirubinemia model was established. The expression levels of Fas protein and N methyl D aspartate (NMDA) receptor and the apoptosis rate of nerve cells in rat hippocampus were detected with immunochemistry, TUNEL method and cytometry. Results Histological changes of nerve cells were found in hippocampal area of rats with hyperbilirubinemia. Significantly increased expression levels of Fas protein and NMDA receptor and apoptosis rate of nerve cells were positively correlated with the bilirubin level in rat brain tissues. Conclusion The bilirubin neurotoxicity is mediated by the excessive activation of NMDA receptor and participation of Fas system, which induces the apoptosis of nerve cells.
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AIM: To investigate the changes of the expression of Bcl-2 and Fas protein and the apoptosis in HL-60 cells induced by cyclosporine A. METHODS: The expression of Bcl-2 and Fas protein and apoptosis in (HL-60) cells were measured by immunohistochemistry analysis and flow cytometric analysis. RESULTS: There was strong expression of Bcl-2 in HL-60 cells, treatment with cyclosporine A (CsA) for 8-10 h down-regulated the expression of Bcl-2. Fas protein expression in HL-60 cells was very low, CsA induced apoptosis of HL-60 cells, but didn't induce Fas protein expression. CONCLUSION: CsA induces apoptosis in HL-60 cells by down-regulating Bcl-2 expression. [
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Objective To explore the mechanism of Xiao Chaihu decoction in t he treatment of endometriosis in rats.Methods The rat model of endometriosis w as established. Fas and Caspase- 3 protein expression in the eutopic endometriu m and eutopic endometrium were observed by immunohistochemical method.Results The protein expression of Fas and Caspase- 3 in ectopic endometrium of Xiao Cha ihu decoction group was higher than that in the eutopic endometrium, while the r esult in the control group was just the opposite. No significant difference was shown in Danazol group. Conclusion The therapeutic mechanism of Xiao Chaihu de coction for endometriosis may be related to the promotion the apoptosis of ectop ic endometrium tissue by increasing Fas protein expression.
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Objective To construct Fas-targeting siRNA-expressing plasmid, and explore the significance of Fas inhibition in the treatment of acute aplastic anemia. Methods U6 promoter cassette and siFas sequence were obtained by PCR method, and cloned into modified pcDNA3.1 to produce plasmid pU6-siFas, which was transfected into P815 cells with limpofectin 2000, and then Fas expression was detected by immunohistochemistry. Results The plasmid pU6-siFas could efficiently reduce the expression of Fas and confer G-418 resistance in P815 cells. Conclusion The successful construction of the siRNA expressing plasmid will facilitate the application of RNA interference technique, and lay foundation for further studies of the therapeutic effect of Fas inhibition on acute aplastic anemia.