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- W2370558070 abstract "AIM: To investigate the role of endoplasmic reticulum stress ( ERS)-induced apoptosis in lung injury following limbs ischemia reperfusion ( LIR) in rats and to observe the effects of taurine. METHODS: Adult male Sprague-Dawley rats ( n = 40) were randomly divided into 4 groups: control group,LIR group,LIR + saline group and LIR + taurine group. The changes of blood gas,the activity of superoxide dismutase ( SOD) and catalase ( CAT) ,and the level of malondialdehyde ( MDA) were detected by biochemical methods. Apoptosis in lung tissues was observed using TdT-mediated dUTP nick end labeling ( TUNEL) assay. The mRNA expression of C/EBP homologous protein ( CHOP) ,activating transcription factor 4 ( ATF4) and X-box binding protein 1 ( XBP1) in the lung tissues was observed by real-time PCR. The protein level of CHOP in the lung tissues was detected by Western blotting. The morphologic changes of the lung tissues were observed under microscope. RESULTS: Compared with control group,PaO2 and PaCO2 in LIR group were reduced,and MDA content was increased. The activity of SOD and CAT was decreased. The cell apoptosis was increased. The protein level of CHOP and mRNA expression of ATF4,XBP1 and CHOP were upregulated. However,taurine significantly attenuated the lung injury following LIR,as showed by reducing the MDA content,decreasing cell apoptosis and inhibiting the mRNA expression of ATF4,XBP1 and CHOP. Furthermore,PaO2 and the activity of SOD and CAT were higher in taurine pretreatment group than those in LIR group. CONCLUSION: The results suggest that taurine attenuates ERS-induced apoptosis in the lungs of the rats with limb ischemia reperfusion." @default.
- W2370558070 created "2016-06-24" @default.
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- W2370558070 date "2010-01-01" @default.
- W2370558070 modified "2023-09-22" @default.
- W2370558070 title "Effects of taurine on endoplasmic reticulum stress-induced cell apoptosis in lung inury following limbs ischemia reperfusion in rats" @default.
- W2370558070 hasPublicationYear "2010" @default.
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