AIM: To detect the changes of heme oxygenase-1 (HO-1) expression in kidney following ischemia-reperfusion of hindlimbs and to elucidate their significance. METHODS: Health SD rats were randomly divided into normal (N), sham (S), 4h ischemia without reperfusion (I), 4 h ischemia-2, 6, 12, 18 or 24 h reperfusion (I-R) groups and I-R18h+zinc protoporphyrin (ZnPP) group. I-R was established using the occlusion for 4 h and re-opening for 2-24 h of the femoral arteries. In I-R 18 h+ZnPP group, ZnPP (5 ?mol?kg~(-1) body weight) was intravenously injected 6 h and 12 h after reperfusion, respectively. The expression of HO-1 mRNA in kidney was detected with reverse transcription-polymerase chain reaction (RT-PCR). The expression and location of HO-1 protein were detected with immunohistochemical technique. The observation of pathologic changes of kidney was made following the inhibition of HO-1 by ZnPP. RESULTS: The relative expression level of HO-1 mRNA significantly increased in I-R group, compared to those in the control groups, It was maximal in I-R 18 h group, and thereafter expression level of HO-1 mRNA decreased, however significant expression was still detected in I-R 24 h group (P

AIM: To investigate the pathologic changes in the brain and its underlying mechansims during ischemia-reperfusion of rat hindlimbs.METHODS: SD rats were divided into the normal(N), sham(S), 4 h ischemia without reperfusion(I), and 4 h ischemia-2, 6,12,18 or 24 h reperfusion (I-R) groups at random. Ischemia and ischemia-reperfusion were established with the occlusion or/and re-opening of the terminal of abdominal aorta, respectively. The pathologic changes in the brain tissue were morphologically observed. The expression of inducible nitric oxide synthase ( iNOS ) mRNA, and iNOS protein and the nitrotyrosine, a marker of peroxynitrite (ONOO -),in the brain tissue were detected with RT-PCR and immunohistochemical technique, respectively. The brain superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents were spectraphotometrically measured.RESULTS: Hydropic degeneration and severe injury to neurons were only showed in I-R group. Expressions of iNOS mRNA and protein were demonstrated in I-R, I and S groups, which were maximal in I-R 6 h group. iNOS positive neurons and microglias were more spread in I-R 6 h group than those in S and I groups. NT positive neurons were localized in the cerebral cortex and hippcampus of I-R 6 h group. The contents of MDA markedly increased, while the activity of SOD significantly decreased in I-R 6 h group compared to the N, S and I groups. There were no significant changes in MDA and SOD in N, S and I groups.CONCLUSION: Severe ischemia-reperfusion of rat hindlimbs could induce brain injury, and its mechanisms might be related to enhanced expression of iNOS -NO-ONOO - in the brain.

AIM: To study the role of high level of endogenous nitric oxide (NO) in apoptosis of alveolar epithelial cells in the development of pulmonary fibrosis in rats. METHODS: The content of nitrite/nitrate (NO 2-/NO 3-) in out-flowing pulmonary blood (OPB) was assayed by nitric acid reduction method. The apoptosis of alveolar epithelial cells was observed by TdT-mediated dUTP nick-end labeling (TUNEL) and electron microscopy, respectively. The above indices were observed on the day 14 and the day 30 after intratracheal administration of BLMA 5 alone or along with blockade of iNOS by aminoguanidine (AG) in rats. RESULTS: (1) Both the content of NO 2-/NO 3- in OPB and the number of apoptotic alveolar epithelial cells in lung were increased in BLMA 5 14 d group, compared with normal control group and BLMA 5 30 d group, respectively (P

AIM: To detect the changes of heme oxygenase-1(HO-1) expression in brain following ischemia-reperfusion of hindlimbs in rats and to elucidate their significance. METHODS: Ischemia-reperfusion was established using the occlusion for 4 h and re-opening for 2-24 h of the femoral arteries. The expression of HO-1 mRNA in brain was detected with reverse transcription-polymerase chain reaction (RT-PCR). The expression and location of HO-1 protein were detected with immunohistochemical technique. The observation of pathologic changes of brain was made following the inhibition of HO-1 by zinc protoporphyrin (ZnPP). RESULTS: The relative expression level of HO-1 mRNA significantly increased in I-R group, compared to those in control group. It was maximal in I-R 12 h group, and thereafter expression level of HO-1 mRNA decreased, however significant expression was still detected in I-R 24 h group (P

AIM:To investigate the pathologic changes in the brain and its underlying mechansims during ischemia-reperfusion of rat hindlimbs.METHODS:SD rats were divided into the normal(N), sham(S), 4 h ischemia without reperfusion(I), and 4 h ischemia-2, 6,12,18 or 24 h reperfusion (I-R) groups at random. Ischemia and ischemia-reperfusion were established with the occlusion or/and re-opening of the terminal of abdominal aorta, respectively. The pathologic changes in the brain tissue were morphologically observed. The expression of inducible nitric oxide synthase (iNOS) mRNA, and iNOS protein and the nitrotyrosine, a marker of peroxynitrite (ONOO-)，in the brain tissue were detected with RT-PCR and immunohistochemical technique, respectively. The brain superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents were spectraphotometrically measured.RESULTS:Hydropic degeneration and severe injury to neurons were only showed in I-R group. Expressions of iNOS mRNA and protein were demonstrated in I-R, I and S groups, which were maximal in I-R 6 h group. iNOS positive neurons and microglias were more spread in I-R 6 h group than those in S and I groups. NT positive neurons were localized in the cerebral cortex and hippcampus of I-R 6 h group. The contents of MDA markedly increased, while the activity of SOD significantly decreased in I-R 6 h group compared to the N, S and I groups. There were no significant changes in MDA and SOD in N, S and I groups.CONCLUSION:Severe ischemia-reperfusion of rat hindlimbs could induce brain injury, and its mechanisms might be related to enhanced expression of iNOS-NO-ONOO- in the brain.