AIM: To investigate the role of heme oxygenase-1 (HO-1) in pathogenesis of experimental hepatorenal syndrome (HRS). METHODS: Rats were divided into liver cirrhotic group, zinc protoporphyrin IX (ZnPP) treatment group,...AIM: To investigate the role of heme oxygenase-1 (HO-1) in pathogenesis of experimental hepatorenal syndrome (HRS). METHODS: Rats were divided into liver cirrhotic group, zinc protoporphyrin IX (ZnPP) treatment group, cobalt protoporphyrin (CoPP) treatment group and sham group. Biliary cirrhosis was established by bile duct ligation in the first three groups. Rats in the ZnPP and CoPP treatment groups received intraperitoneal injection of ZnPP and CoPP, respectively, 24 h before sample collection. Expression of HO-1 mRNA in kidney was detected by reverse-transcription polymerase chain reaction, while protein expression was determined by immunohis-tochemical analysis. Hematoxylin and eosin staining was performed to observe liver cirrhosis and renal structure. Renal artery blood flow, mean arterial pressure and portal vein pressure, 24 h total urinary volume, serum and urine sodium concentrations, and creatinine clearance rate (Ccr) were also measured.RESULTS: The HO-1 mRNA and protein expression levels in kidney, 24 h total urinary volume, renal artery blood flow, serum and urine sodium concentration and Ccr were lower in cirrhotic group than in sham group (P < 0.05). However, they were significantly lower in ZnPP treatment group than in cirrhotic group and significantly higher in CoPP treatment group than in cirrhotic group (P < 0.05). CONCLUSION: Low HO-1 expression level in kidney is an important factor for experimental HRS.展开更多
目的探讨锌原卟啉(Znpp)对高体积分数氧(高氧)肺损伤早产大鼠的影响。方法出生3 d SD早产大鼠随机分为空气对照组(Ⅰ组),高氧对照组(Ⅱ组),空气加Znpp组(Ⅲ组),高氧加Znpp组(Ⅳ组)。Ⅱ组、Ⅳ组吸入氧体积分数≥900 mL/L,Ⅲ组和Ⅳ组每日...目的探讨锌原卟啉(Znpp)对高体积分数氧(高氧)肺损伤早产大鼠的影响。方法出生3 d SD早产大鼠随机分为空气对照组(Ⅰ组),高氧对照组(Ⅱ组),空气加Znpp组(Ⅲ组),高氧加Znpp组(Ⅳ组)。Ⅱ组、Ⅳ组吸入氧体积分数≥900 mL/L,Ⅲ组和Ⅳ组每日腹腔注射Znpp 45μmol/(kg.d)。于实验第3、7天,分别检测其肺组织匀浆血红蛋白氧合酶-1(HO-1)活性、碳氧血红蛋白(HbCO)水平及支气管肺泡灌洗液TNF-α、总蛋白、丙二醛(MDA)水平,测定肺湿/干质量比值(W/D),光镜下观察其肺组织病理学变化。结果实验第3天,Ⅱ组早产大鼠HO-1活性、HbCO水平、肺W/D及TNF-α水平、总蛋白、MDA水平明显高于Ⅰ组(Pa<0.05,0.01);Ⅳ组HO-1活性、HbCO水平、肺W/D及TNF-α水平、MDA水平明显低于Ⅱ组(Pa<0.01,0.05);实验第7天,Ⅱ组HO-1活性、HbCO水平及TNF-α水平、总蛋白、MDA水平明显高于Ⅰ组(Pa<0.01);Ⅳ组HO-1活性、HbCO水平及TNF-α水平、总蛋白、MDA水平明显低于Ⅱ组(Pa<0.01,0.05)。第3天,Ⅱ组肺组织呈急性炎性反应性改变,Ⅳ组炎性反应减轻明显;第7天,Ⅱ组呈亚急性炎性反应性改变、肺间质纤维化、肺泡发育障碍等,Ⅳ组病理损害有所减轻。结论HO-1参与早产大鼠高氧肺损伤。Znpp可通过抑制HO-1活性,减轻早产鼠高氧肺损伤。展开更多
基金Supported by National Natural Science Foundation of China, No. 30970886Science and Technology Project of Dalian,No. 2008E13SF193
文摘AIM: To investigate the role of heme oxygenase-1 (HO-1) in pathogenesis of experimental hepatorenal syndrome (HRS). METHODS: Rats were divided into liver cirrhotic group, zinc protoporphyrin IX (ZnPP) treatment group, cobalt protoporphyrin (CoPP) treatment group and sham group. Biliary cirrhosis was established by bile duct ligation in the first three groups. Rats in the ZnPP and CoPP treatment groups received intraperitoneal injection of ZnPP and CoPP, respectively, 24 h before sample collection. Expression of HO-1 mRNA in kidney was detected by reverse-transcription polymerase chain reaction, while protein expression was determined by immunohis-tochemical analysis. Hematoxylin and eosin staining was performed to observe liver cirrhosis and renal structure. Renal artery blood flow, mean arterial pressure and portal vein pressure, 24 h total urinary volume, serum and urine sodium concentrations, and creatinine clearance rate (Ccr) were also measured.RESULTS: The HO-1 mRNA and protein expression levels in kidney, 24 h total urinary volume, renal artery blood flow, serum and urine sodium concentration and Ccr were lower in cirrhotic group than in sham group (P < 0.05). However, they were significantly lower in ZnPP treatment group than in cirrhotic group and significantly higher in CoPP treatment group than in cirrhotic group (P < 0.05). CONCLUSION: Low HO-1 expression level in kidney is an important factor for experimental HRS.
文摘目的探讨锌原卟啉(Znpp)对高体积分数氧(高氧)肺损伤早产大鼠的影响。方法出生3 d SD早产大鼠随机分为空气对照组(Ⅰ组),高氧对照组(Ⅱ组),空气加Znpp组(Ⅲ组),高氧加Znpp组(Ⅳ组)。Ⅱ组、Ⅳ组吸入氧体积分数≥900 mL/L,Ⅲ组和Ⅳ组每日腹腔注射Znpp 45μmol/(kg.d)。于实验第3、7天,分别检测其肺组织匀浆血红蛋白氧合酶-1(HO-1)活性、碳氧血红蛋白(HbCO)水平及支气管肺泡灌洗液TNF-α、总蛋白、丙二醛(MDA)水平,测定肺湿/干质量比值(W/D),光镜下观察其肺组织病理学变化。结果实验第3天,Ⅱ组早产大鼠HO-1活性、HbCO水平、肺W/D及TNF-α水平、总蛋白、MDA水平明显高于Ⅰ组(Pa<0.05,0.01);Ⅳ组HO-1活性、HbCO水平、肺W/D及TNF-α水平、MDA水平明显低于Ⅱ组(Pa<0.01,0.05);实验第7天,Ⅱ组HO-1活性、HbCO水平及TNF-α水平、总蛋白、MDA水平明显高于Ⅰ组(Pa<0.01);Ⅳ组HO-1活性、HbCO水平及TNF-α水平、总蛋白、MDA水平明显低于Ⅱ组(Pa<0.01,0.05)。第3天,Ⅱ组肺组织呈急性炎性反应性改变,Ⅳ组炎性反应减轻明显;第7天,Ⅱ组呈亚急性炎性反应性改变、肺间质纤维化、肺泡发育障碍等,Ⅳ组病理损害有所减轻。结论HO-1参与早产大鼠高氧肺损伤。Znpp可通过抑制HO-1活性,减轻早产鼠高氧肺损伤。
