AIMTo explore the effect of hydrogen sulfide (H<sub>2</sub>S) on restraint water-immersion stress (RWIS)-induced gastric lesions in rats and the influence of adenosine triphosphate (ATP)-sensitive potassiu...AIMTo explore the effect of hydrogen sulfide (H<sub>2</sub>S) on restraint water-immersion stress (RWIS)-induced gastric lesions in rats and the influence of adenosine triphosphate (ATP)-sensitive potassium (K<sub>ATP</sub>) channels and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway on such an effect.METHODSMale Wistar rats were randomly divided into a control group, a physiological saline (PS) group, a sodium hydrosulfide (NaHS) group, a glibenclamide (Gl) group, Gl plus NaHS group, a pyrrolidine dithiocarbamate (PDTC) group, and a PDTC plus NaHS group. Gastric mucosal injury was induced by RWIS for 3 h in rats, and gastric mucosal damage was analyzed after that. The PS, NaHS (100 μmol/kg body weight), Gl (100 μmol/kg body weight), Gl (100 μmol/kg or 150 μmol/kg body weight) plus NaHS (100 μmol/kg body weight), PDTC (100 μmol/kg body weight), and PDTC (100 μmol/kg body weight) plus NaHS (100 μmol/kg body weight) were respectively injected intravenously before RWIS.RESULTSRWIS induced serious gastric lesions in the rats in the PS pretreatment group. The pretreatment of NaHS (a H<sub>2</sub>S donor) significantly reduced the damage induced by RWIS. The gastric protective effect of the NaHS during RWIS was attenuated by PDTC, an NF-κB inhibitor, and also by glibenclamide, an ATP-sensitive potassium channel blocker, in a dose-dependent manner.CONCLUSIONThese results suggest that exogenous H<sub>2</sub>S plays a protective role against RWIS injury in rats, possibly through modulation of K<sub>ATP</sub> channel opening and the NF-κB dependent pathway.展开更多
ATP-sensitive potassium channel(KATP) consists of a 4.4 complex of an inwardly rectifying Kir6.x pore plus a sulfonylurea receptor,which is an ATP-binding cassette transporter.KATP has been indentified in a variety of...ATP-sensitive potassium channel(KATP) consists of a 4.4 complex of an inwardly rectifying Kir6.x pore plus a sulfonylurea receptor,which is an ATP-binding cassette transporter.KATP has been indentified in a variety of tissues and recognized as an important drug target.It connects cell metabolism with cell electric activity.KATP has been proposed to play protective roles during heart failure,arrhythmia,myocardial infarction,stress,myocardial ischemia and hypertension.In this review,a summary of KATP is presented with molecular structure,localization,regulation,cardiovascular protective effect and its mechanisms.展开更多
目的探讨辛伐他汀预处理对缺血再灌注损伤的保护作用及其作用机制。方法结扎冠状动脉左前降支3h后再开放60min,在20只血脂正常兔建立缺血再灌注模型,随机分为对照组、辛伐他汀组、格列苯脲组和格列苯脲加辛伐他汀组。再灌注结束后,测定...目的探讨辛伐他汀预处理对缺血再灌注损伤的保护作用及其作用机制。方法结扎冠状动脉左前降支3h后再开放60min,在20只血脂正常兔建立缺血再灌注模型,随机分为对照组、辛伐他汀组、格列苯脲组和格列苯脲加辛伐他汀组。再灌注结束后,测定各组血清心肌型肌酸激酶同工酶(MB isoenzyme of creatine kinase,CK-MB)活性,用伊文蓝及氯化三苯四唑啉染色计算心肌梗死面积。结果辛伐他汀组心肌梗死面积及CK-MB活性较对照组和格列苯脲组减少(P<0.01),格列苯脲组与对照组差异无统计学意义(P>0.05),格列苯脲加辛伐他汀组较对照组减小(P<0.05),但仍明显高于辛伐他汀组(P<0.05)。结论辛伐他汀可明显减小缺血再灌注模型的心肌梗死面积,对缺血再灌注损伤具有保护作用,可能与辛伐他汀激活三磷腺苷敏感性钾通道有关。展开更多
基金Natural Science Foundation of Shandong Province,No.ZR2015CL016 and No.ZR2011CL012Colleges and Universities of Shandong Province Science and Technology Plan Projects,No.J11LC17
文摘AIMTo explore the effect of hydrogen sulfide (H<sub>2</sub>S) on restraint water-immersion stress (RWIS)-induced gastric lesions in rats and the influence of adenosine triphosphate (ATP)-sensitive potassium (K<sub>ATP</sub>) channels and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway on such an effect.METHODSMale Wistar rats were randomly divided into a control group, a physiological saline (PS) group, a sodium hydrosulfide (NaHS) group, a glibenclamide (Gl) group, Gl plus NaHS group, a pyrrolidine dithiocarbamate (PDTC) group, and a PDTC plus NaHS group. Gastric mucosal injury was induced by RWIS for 3 h in rats, and gastric mucosal damage was analyzed after that. The PS, NaHS (100 μmol/kg body weight), Gl (100 μmol/kg body weight), Gl (100 μmol/kg or 150 μmol/kg body weight) plus NaHS (100 μmol/kg body weight), PDTC (100 μmol/kg body weight), and PDTC (100 μmol/kg body weight) plus NaHS (100 μmol/kg body weight) were respectively injected intravenously before RWIS.RESULTSRWIS induced serious gastric lesions in the rats in the PS pretreatment group. The pretreatment of NaHS (a H<sub>2</sub>S donor) significantly reduced the damage induced by RWIS. The gastric protective effect of the NaHS during RWIS was attenuated by PDTC, an NF-κB inhibitor, and also by glibenclamide, an ATP-sensitive potassium channel blocker, in a dose-dependent manner.CONCLUSIONThese results suggest that exogenous H<sub>2</sub>S plays a protective role against RWIS injury in rats, possibly through modulation of K<sub>ATP</sub> channel opening and the NF-κB dependent pathway.
文摘ATP-sensitive potassium channel(KATP) consists of a 4.4 complex of an inwardly rectifying Kir6.x pore plus a sulfonylurea receptor,which is an ATP-binding cassette transporter.KATP has been indentified in a variety of tissues and recognized as an important drug target.It connects cell metabolism with cell electric activity.KATP has been proposed to play protective roles during heart failure,arrhythmia,myocardial infarction,stress,myocardial ischemia and hypertension.In this review,a summary of KATP is presented with molecular structure,localization,regulation,cardiovascular protective effect and its mechanisms.
文摘目的探讨辛伐他汀预处理对缺血再灌注损伤的保护作用及其作用机制。方法结扎冠状动脉左前降支3h后再开放60min,在20只血脂正常兔建立缺血再灌注模型,随机分为对照组、辛伐他汀组、格列苯脲组和格列苯脲加辛伐他汀组。再灌注结束后,测定各组血清心肌型肌酸激酶同工酶(MB isoenzyme of creatine kinase,CK-MB)活性,用伊文蓝及氯化三苯四唑啉染色计算心肌梗死面积。结果辛伐他汀组心肌梗死面积及CK-MB活性较对照组和格列苯脲组减少(P<0.01),格列苯脲组与对照组差异无统计学意义(P>0.05),格列苯脲加辛伐他汀组较对照组减小(P<0.05),但仍明显高于辛伐他汀组(P<0.05)。结论辛伐他汀可明显减小缺血再灌注模型的心肌梗死面积,对缺血再灌注损伤具有保护作用,可能与辛伐他汀激活三磷腺苷敏感性钾通道有关。
