The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

内毒素血症新生大鼠肾组织核因子κB和转化生长因子β1表达及超微结构的动态变化

目的 探讨新生大鼠内毒素血症时肾脏损伤与修复的可能机制.方法 将80只健康7日龄Wistar大鼠随机分为2组,每组40只,对照组腹腔内注射0.9%氯化钠溶液0.1 ml;内毒素组(LPS组)腹腔注射等容积LPS 5 mg/kg.每组大鼠分别于腹腔注射后1、4、8和12 h处死.采用免疫组织化学方法检测肾组织中核因子(NF)-κB及转化生长因子(TGF)-β1表达的动态变化,用透射电镜观察.肾组织超微结构变化.结果 NF-κB在对照组基本无表达,LPS组主要在肾小管上皮细胞表达,于实验后1 h即有升高,8 h达高峰,12 h略有下降.TGF-β1在对照组肾小管中少量表达,LPS组1、4及8 hTCF-β1表达较对照组差异无显著性,而12 h显著升高.电镜下观察到,LPS组于实验后4 h可见肾小球上皮细胞足突融合减少,肾小管上皮细胞线粒体空泡形成,刷状缘无明显改变;12 h肾小球上皮细胞足突明显融合,系膜细胞线粒体嵴断裂,肾小管上皮细胞线粒体扩张.结论 NF-κB参与了新生大鼠内毒素血症时肾损害的病理过程,而TGF-β1可能促进肾组织修复,同时可能抑制NF-κB产生.     

The role of TGF-β/BMP signaling pathway in the development of cardiac outflow tract

Conotruncal anomaly is composed of a group of complex congenital heart diseases. Cardiac outflow tract (OFT) plays an essential role in the cardiac conotruncal development. Recently, transforming growth factor β/bone morphogenetic protein signaling pathway has become a research hotspot, which is recognized as a important regulation mechanism in many processes of the cardiac development, such as separation of OFT and maturation of septums. In this paper we describe the role of the signaling pathway and its effect on the development of cardiac OFT.     

IL-1β诱导NF-κB通路对肠三叶因子治疗坏死性小肠结肠炎的影响及意义

目的 研究肠三叶因子(ITF)对坏死性小肠结肠炎(NEC)新生大鼠的肠黏膜中白细胞介素1β(IL-1β)含量的影响,观察ITF对NEC新生大鼠中核因子-κB(NF-κB)的活化及胞内分布规律,探讨其在NEC发病机制中的作用.方法 50只新生Wistar大鼠随机分为5组(正常对照组、正常对照给予ITF组、NEC模型组、NEC给予生理盐水组、NEC给子ITF组),每组10只,并于NEC模型后,母鼠身边喂养3 d.第四天处死并取回盲部组织1～2 cm固定、包埋、切片、HE染色,观察组织学变化及免疫组化表现NF-κB的表达,其他肠组织制备组织匀浆,取上清液检测IL-1β含量.结果 NEC新生大鼠模型中损伤肠组织IL-1β含量明显增多,NF-κB表达增强.ITF治疗组能明显的抑制NEC新生大鼠肠组织IL-1β的产生和NF-κB(P65)的表达.结论 NF-κB信号通路可能参与了NEC发病过程,并起着信号转导作用;ITF通过抑制NF-κB信号通路,减轻小肠结肠组织炎症反应,起到保护肠黏膜的作用.