肠三叶因子对新生鼠NEC模型PI3K和caspase-3/9的影响

目的 利用PI3K的特异性抑制剂Wortmannin阻断PI3K/Akt细胞信号转导通路,观察ITF对新生鼠NEC模型caspase-3及caspase-9水平的影响,探讨ITF对NEC的保护作用机制.方法 建立NEC模型,对新生一日龄Wistar大鼠予100%氮气,1 min后放4℃冷环境中持续10min,每日2次,随后放回自制的保温箱内人工喂养,第四天处死,取肠组织待检.新生鼠50只随机分为5组,每组10只,A组为NEC模型后予以腹腔注射生理盐水0.2 ml;B组NEC模型后予以腹腔注射ITF0.2 mg;C组为NEC模型后腹腔内注射wortmannin(0.1 mg/kg);D组为NEC模型后腹腔内注射ITF+wortmannin;E组为正常对照组.取近回盲部1～2 cm肠道组织固定包埋、切片、HE染色做病理学检查,其他肠道组织制备组织匀浆取上清液应用ELISA试剂盒检测PI3K的含量及用分光光度法检测caspase-3/9的活性.结果 病理切片显示A组HE染色见肠壁损伤轻重不一,可见全肠黏膜绒毛坏死,病理评分中位积分3分;B组病变明显减轻,肠上皮细胞少量脱落,顶端绒毛坏死,病理评分中位积分1分;C、D组病理评分中位积分3分.A组组织匀浆中PI3K的含量(pg/ml)较E组略升高(P<0.05),与D组差异无统计学意义(P>0.05);B组PI3K表达水平较其他组显著升高(P<0.01);C组与E组比较显著降低,差异有统计学意义(P<0.01).Caspase-3及caspase-9活性在A组较B、E组明显升高,差异有统计学意义(P<0.01),C组更加明显升高(P<0.01),A、D组及B、E组之间,差异无统计学意义(P>0.05).结论 通过腹腔注射ITF可以减轻NEC后的肠道炎症反应,ITF有可能为治疗NEC提供新的方法 ;PI3K/Akt细胞信号转导通路参与了NEC发病过程,并起着信号转导作用.而ITF可能是通过激活PI3K/Akt信号转导途径来下调caspase-3/9的水平,从而保护新生Wistar大鼠NEC模型肠道损伤.     

肠三叶因子对新生鼠NEC模型PI3K和caspase-3/9的影响

Objective To study the effects of ITF on PI3K (phosphatidylinositol 3-kinase) and caspases-3/9 (cysteinyl aspartate-specific protea-ses) in neonatal rat NEC model. Methods NEC model of neonatal rats was established. Asphyxia stress was accomplished by exposure to l00% nitrogen for 60s, followed by exposure to coldness (4 ℃ ) for 10 min twice daily. Neonatal rats were fed formula (200 kcal/kg/day) every 3 h via an gavage tube. The feeding volume began at 0. 1 cc every 3 h and was increased incrementally. This procedure is done once everyday and continued for 3 days. On the 4th day,all the subjects were sacrificed. Fifty neonatal rats were randomized into five groups: A) NEC + NS0. 2mi, (B) NEC + ITF 0. 2 mg, (C) NEC(Wortmannin (0. 1 mg/kg) (D) NEC + ITF 0. 2 mg + Wortmannin (0. 1 mg/kg), (E) control. The intestinal tissue located at the boundary of ileum and cecum was sampled for histology. The remaining intestinal tissue was homogenized. After the homogenate was centrifuged,supernatants were used to assay PI3K and Caspase-3 and caspase-9. Results The pathological lesions showed that intestinal necrosis was severe in group A、C and D, which was graded as 3points. They were significantly decreased in group B,which was graded 1 point. The level of PI3K(pg/ml)in Group A was higher than those in group E (P<0. 05), the latter had difference with those in group D(P>0. 05). The level of PI3K(pg/ml) were the strongest in group B and were lowest in group C. The activity of Caspase-3 and Caspase-9 were significantly increased in group A compared to those in group B and E (P<0. 01 ),and was significantly increased in Group C(P<0. 01 ). Caspase-3 and Caspase-9 levels of group A and D,group B and E showed no significant difference(P>0. 05). Conclusions Intestinal inflammation was ameliorated by intraperitoneal ITF. ITF may provide a new therapy for NEC; PI3K/Akt signal pathways might play important roles in signal transduction during NEC;ITF may protect the intestinal injury of neonatal Wistar rat by activation of PI3K/Akt signal transduction pathway, and down regulation of caspase-9.     

肠三叶因子对坏死性小肠结肠炎新生鼠白细胞介素-6的影响

目的探讨肠三叶因子（ITF）对坏死性小肠结肠炎（NEC）新生大鼠肠黏膜组织IL-6水平的影响，分析ITF对NEC的保护作用机制。方法新生鼠32只随机分为4组，每组各8只，正常对照组（A组）；NEC模型组（B组）；NEC模型后予以皮下注射9g/L盐水0．2mL（C组）；NEC模型后予以皮下注射ITF0.2mg（D组）。取近回盲部1-2cm肠道组织固定包埋、切片、HE染色做病理学检查，其他肠道组织制备组织匀浆取上清液检测IL-6水平。结果B、C组组织匀浆IL-6的水平较A、D组显著增高（Pa〈0.05，0．01），A与D组无明显差异（P〉0．05）。病理切片显示C、D组HE染色切片见肠壁损伤轻重不一，可见全肠黏膜绒毛坏死，病理评分的中位积分为3分；D组肠上皮细胞少量脱落，顶端绒毛坏死，病理评分的中位积分为1分。结论通过皮下注射ITF可减轻NEC后的肠道炎性反应。ITF有可能为治疗NEC提供新的方法。     

新生儿低钠血症22例临床分析

1989年3月～12月,我们对部分住院新生儿患儿进行血清钠测定。其中22例伴有低钠血症,现报道如下: 一、一般资料:22例中,男16例,女6例,足月儿19例,早产儿2例,过期产儿1例,体重≥2500g19例,<2500g 3例;日龄2～7天12例,～14天8例,～28天名例。其中化脓性脑膜炎1例,缺血缺氧性脑     

晚期妊娠妇女与非妊娠健康妇女骨矿含量对应研究

８６例妊娠晚期妇女及８９例非妊娠健康妇女的桡骨骨宽（ＢＷ）、骨矿含量（ＢＭＣ）及血清Ｃａ（２＋）、Ｐ（２－）、总蛋白（ＴＰ）、白蛋白（ＡＬＢ）、碱性磷酸酶（ＡＬＰ）的对照研究，结果表明：两者的ＢＷ差异无显著性（Ｐ＜０．０５），而ＢＷＣ、Ｃａ（２＋）、Ｐ（２－）、ＴＰ、ＡＬＢ的测定值，妊娠晚期妇女明显低于非妊娠健康妇女，有差异显著性（Ｐ＜０．０５）。说明我市妊娠妇女的Ｃａ（２＋）、Ｐ（２－）和蛋白质摄入不足，应注意补充。     

亲环素 A/CD147信号通路与新生儿缺氧缺血性脑损伤相关性研究进展

新生儿缺氧缺血性脑损伤( HIBD)是围产期窒息的严重并发症,影响着病儿的早期存活和远期预后。亲环素 A(Cy- pA)/CD147信号通路参与细胞的增殖、趋化、凋亡、炎症以及神经元代谢等过程,与 HIBD的发生发展密切相关,因此研究 Cy- pA/CD147的作用机制对 HIBD诊断与治疗具有重要意义。该研究阐述了 CypA/CD147的信号通路与缺血缺氧性脑损伤关系最新研究进展,以期为 HIBD的治疗提供新的思路与方向。     

肠三叶因子对新生鼠NEC模型PI3K和caspase-3/9的影响

Objective To study the effects of ITF on PI3K (phosphatidylinositol 3-kinase) and caspases-3/9 (cysteinyl aspartate-specific protea-ses) in neonatal rat NEC model. Methods NEC model of neonatal rats was established. Asphyxia stress was accomplished by exposure to l00% nitrogen for 60s, followed by exposure to coldness (4 ℃ ) for 10 min twice daily. Neonatal rats were fed formula (200 kcal/kg/day) every 3 h via an gavage tube. The feeding volume began at 0. 1 cc every 3 h and was increased incrementally. This procedure is done once everyday and continued for 3 days. On the 4th day,all the subjects were sacrificed. Fifty neonatal rats were randomized into five groups: A) NEC + NS0. 2mi, (B) NEC + ITF 0. 2 mg, (C) NEC(Wortmannin (0. 1 mg/kg) (D) NEC + ITF 0. 2 mg + Wortmannin (0. 1 mg/kg), (E) control. The intestinal tissue located at the boundary of ileum and cecum was sampled for histology. The remaining intestinal tissue was homogenized. After the homogenate was centrifuged,supernatants were used to assay PI3K and Caspase-3 and caspase-9. Results The pathological lesions showed that intestinal necrosis was severe in group A、C and D, which was graded as 3points. They were significantly decreased in group B,which was graded 1 point. The level of PI3K(pg/ml)in Group A was higher than those in group E (P<0. 05), the latter had difference with those in group D(P>0. 05). The level of PI3K(pg/ml) were the strongest in group B and were lowest in group C. The activity of Caspase-3 and Caspase-9 were significantly increased in group A compared to those in group B and E (P<0. 01 ),and was significantly increased in Group C(P<0. 01 ). Caspase-3 and Caspase-9 levels of group A and D,group B and E showed no significant difference(P>0. 05). Conclusions Intestinal inflammation was ameliorated by intraperitoneal ITF. ITF may provide a new therapy for NEC; PI3K/Akt signal pathways might play important roles in signal transduction during NEC;ITF may protect the intestinal injury of neonatal Wistar rat by activation of PI3K/Akt signal transduction pathway, and down regulation of caspase-9.     

33例冠心病后代的血清脂质分析

３３例冠心病后代的血清脂质分析湖北医科大学附属第一医院儿科教研室（４３００６０）唐红敏田鸾英张丙宏周于新刘仲熊１９９２年４月～１９９５年１２月，我们对有冠心病家族史的健康父母及新生儿各３３名进行了血清胆固醇（ＴＣ）、甘油三酯（ＴＧ）、载脂蛋白Ａ１（Ａ...     

小胶质细胞在新生儿缺氧缺血性脑病中的作用的研究进展

小胶质细胞作为中枢神经系统的固有免疫细胞,参与了新生儿大脑发育和功能稳态的维持。目前认为小胶质细胞在中枢神经系统损伤中的作用是双重的,既可以加剧神经损伤,也可以通过分泌生长因子、吞噬清除细胞碎片等方式限制炎症信号,促进神经功能的恢复。本文就小胶质细胞在新生儿脑发育及缺氧缺血性脑病中的作用进行综述,旨在为未来靶向小胶质细胞治疗缺氧缺血性脑病提供新的观点。     

维生素D与早产儿呼吸窘迫综合征的临床分析

目的 分析早产儿血清维生素D[25-(OH)D₃]水平与早产儿呼吸窘迫综合征(RDS)发生的相关性,为早产儿RDS的治疗提供科学依据。方法 选取2018年9月-2019年3月在武汉大学人民医院新生儿科住院的131例RDS早产儿为实验组,29例非RDS早产儿为对照组。收集所有患儿一般临床资料(性别、分娩方式、母孕情况及Apgar 评分等)及血清25-(OH)D₃结果,分析25-(OH)D₃ 水平与RDS发生之间的关系。结果 RDS组25-(OH)D₃水平低于对照组,差异均有统计学意义(t=2.682,P＜0.05),且CPAP时间、吸氧时间、静脉营养天数、住院天数均明显高于对照组,差异均有统计学意义(t=2.969、2.380、2.571、1.999,P＜0.05)。Logistic 回归分析显示:维生素 D 缺乏是早产儿发生RDS 的危险因素(OR=0.050,95%CI:0.013~0.186,P＜0.05)。结论 早产儿更易发生维生素D缺乏,且维生素D缺乏可能是早产儿RDS发生的危险因素,预防维生素D缺乏有重大意义。