目的:研究双嘧达莫片联合维生素C治疗小儿过敏性紫癜对血清血栓调节蛋白(TM)、正五聚蛋白3(PTX3)、白细胞介素-23(IL-23)的变化影响.方法:选取我院于2017年5月～2020年5月收治的小儿过敏性紫癜患儿100例,分为2组.对照组给予常规对症治疗,观察组在对照组基础上给予双嘧达莫片联合维生素C治疗.统计2组有效率和6个月内的复发率,检测2组TM、PTX3、炎症因子的变化.结果:观察组的总有效率为92.00％,高于对照组的76.00％,组间比较发现,有统计学意义.治疗前组间比较发现,2组TM、PTX3、炎症因子水平无统计学意义.治疗后组间比较发现,观察组TM、PTX3、白细胞介素-4(IL-4)、白细胞介素-8(IL-8)、IL-23、肿瘤坏死因子-α(TNF-α)低于对照组.观察组6个月内的复发率为4.00％,与对照组的10.00％进行组间比较发现,无统计学意义.结论:双嘧达莫片联合维生素C治疗小儿过敏性紫癜可降低TM、PTX3及炎症因子的表达水平,提高疗效.

目的 分析益生菌辅治小儿支气管哮喘(BA)及对S100β 蛋白、TLR4与炎性免疫因子的影响;方法 选择我院2016年1月至2019年12月收治的BA患儿78例,按照随机数字表法分为观察组41例、对照组37例,对照组给予常规治疗+沙美特罗替卡松粉吸入剂治疗.观察组在对照组基础上给予布拉氏酵母菌散治疗.观察两组哮喘控制情况,不良反应.两组治疗前后最大呼吸流量(PEF)、第一秒用力呼吸容积(FEV1)、用力肺活量(FVC)等肺功能指标,血清CD4+、CD8+、CD4+/CD8+等免疫因子水平,血清S100β蛋白、TLR4水平;血清IL-17、IL?22、IL?35等炎性因子水平;结果 治疗后,观察组FPE、FEV1、FVC均高于对照组(P<0.05).治疗后,观察组CD4+、CD4+/CD8+均高于对照组,CD8+小于对照组(P<0.05).治疗后,观察组100β蛋白、TLR4低于对照组(P<0.05).治疗后,观察组IL?17、IL?22均低于对照组,IL?35高于对照组(P<0.05).观察组总控制率(92.19％)大于对照组(78.13％)(P<0.05).治疗期间两组均无显著不良反应;结论 益生菌辅治小儿支气管哮喘可提高免疫功能,缓解机体炎性反应,改善血清炎性因子水平,抑制100β蛋白、TLR4生成,疗效显著,安全.

BACKGROUND:The reasonable use of amino acids (AAs) in parenteral nutrition (PN) is very critical to the growth and development of premature infants. However, the appropriate dose of AAs has not been determined. Our study was designed to investigate the clinical effect of two different doses of AAs in PN for low birth weight premature infants. MATERIALS AND METHODS:This randomized controlled study included 191 preterm infants who admitted to the neonatal intensive care unit of the First Affiliated Hospital of Nanjing Medical University from June 2015 to December 2016 and they were randomly divided into Group 1 (n = 81) and Group 2 (n = 110). In Group 1, the starting dose of AAs dose was 1.0-1.5 g/kg/day, which was increased by 0.5 g/kg with the maximum dose at 3.5 g/kg/day. In Group 2, the starting dose of AAs was 1.8-2.5 g/kg/day and was increased by 1.0 g/kg with the maximum dose at 4.0-4.5 g/kg/day. We analyzed the clinical characteristics, body weight, body length, total calorie intake, nonprotein calorie intake, total protein intake, liver and kidney function, and complications of the two groups of preterm infants. RESULTS:The start of enteral feeding and the recovery of birth weight in Group 2 were earlier than those in Group 1 (3.83 ± 3.15 day vs. 5.53 ± 5.63 day, P = 0.016 and 6.36 ± 4.88 day vs. 8.48 ± 9.27 day, P = 0.043, respectively). The duration of PN and the time before total enteral nutrition were shorter in Group 2 than in Group 1 (16.46 ± 10.33 day vs. 21.41 ± 18.00 day, P = 0.029 and 15.47 ± 10.54 day vs. 19.47 ± 14.57 day, P = 0.038; respectively). The duration of mechanical ventilation (1.12 ± 2.62 day vs. 3.31 ± 8.13 day, P = 0.028) in Group 2 was shorter than that in Group 1. CONCLUSION:High doses of AAs in the early PN for preterm infants facilitate the promotion of early growth and development, advance recovery of birth weight, reduce the duration of PN, and reduce respiratory support without increasing the incidence of complications.

目的:探讨原发性肾病综合征(PNS)患儿血管内皮生长因子(VEGF)、血同型半胱氨酸(Hcy)及其与急性肾损伤(AKI)的关系.方法:选取2016年7月 ～2019年7月本院收治的67例原发性肾病综合征患儿为研究对象.收集所有患儿的性别、年龄、身体质量指数(BMI)、24 h尿蛋白定量、血清肌酐(SCr)、肾小球滤过率估计值(eGFR)资料,检测VEGF、Hcy水平.采用Pearson相关性分析VEGF、Hcy水平与肾功能指标及AKI分期之间的的相关性.结果:PNS合并AKI组患儿的24 h尿蛋白定量、SCr、VEGF、Hcy水平明显高于PNS未合并AKI组,eGFR水平明显低于PNS未合并AKI组.VEGF水平与24 h尿蛋白定量、SCr、AKI分期呈正相关关系,与eGFR呈负相关关系;Hcy水平与24 h尿蛋白定量、SCr、AKI分期呈正相关关系,与eGFR呈负相关关系.结论:VEGF、Hcy水平与AKI关系密切,监测PNS患儿的VEGF、Hcy水平可能对监控患儿肾功能水平及AKI程度具有积极意义.

Objective To explore the effect of early administration of high-dose amino acids in parenteral nutrition for low birth weight infants of prematurity.Methods A total of 191 prematures admitted to the First Affiliated Hospital of Nanjing Medical University from June 2015 to December 2016 were selected,and they were randomly divided into the study group (n =110) and the control group (n =81).The starting amino acid dose was 1.8-2.5 g/(kg · d)and 1.0-1.5 g/(kg · d) in the study group and the control group,respectively.Lipids,glucose,and electrolytes in parenteral nutrition were applied according to standard protocol of the guideline.And the start of enteral feeding,the recovery of birth weight,the duration of parenteral nutrition,the time before total enteral nutrition,duration of hospital stay,incidence of respiratory distress syndrome,duration of mechanical ventilation and incidence of kaliopenia were compared between the 2 groups.Results The start of enteral feeding,the recovery of birth weight,the duration of parenteral nutrition,the time before total enteral nutrition in the study group were earlier than those in the control group [(3.83 ±3.15) d vs.(5.53 ±5.63) d,(15.47±10.54) d vs.(19.47 ± 14.57) d,(16.46 ± 10.33) d vs.(21.41 ±18.00) d,(6.36 ± 4.88) d vs.(8.48 ± 9.27) d],and the differences were all statistically significant (t =2.455,2.097,2.217,2.041,P =0.016,0.038,0.029,0.043).The duration of hospital stay was shorter and the hospitalization expenses were lower in the study group than those in the control group,but the differences were not significant (all P ＞ 0.05).The incidence of respiratory distress syndrome in the study group was significantly lower than that in the control group[20.91％ (23/110 cases) vs.35.80％ (29/81 cases)],and the difference was statistically significant (x2 =5.223,P =0.022).The duration of mechanical ventilation in study group was shorter than that in control [(1.12 ± 2.62) d vs.(3.31 ± 8.13) d],and the difference was statistically significant (t =2.231,P =0.028).The incidence of kaliopenia in the study group was higher than that in the control group [30.91％ (34/110 cases)vs.17.28％ (14/81 cases)],and the difference was statistically significant (x2 =4.603,P =0.032).There were not significant differences in terms of complications of necrotizing enterocolitis,sepsis,extrauterine growth retardation,hospital infection,metabolic acidosis,hyperglycemia,glucopenia,patent ductus arteriosus and respiratory distress syndrome between 2 groups (all P ＞ 0.05).Conclusions Early administration of high-dose amino acids in parenteral nutrition for preterm infants can result in earlier enteral nutrition,shorter parenteral nutrition duration without increasing incidence of complications and hospitalization expenses.

The present study examined whether lipoxin A4 (LXA4) increases the expression of HO‑1, and inhibits the production of interleukin 6 (IL‑6) and monocyte chemotactic protein 1 (MCP‑1) in LXA4‑induced protection during hyperoxia‑induced injury in murine lung epithelial cells (MLE‑12) and what signal pathway may participate in the actions of LXA4 inhibiting IL‑6 and MCP‑1. MLE‑12 cells were exposed to air or hyperoxia with or without pretreatment with LXA4, Zinc protoporphyrin IX (ZnPP‑IX), IL‑6, anti‑IL‑6, MCP‑1, anti‑MCP‑1, inhibitors of p38 mitogen‑activated protein kinase (p38 MAPK), protein kinase B (Akt) and extracellular signal‑regulated kinase 1/2 (ERK1/2) signaling pathways. The cell survival rates, cell viability, apoptosis rates, expression of superoxide dismutase (SOD), heme oxygenase‑1 (HO‑1), IL‑6 and MCP‑1, and the activations of p38 MAPK, ERK1/2 and Akt were measured. LXA4 significantly increased the cell survival rates, cell viability, SOD levels and HO‑1 expression, reduced the apoptosis rates, and inhibited the MCP‑1 and IL‑6 levels induced by hyperoxia in cells. ZnPP‑IX, an inhibitor of HO‑1, blocked LXA4‑induced protection on cell viability in cells exposed to hyperoxia. Anti‑IL‑6 and anti‑MCP‑1 improved the cell viability of cells exposed to hyperoxia. Inhibition of p38 MAPK and ERK1/2 blocked the expression of MCP‑1 and IL‑6 induced by hyperoxia. LXA4 inhibited the activation of p38 MAPK and ERK1/2 induced by hyperoxia, and increased the activation of the Akt signaling pathway, which was inhibited by hyperoxia. Therefore, LXA4 attenuated hyperoxia‑induced injury in MLE‑12 cells via the upregulation of HO‑1 expression. The protection of LXA4 in hyperoxia‑induced cell injury may be associated with the downregulation IL‑6 and MCP‑1 levels via the inhibition of the p38 MAPK and ERK1/2 signaling pathways.

Objective:To investigate protectory effects and possible mechanisms of lipoxin A4(LXA4)on the type Ⅱ alveolar epithelial cell line MLE-12 with hyperoxia injury.Methods:MLE-12 cells were cultured and divided into five groups randomly:I:air group,Ⅱ:hyperoxia group,Ⅲ:hyperoxia+ LXA4 group,Ⅳ:hyperoxia+ TGF-β1 neutralizing antibodies,Ⅴ:hyperoxia+ TGF-β1 neutralizing antibodies+ LXA4.The growth state and morphological changes of the cells were observed by the inverted phase microscope;the mRNA expression of collagen Ⅰ,tenascin-C,TGF-β1 receptor(TGF-βR1),TGF-βR2 and Smad3 were measured by real-time quantitative PCR;the protein levels of TGF-ββ1/Smads signaling pathway(TGFβR1,Smad2,Smad3,Smad4,p-Smad2 and p-Smad3)were detected by Western blot.Results:①Morphological change:the cells under hyperoxia lost their normal shapes and showed necrosis,while the cells cultured with LXA4 and/lor TGF-β 1 neutralizing antibodies were normal appropriately.②The mRNA expression of extracellular matrix (ECM):LXA4 and TGF-β1 neutralizing antibodies attenuated the mRNA expression of collagen Ⅰ,tenascin-C markedly (P ＜ 0.05),which expressed in the group hyperoxia+TGF-ββ1 neutralizing antibodies + LXA4 decreased most obviously.③The mRNA and protein levels of TGF-β1/Srnads signaling pathway:Compared with that of the hyperoxia group,the mRNA expression of TGF-βR1,TGF-βR2 and Smad3 decreased(P ＜ 0.05),while the protein level of TGF-β1/Smads signaling pathway had the same change in intervention group,and it in the the group hyperoxia+ TGF-β1 neutralizing antibodies +LXA4 decreased most obviously (P ＜ 0.05).Conclusion:LXA4 can achieve protection of hy-peroxia-induced injury to MLE-12 which may be related to collagen Ⅰ,tenascin-C and TGF-ββ1/Smads signaling pathway.

Objective To investigate the protective effects of lipoxin A4 (LXA4) on the lung epithelial cells (MLE-12) in mice with hyperoxia injury.Methods MLE-12 cells were cultured in vitro and divided into air group,air + LXA4 group,hyperoxia group and hyperoxia + LXA4 group.The receptor of LXA4 (ALX) was verified by using reverse transcription-polymerase chain reaction (RT-PCR).MLE-12 cells were exposed to hyperoxia (＞ 850 mL/L oxygen concentration) for 12 h followed by pretreatment of 1 nmol/L,10 nmol/L and 50 nmol/L LXA4 for 1 h,6 h,12 h and 24 h.Quantitative real-time PCR (qRT-PCR) was applied to analyze the heme oxygenase 1 (HO-1) expression to determine the optimal concentration and the optimal pretreatment time of LXA4.The cell morphology was observed by using inverted microscope.The survival rates and cell viability were determined by using Trypan Blue stain and cell counting kit-8 (CCK-8).The superoxide dismutase (SOD) level was determined by using hydroxylamine method.The expressions of mRNA and protein of HO-1 were measured by using qRT-PCR,western blot and immunofluorescence assay,respectively.The interleukin-6 (IL-6) and monocyte chemotactic protein 1 (MCP-1) were determined by using enzyme-linked immunosorbent assay.Results ALX was expressed in MLE-12 cells.The optimal intervention concentration and time of LXA4 was 10 nmol/L for 12 h.Compared with air group [(84 ± 5) ％,1.22 ± 0.27,(5.33 ± 1.16) kU/L],the cell survival rate,viability and SOD level of hyperoxia group [(66 ± 8) ％,0.67 ± 0.21,(2.38 ± 0.65) kU/L] decreased,and the differences were significant (t =3.98,2.55,4.86;P =0.01,0.03,0.00);compared with the hyperoxia group,the cell survival rate,viability and SOD level of hyperoxia + LXA4 group [(88 ± 5) ％,1.43 ± 0.05,(6.50 ± 0.19) kU/L] significantly increased,and the differences were significant (t =4.83,3.52,6.78;P =0.01,0.02,0.00).The HO-1 mRNA and protein expression of hyperoxia group (0.57 ± 0.03,1.31 ± 0.11) increased as compared to air group (0.13 ± 0.03,0.24 ± 0.10),and the differences were significant (t =8.00,10.10;all P =0.00);the HO-1 expression of hyperoxia + LXA4 group (0.78 ± 0.08,1.82 ± 0.09) significantly increased as compared to hyperoxia group,and the differences were significant (t =3.94,8.82,all P=0.00).The levels of MCP-1 and IL-6 of hypemxia group [(1 025.18 ±35.51) rig/L,(1 136.65 ±160.01) ng/L] significantly increased as compared to air group [(467.63 ± 13.69) ng/L,(470.03 ± 118.22) ng/L],and the differences were significant (t =16.51,7.48;all P =0.00);the MCP-1 and IL-6 of hyperoxia + LXA4 group [(640.25 ± 61.03) ng/L,(655.48 ± 88.57) ng/L] significantly decreased as compared to hyperoxia group,and thedifferences were significant (t =11.40,5.40,all P =0.00).Conclusions LXA4 can attenuate hyperoxia-induced injury in MLE-12 cells.The protective role of LXA4 in the hyperoxia-induced cell injury is related to the up-regulation of HO-1 expression and down-regulation of IL-6 and MCP-1 levels.

Transforming growth factor-β (TGF-β) superfamily members are key regulators for lung development and progress of bronchopulmonary dysplasia (BPD). The mechanisms by which lipoxin A 4 (LXA 4 ) attenuates development of BPD have not been clarified. Neonatal murine BPD models were inducted by hyperoxia treatment. Neonatal mice were exposed to room air or 85% O 2 hyperoxia with or without treatment with 5S,6R-methyl-LXA 4 or anti-TGF-β antibodies. Mouse lung epithelial cells (MLE-12 cells) and mouse embryonic fibroblasts (NIH/3T3 cells) were cultured in room air or 85% O 2 followed by treatment of LXA 4 , anti-TGF-β antibodies, and let-7c mimic/anti-microRNA transfections. Treatment with 5S,6R-methyl-LXA 4 and anti-TGF-β antibodies both attenuated the mice alveolar simplification induced by hyperoxia. Hyperoxia treatment significantly altered pulmonary basal mRNA and protein expressions of several important extracellular matrix (ECM) and ECM remodeling proteins including fibronectin, α-smooth muscle actin (α-SMA), tissue inhibitor of metalloproteinase-1 (TIMP-1), elastin, tenascin C, collagen I, and matrix metalloproteinase-1 (MMP-1). 5S,6R-methyl-LXA 4 and anti-TGF-β antibodies suppressed the mRNA and protein expressions of TGF-β 1 and TGF-βR1 but not TGF-βR2 in the lungs exposed to hyperoxia. Treatment with LXA 4 and anti-TGF-β antibodies alleviated hyperoxia-induced injury of the NIH/3T3 cells identified by morphologic observation and flow cytometry, and expressions of ECM, ECM remodeling proteins, and TGF-β 1 signaling pathway, but reversed by transfection with let-7c anti-miRNA. LXA 4 upregulated the let-7c expression in MLE-12 cells, transfection with let-7c anti-miRNA, inhibited the LXA 4 -induced let-7c expression in MLE-12 cells exposed to hyperoxia and reduced the relative luciferase activity of let-7c binding with let-7c binding sites of the TGF-βR1 3′ UTR. Treatment with 5S,6R-methyl-LXA 4 and anti-TGF-β antibodies significantly improved histology, ECM, and ECM remodeling proteins in the lungs isolated from the murine BPD model induced by hyperoxia. The LXA 4 -imparted protective effects on hyperoxia-induced lung injury are mediated by upregulation of let-7c and inhibition of TGF-β 1 and subsequent downregulation of TGF-β 1 signaling pathway.

Objective To evaluate the appropriate strategies of parenteral nutrition for premature infants.Methods One hundred and seven preterm babies with birth weights ranging from 1 000-2 500 g received parenteral nutrition within 2 h after birth during June 2015 to January 2016.Lipids,glucose and electrolytes were applied with standard protocol of parenteral nutrition;while the amino acids contents were1.0-1.5 g · kg-1 · d-1 in 81 cases (control group) and 2-2.5 g · kg-1 · d-1 in 26 cases (study group).The data of demographics,development,laboratory findings and complications were documented.Results There were no significant differences in the baseline data of gestational age,birth weight between two groups (P ＞ 0.05).There were also no significant differences in total protein intake and target non-protein calorie intake within the first week after birth and the total calorie intake during the first two weeks between study group and control group (P ＞ 0.05).The start of enteral feeding [(3.54 ± 3.18) d vs.(5.64±5.81) d,P=0.02)],the start of total enteral nutrition [(16.50±9.54) d vs.(21.21 ±15.63) d,P=0.07)],the recovery of birth weight [(7.35±4.55) vs.(9.19±9.50) d,P=0.19)] in study group were earlier than those in control group.The duration of parenteral nutrition [(16.88 ± 8.99) d vs.(22.33 ± 18.10) d,P =0.04],the duration of hospital stay [(20.62 ± 10.41] d vs.(24.22 ± 15.62) d,P =0.18] were shorter and the hospitalization expenses [(21 929.00 ± 11 945.42] Yuan vs.(37 499.58 ±71 146.80) Yuan,P =0.14] were lower in study group than those in control group.The incidence of metabolic acidosis was significantly lower in study group than that in control group (19.23％ vs.45.68％,P =0.02).There were no significant differences in complications of necrotizing enterocolitis,sepsis,extrauterine growth retardation,parenteral nutrition-associated cholestasis,patent ductus arteriosus,respiratory distress syndrome,nosocomial and the duration of artificial ventilation and oxygen therapy between two groups (P ＞ 0.05).The incidence of metabolic disorders (hyperglycemia,hypoglycemia,hypocalcemia,hyponatremia,hypokalemia and hypomagnesemia) was similar in two groups (P ＞ 0.05).Conclusion Amino acids should be apply to the premature infants within 2 h after birth,and the contents in parenteral nutrition should be ＞ 2.0 g · kg-1 · d-1.

Objective To study the protective mechanisms of lipoxin A 4 ( LXA4 ) for hyperoxia-induced lung injury through modulation of let-7c/TGF-β1 signal pathway in mice.Method MLE-12 cells was transfected with let-7c mimic, mimic negative control ( NC) , let-7c inhibitor and inhibitor NC.The cells were assigned into hyperoxia group , LXA4 group, let-7c over-expression group, let-7c silence group, let-7c silence+LXA4 group, and all exposed to 85% oxygen.The mRNA level of the extracellular matrixα-smooth muscle actin (α-SMA) and collagen Ⅰ( COL-Ⅰ) , and the expression of related genes in TGF-β1 signaling pathway (Smad 2, Smad 3, Smad 4, TGF-βR1, TGF-βR2) were examined using qPCR.The protein expressions in TGF-β1 signaling pathway was examined using Western blot .Result The mRNA expressions of α-SMA, COL-Ⅰ, Smad 3, Smad 4, TGF-βR1 and TGF-βR2 in LXA4 group [(24.3 ±2.1), (14.6 ±0.2), (17.0 ±0.0), (14.9 ±0.1), (20.8 ±0.1), (9.0 ±0.0) ] and let-7c over-expression group [ ( 12.2 ±0.5 ) , ( 3.0 ±0.0 ) , ( 3.1 ±0.0 ) , ( 9.6 ±0.4 ) , ( 28.5 ±0.2 ) , ( 7.6 ± 0.1)] were decreased comparing with the hyperoxia group [(51.4 ±0.5), (32.0 ±0.1), (40.6 ±0.2), (16.3 ±0.1), (89.1 ±1.1), (19.3 ±0.2)].These expressions were increased in both let-7c silence group [(87.3 ±7.0), (38.5 ±0.3), (48.0 ±0.2), (56.5 ±0.2), (126.0 ±0.9), (33.1 ±1.0)] and let-7c silence +LXA4 group [(144.5 ±12.9), (86.3 ±3.0), (91.5 ±4.7), (86.5 ±3.3), (109.0 ±4.5), (45.6 ±1.6)].The protein levels of Smad 2, Smad 3, Smad 4, p-Smad 2, p-Smad 3 and TGF-βR1 of LXA4 group and let-7c over-expression group were decreased comparing with the hyperoxia group, while p-Smad 2, p-Smad 3 of let-7c silence+LXA4 group were increased(P<0.05).Conclusion LXA4 may play a protective role through let-7c /TGF-β1 signal pathway of lung epithelial cells for hyperoxia-induced lung injury in mice .

目的:探讨脂氧素A4(lipoxin A4,LXA4)对新生小鼠高氧诱导所致的支气管发育不良(bronchopulmonary dysplasia,BPD)的保护作用及可能机制.方法:利用高氧损伤诱导BPD动物模型,将新生C57BL/6J小鼠随机分成:空气对照组、模型组、LXA4干预组、转化生长因子-β1 (transforming growth factor-β1,TGF-β1)中和抗体(1D11)干预组,记录仔鼠体重和生存情况,HE染色观察出生后肺组织病理改变,qPCR法检测肺纤维化指标及转化生长因子-β I型受体(transforming growth factor-β receptor 1,TGF-βR1)和转化生长因子-βⅡ型受体(transforming growth factor-β receptor 2,TGF-βR2)的表达水平.结果:①模型组新生小鼠较空气对照组体重减低且活力差.②肺组织大体标本观察:与空气对照组相比,各组小鼠肺体积减小,色泽暗淡.与空气对照组(d13)相比,LXA4干预组和1D11干预组小鼠肺外观与之相仿.③HE染色:除空气对照组外,各组肺组织均产生类似BPD的病理损伤.较模型组(d13)相比,LXA4干预组与1D11干预组的肺泡结构趋于正常化.④qPCR:与空气对照组相比,各组肺纤维化指标:纤维连接蛋白、平滑肌肌动蛋白--α、弹性蛋白、肌腱蛋白C、组织金属蛋白抑制剂-1及TGF-βR1、TGF-βR2的表达量均增加(P＜0.05).与空气对照组相比,各组基质金属蛋白酶1相对表达量减少(P＜0.05);其中与模型组相比,LXA4干预组和1D11干预组基质金属蛋白酶1表达量上调(P＜0.05),且LXA4干预组上调更为显著(P＜0.05).与空气组对照比较,模型组、LXA4干预组和1D11干预组I型胶原表达量增高(P＜0.05);其中与模型组相比,LXA4干预组和1D11干预组I型胶原表达减少(P＜0.05).结论:LXA4可能是通过抑制TGF-β1信号通路下调肺纤维化相关因子,实现对高氧诱导BPD的保护作用.

MicroRNA（miRNA）是一类内源性、广泛分布的非编码 RNA，这些非编码 RNA 通过调控基因表达的方式参与生命活动的一系列重要的过程，包括细胞增殖、凋亡、分化、个体发育等。Let-7家族是继 Lin -4之后于2000年发现的第二个 miRNA 家族，目前认为Let-7家族与肿瘤、心血管疾病、病毒感染等发生发展有关，尤其是与肺部疾病关系密切。本文将针对Let-7家族与肺部疾病（肺癌、肺发育不良、肺损伤、特发性肺纤维化、肺部炎症）的研究进展进行综述。