荔枝GRF基因家族的全基因组鉴定及表达分析

为揭示荔枝(Litchi chinensis)GFR基因的功能,对荔枝生长调控因子(LcGRF)基因家族进行了全基因组鉴定和分析,并研究其在荔枝中的表达模式。基于荔枝基因组数据库,使用生物信息学软件对LcGRFs家族成员进行全基因组鉴定,分析基本理化性质、染色体定位、基因结构、进化关系、蛋白保守基序、顺式作用元件和时空表达情况进行系统分析。共获得12个GRF基因,不均匀地分布在10条染色体上,内含子2~5个。蛋白保守基序分析发现,荔枝GRF蛋白均含有保守的motif1(WRC)和motif2(QLQ),进化分析LcGRF划分为5个亚家族,LcGRFs启动子上存在大量的光、植物激素、非生物胁迫响应以及生长发育相关的顺式作用元件。不同转录组表达模式结果显示,各个组织中呈现出多样化的表达特征,表明不同成员可能在荔枝不同生长发育过程中发挥调控作用,参与调节荔枝的生长发育。研究显示,荔枝GRF家族成员有12个,划分为5个亚家族。

Emodin regulating excision repair cross-complementation group 1 through fibroblast growth factor receptor 2 signaling

AIM: To investigate the molecular mechanisms underlying the reversal effect of emodin on platinum resistance in hepatocellular carcinoma. METHODS: After the addition of 10 μmol/L emodin to HepG2/oxaliplatin (OXA) cells, the inhibition rate (IR), 50% inhibitory concentration (IC 50 ) and reversal index (IC 50 in experimental group/IC 50 in control group) were calculated. For HepG2, HepG2/OXA, HepG2/OXA/T, each cell line was divided into a control group, OXA group, OXA + fibroblast growth factor 7 (FGF7) group and OXA + emodin group, and the final concentrations of FGF7, emodin and OXA in each group were 5 ng/mL, 10 μg/mL and 10 μmol/L, respectively. Single-cell gel electrophoresis was conducted to detect DNA damage, and the fibroblast growth factor receptor 2 (FGFR2), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and excision repair cross-complementing gene 1 (ERCC1) protein expression levels in each group were examined by Western blotting. RESULTS: Compared with the IC50 of 120.78 μmol/L in HepG2/OXA cells, the IC 50 decreased to 39.65 μmol/L after treatment with 10 μmol/L emodin; thus, the reversal index was 3.05. Compared with the control group, the tail length and Olive tail length in the OXA group, OXA + FGF7 group and OXA + emodin group were significantly increased, and the differences were statistically significant (P < 0.01). The tail length and Olive tail length were lower in the OXA + FGF7 group than in the OXA group, and this difference was also statistically significant. Compared with the OXA + FGF7 group, the tail extent, the Olive tail moment and the percentage of tail DNA were significantly increased in the OXA + emodin group, and these differences were statistically significant (P < 0.01). In comparison with its parental cell line HepG2, the HepG2/OXA cells demonstrated significantly increased FGFR2, p-ERK1/2 and ERCC1 expression levels, whereas the expression of all three molecules was significantly inhibited in HepG2/ OXA/T cells, in which FGFR2 was silenced by FGFR2 shRNA. In the examined HepG2 cells, the FGFR2, p-ERK1/2 and ERCC1 expression levels demonstrated increasing trends in the OXA group and OXA + FGF7 group. Compared with the OXA group and OXA + FGF7 group, the FGFR2, p-ERK1/2, and ERCC1 expression levels were significantly lower in the OXA + emodin group, and these differences were statistically significant. In the HepG2/OXA/T cell line that was transfected with FGFR2 shRNA, the FGFR2, p-ERK1/2 and ERCC1 expression levels were significantly inhibited, but there were no significant differences in these expression levels among the OXA, OXA + FGF7 and OXA + emodin groups. CONCLUSION: Emodin markedly reversed OXA resistance by enhancing OXA DNA damage in HepG2/OXA cells, and the molecular mechanism was related to the inhibitory effect on ERCC1 expression being mediated by the FGFR2/ERK1/2 signaling pathway.

Expression of vascular endothelial growth factor and its role in oncogenesis of human gastric carcinoma

AIM: To establish the role of vascular endothelial growth factor (VEGF) in the oncogenesis of human gastric carcinoma more directly. METHODS: The expression of VEGF and its receptor kinase-domain insert containing receptor (KDR) in human gastric cancer tissue were observed by immunohistochemical staining. VEGF levels were manipulated in human gastric cancer cell using eukaryotic expression constructs designed to express the complete VEGF(165) complimentary DNA in either the sense or antisense orientation. The biological changes of the cells were observed in which VEGF was up-regulated or down-regulated. RESULTS: VEGF-positive rate was 50%, and VEGF was mainly localized in the cytoplasm and membrane of the tumor cells, while KDR was mainly located in the membrane of vascular endothelial cells in gastric cancer tissues and peri-cancerous tissue. In 2 cases of 50 specimens, the gastric cancer cells expressed KDR, localized in both the cytoplasm and membrane. Introduction of VEGF(165) antisense into human gastric cancer cells (SGC-7901, immunofluorescence intensity, 31.6%)) resulted in a significant reduction in VEGF-specific messenger RNA and total and cell surface VEGF protein (immunofluorescence intensity, 8.9%) (P【0.05). Conversely, stable integration of VEGF(165) in the sense orientation resulted in an increase in cellular and cell surface VEGF (immunofluorescence intensity, 75.4%) (P【0.05). Lowered VEGF levels were associated with a marked decrease in the growth of nude mouse xenografted tumor (at 33 days postimplantation, tumor volume: 345.40 +/- 136.31 mm3)(P【0.05 vs control SGC-7901 group: 1534.40 +/- 362.88 mm3), whereas up-regulation of VEGF resulted in increased xenografted tumor size (at 33 days postimplantation, tumor volume: 2350.50 +/- 637.70 mm3) (P【0.05 vs control SGC-7901 group). CONCLUSION: This study provides direct evidence that VEGF plays an important role in the oncogenesis of human gastric cancer.

Post-transcriptional regulation of vascular endothelial growth factor: Implications for tumor angiogenesis

Vascular endothelial growth factor （VEGF） is a potent secreted mitogen critical for physiologic and tumor angiogenesis. Regulation of VEGF occurs at several levels, including transcription, mRNA stabilization, translation, and differential cellular localization of various isoforms. Recent advances in our understanding of post-transcriptional regulation of VEGF include identification of the stabilizing mRNA binding protein, HuR, and the discovery of internal ribosomal entry sites in the 5＇UTR of the VEGF mRNA. Monoclonal anti-VEGF antibody was recently approved for use in humans, but suffers from the need for high systemic doses. RNA interference （RNAi） technology is being used in vitro and in animal models with promising results. Here, we review the literature on post-transcriptional regulation of VEGF and describe recent progress in targeting these mechanisms for therapeutic benefit.

Biological characteristics of dynamic expression of nerve regeneration related growth factors in dorsal root ganglia after peripheral nerve injury

The regenerative capacity of peripheral nerves is limited after nerve injury.A number of growth factors modulate many cellular behaviors,such as proliferation and migration,and may contribute to nerve repair and regeneration.Our previous study observed the dynamic changes of genes in L4–6 dorsal root ganglion after rat sciatic nerve crush using transcriptome sequencing.Our current study focused on upstream growth factors and found that a total of 19 upstream growth factors were dysregulated in dorsal root ganglions at 3,9 hours,1,4,or 7 days after nerve crush,compared with the 0 hour control.Thirty-six rat models of sciatic nerve crush injury were prepared as described previously.Then,they were divided into six groups to measure the expression changes of representative genes at 0,3,9 hours,1,4 or 7 days post crush.Our current study measured the expression levels of representative upstream growth factors,including nerve growth factor,brain-derived neurotrophic factor,fibroblast growth factor 2 and amphiregulin genes,and explored critical signaling pathways and biological process through bioinformatic analysis.Our data revealed that many of these dysregulated upstream growth factors,including nerve growth factor,brain-derived neurotrophic factor,fibroblast growth factor 2 and amphiregulin,participated in tissue remodeling and axon growth-related biological processes Therefore,the experiment described the expression pattern of upstream growth factors in the dorsal root ganglia after peripheral nerve injury.Bioinformatic analysis revealed growth factors that may promote repair and regeneration of damaged peripheral nerves.All animal surgery procedures were performed in accordance with Institutional Animal Care Guidelines of Nantong University and ethically approved by the Administration Committee of Experimental Animals,China(approval No.20170302-017)on March 2,2017.

The involvement of p38 MAPK in transforming growth factor β1-induced apoptosis in murine hepatocytes

We reported in this manuscript that TGF-beta1 induces apoptosis in AML12 murine hepatocytes, which is associated with the activation of p38 MAPK signaling pathway. SB202190, a specific inhibitor of p38 MAPK, strongly inhibited the TGF-beta1-induced apoptosis and PAI-1 promoter activity. Treatment of cells with TGF-beta1 activates p38. Furthermore, over-expression of dominant negative mutant p38 also reduced the TGF-beta1-induced apoptosis. The data indicate that the activation of p38 is involved in TGF-beta1-mediated gene expression and apoptosis.

Involvement of PI3K and ERK1/2 pathways in hepatocyte growth factor-induced cholangiocarcinoma cell invasion

AIM:To investigate the role of hepatocyte growth factor(HGF) in cholangiocarcinoma(CCA) cell invasiveness and the mechanisms underlying such cellular responses. METHODS:Effects of HGF on cell invasion and motility were investigated in two human CCA cell lines,HuCCA-1 and KKU-M213,using Transwell in vitro assay.Levels of proteins of interest and their phosphorylated forms were determined by Western blotting.Localization of E-cadherin was analyzed by immunofluorescence staining and visualized under confocal microscope. Activities of matrix degrading enzymes were determined by zymography. RESULTS:Both CCA cell lines expressed higher Met levels than the H69 immortalized cholangiocyte cell line.HGF induced invasion and motility of the cell lines and altered E-cadherin from membrane to cytoplasm localization,but did not affect the levels of secreted matrix metalloproteinase(MMP) -2,MMP-9 andurokinase plasminogen activator,key matrix degrading enzymes involved in cell invasion.Concomitantly,HGF stimulated Akt and extracellular signal-regulated kinase(ERK) 1/2 phosphorylation but with slightly different kinetic profiles in the two cell lines.Inhibition of the phosphoinositide 3-kinase(PI3K) /Akt pathway by the PI3K inhibitor,LY294002,markedly suppressed HGFstimulated invasion of both CCA cell lines,and inhibition of the ERK pathway by U0126 suppressed HGF-induced invasion of the KKU-M213 cell line but had a moderate effect on HuCCA-1 cells. CONCLUSION:These data indicate that HGF promotes CCA cell invasiveness through dys-localization of E-cadherin and induction of cell motility by distinct signaling pathways depending on cell line type.

Vascular endothelial growth factor B inhibits insulin secretion in MIN6 cells and reduces Ca2+ and cyclic adenosine monophosphate levels through PI3K/AKT pathway

BACKGROUND Type 2 diabetes(T2 D) is characterized by insufficient insulin secretion caused by defective pancreatic β-cell function or insulin resistance,resulting in an increase in blood glucose.However,the mechanism involved in this lack of insulin secretion is unclear.The level of vascular endothelial growth factor B(VEGF-B) is significantly increased in T2 D patients.The inactivation of VEGF-B could restore insulin sensitivity in db/db mice by reducing fatty acid accumulation.It is speculated that VEGF-B is related to pancreatic β-cell dysfunction and is an important factor affecting β-cell secretion of insulin.As an in vitro model of normal pancreatic β-cells,the MIN6 cell line can be used to analyze the mechanism of insulin secretion and related biological effects.AIM To study the role of VEGF-B in the insulin secretion signaling pathway in MIN6 cells and explore the effect of VEGF-B on blood glucose regulation.METHODS The MIN6 mouse pancreatic islet β-cell line was used as the model system.By administering exogenous VEGF-B protein or knocking down VEGF-B expression in MIN6 cells,we examined the effects of VEGF-B on insulin secretion,Ca2+ and cyclic adenosine monophosphate(cAMP) levels,and the insulin secretion signaling pathway.RESULTS Exogenous VEGF-B inhibited the secretion of insulin and simultaneously reduced the levels of Ca2+ and cAMP in MIN6 cells.Exogenous VEGF-B also reduced the expression of phospholipase C gamma 1(PLCγ1),phosphatidylinositol 3-kinase(PI3 K),serine/threonine kinase(AKT),and other proteins in the insulin secretion pathway.Upon knockdown of VEGF-B,MIN6 cells exhibited increased insulin secretion and Ca2+ and cAMP levels and upregulated expression of PLCγ1,PI3 K,AKT,and other proteins.CONCLUSION VEGF-B can regulate insulin secretion by modulating the levels of Ca2+ and cAMP.VEGF-B involvement in insulin secretion is related to the expression of PLCγ1,PI3 K,AKT,and other signaling proteins.These results provide theoretical support and an experimental basis for the study of VEGF-B in the pathogenesis of T2 D.

The change of basic fibroblast growth factor and effect of prostacyclin in lung injury

In this study,the changes in activity and mRNA transcript of basic fibroblast growth fac-tor(bFGF)in lung injury and the effect of prostacyclin on the treatment of lung injury wereinvestigated.The result of the experiment revealed that there were not any bioactive bFGF andbFGF mRNA in the lung tissue of normal dogs.bFGF activity and bFGF mRNA were detectedonly in the injured lung tissue.Prostacyclin could slightly elevate the activity of bFGF andsignificantly elevate the level of bFGF mRNA.The findings suggest that(1)the level of bFGF in-creased after lung injury.(2)Prostacyclin could influence the expression of bFGF.(3)bFGF couldplay an important role in the repair of injury lung tissue.

通调针刺法联合康复疗法治疗气虚血瘀型脑梗死后运动障碍临床观察

目的评估通调针刺法联合康复疗法治疗气虚血瘀型脑梗死后运动障碍的临床疗效。方法将60例气虚血瘀型脑梗死后运动障碍患者随机分为对照组和治疗组,每组30例。两组患者均给予基础治疗,对照组患者给予康复治疗,治疗组患者给予康复治疗联合通调针刺法治疗,两组疗程均为4周。比较治疗前后两组患者简化Fugl-Meyer评估(Fugl-Meyer assessment,FMA)量表评分和日常生活活动能力(activity of daily living,ADL)量表评分、气虚血瘀证证候积分、血清转铁蛋白(transferrin,TF)和神经生长因子(nerve growth factor,NGF)水平,对比两组总体疗效。结果治疗组脱落2例患者,对照组脱落1例患者。与治疗前比较,两组患者治疗后FMA量表评分和ADL量表评分均显著上升(P<0.05),气虚血瘀证证候积分显著降低(P<0.05),血清TF和NGF水平显著升高(P<0.05),且治疗组FMA量表评分和ADL量表评分及血清TF和NGF水平升高程度、气虚血瘀证证候积分降低程度均显著大于对照组(P<0.05)。治疗组临床疗效显著优于对照组(P<0.05)。结论通调针刺法联合康复疗法治疗气虚血瘀型脑梗死后运动障碍疗效显著。

生长分化因子15联合沉默信息调节因子1在老年急性心肌梗死患者介入治疗的预后预测价值分析

目的:探讨生长分化因子15(growth differentiation factor-15,GDF15)联合沉默信息调节因子1(silent information regulator 1,SIRT1)在老年急性心肌梗死(acute myocardial infarctio,AMI)患者PCI治疗后预后预测中的价值。方法:选取本院2019年1月至2021年8月收治的209例AMI行PCI老年患者纳入AMI组,另选同期健康体检人群90例纳入对照组,检测AMI患者术前、术后7d以及对照组血清GDF15、SIRT1表达水平,观察AMI术后3个月内AMI组主要不良心血管事件(major adverse cardiovascular events,MACE)发生情况,对比MACE发生与未发生患者血清GDF15、SIRT1表达差异,通过受试者工作曲线(ROC)评估其对患者MACE发生的预测价值。结果:AMI患者术前与术后血清GDF-15水平明显高于对照组,SIRT1水平明显低于对照组(P <0.05);血清GDF-15、SIRT1水平联合检测诊断AMI的发生ROC曲线下面积(AUC)显著高于两项指标单独评估的AUC(P <0.05);209例患者术后3个月内发生MACE者44例(21.1%),发生MACE患者术前及术后血清GDF-15水平高于未发生者,SIRT1水平低于未发生者(P <0.05);术前血清GDF-15、SIRT1水平联合检测评估老年PCI治疗AMI患者MACE的发生ROC曲线下面积为0.816,显著高于两项指标单独评估曲线下面积0.726、0.725(P <0.05);术后血清GDF-15、SIRT1水平联合检测评估老年PCI治疗AMI患者MACE的发生ROC曲线下面积为0.894,显著高于两项指标单独评估曲线下面积0.815、0.811(P <0.05);术后7d血清GDF-15、SIRT1水平检测评估老年PCI治疗AMI患者MACE的发生ROC曲线下AUC高于术前(P <0.05)。结论:AMI患者血清GDF-15呈高表达,SIRT1呈低表达,且其表达水平可在一定程度上预测患者PCI术后MACE的发生,反映患者预后状态。

GRF转录因子对植物生长发育及胁迫响应调控的分子机制

生长调控因子(GRFs)是一类植物特有的转录因子家族。GRFs信号通路介导植物种子发育、根系生长、花的发育等很多重要的生命过程。尽管GRFs的上游基因已被发现,但是其下游靶基因的研究仍鲜见报道。本文对近年来有关GRFs的结构特征、生物学功能及调控机制等方面进行了综述,并结合当前研究现状展望了GRFs未来的研究方向,以期为该领域的相关研究提供参考。

Bt-G033A与3种昆虫生长调节剂混配对番茄潜叶蛾的防治效果评价

为提高生物药剂使用效率,减少化学农药使用量,将50000 IU/mg Bt-G033A WP分别与30%灭蝇胺SC、25%灭幼脲SC和20%虫酰肼SC减量联合应用。共毒因子法初步筛选结果表明,Bt-G033A:灭蝇胺75:25、Bt-G033A:灭幼脲25:75和50:50的配比处理均表现为增效作用,Bt-G033A:灭蝇胺25:75和50:50、Bt-G033A:虫酰肼75:25、Bt-G033A:灭幼脲75:25处理均表现为相加作用。共毒系数法筛选结果表明,Bt-G033A与灭蝇胺平均共毒系数83.75,表现为相加作用;Bt-G033A与灭幼脲复配共毒系数为131.76,表现为增效作用,其中50:50增效最明显,增效系数最大为203.25。最佳复配剂Bt-G033A:灭幼脲50:50田间试验结果表明,药后3~21 d对番茄潜叶蛾防治效果64.76%~89.12%,均可高于灭幼脲和Bt-G033A单剂防效。

基于EGFR/MAPK/ERK信号通路探讨鳖甲煎丸对MHCC-97H肝癌细胞皮下瘤的抑瘤作用

目的基于表皮生长因子受体(epidermal growth factior receptor,EGFR)/丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)/细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)信号通路探究鳖甲煎丸对MHCC-97H肝癌细胞皮下瘤的抑瘤作用及作用机制。方法选取30只雄性BLAB/c裸鼠,建立MHCC-97H肝癌细胞皮下瘤模型。造模成功后随机分为模型组,鳖甲煎丸低、中、高剂量组(0.55、1.1、2.2 g/kg),西药组(乐伐替尼4 mg/kg+吉非替尼80 mg/kg),每组6只。鳖甲煎丸低、中、高剂量组灌胃2次/d,西药组每周灌胃5 d,模型组予以等量生理盐水2次/d灌胃,每组连续干预2周。观察大鼠一般情况;计算各组大鼠抑瘤率;HE染色观察病理形态学变化;RT-qPCR检测瘤体组织中EGFR、丝裂原活化蛋白质激酶激酶(mitogen-activated protein kinase kinase,MEK)、ERK1、ERK2 mRNA表达水平;Western blot检测EGFR、磷酸化的EGFR(p-EGFR)、MEK、磷酸化的MEK(p-MEK)、ERK1、ERK2、磷酸化的ERK1/2(p-ERK1/2)、基质金属蛋白酶-1(matrix metalloproteinase-1,MMP-1)、细胞周期蛋白D1(cell cycle protein D1,Cyclin D1)、神经型钙黏附蛋白(N-cadherin)、上皮型钙黏附蛋白(E-cadherin)相对表达水平。结果与模型组比较,鳖甲煎丸低、中、高剂量组及西药组精神、反应、进食饮水等情况均明显改善。与第0天比较,各组第14天体质量明显降低(P<0.01)。与模型组、鳖甲煎丸低剂量组比较,鳖甲煎丸中、高剂量组和西药组瘤体质量减轻(P<0.05,P<0.01)。鳖甲煎丸低、中、高剂量组和西药组抑瘤率分别为20%、47.73%、55.91%、75.45%。与模型组比较,鳖甲煎丸低、中、高剂量组及西药组肿瘤细胞排列疏松,边界模糊,细胞核固缩、破裂,其中西药组最明显。与模型组比较,鳖甲煎丸低、中、高剂量组和西药组EGFR、MEK、ERK1、ERK2 mRNA表达水平明显下降(P<0.01);与鳖甲煎丸低剂量组比较,鳖甲煎丸高剂量组和西药组EGFR、MEK、ERK1、ERK2 mRNA表达水平显著降低(P<0.01),鳖甲煎丸中剂量组ERK1 mRNA表达水平显著降低(P<0.01);与鳖甲煎丸中剂量组比较,西药组EGFR、ERK2 mRNA表达水平降低(P<0.05,P<0.01)。与模型组比较,鳖甲煎丸中、高剂量组和西药组p-EGFR/EGFR、p-MEK/MEK、p-ERK1/ERK1、p-ERK2/ERK2、MMP-1、Cyclin D1、N-cadherin蛋白相对表达水平下降(P<0.05,P<0.01),E-cadherin蛋白相对表达水平明显升高(P<0.01)。与鳖甲煎丸高剂量组比较,西药组p-EGFR/EGFR、p-ERK1/ERK1、MMP-1、Cyclin D1、N-cadherin蛋白相对表达水平明显下降(P<0.01),E-cadherin蛋白相对表达水平升高(P<0.05)。结论鳖甲煎丸可能通过抑制EGFR/MAPK/ERK信号通路激活,从而下调MMP-1、Cyclin D1、N-cadherin蛋白,上调E-cadherin蛋白表达,进而对MHCC-97H肝癌细胞皮下瘤产生显著的抑制作用。

Organ Abscission in Plants: With Special Emphasis on Bell Pepper

Bell pepper(Capsicum annuum L.),along with potato and tomato,is one of the three most cultivated vegetables in the world.Bell pepper is worldwide accepted due to its characteristics of color,smell,flavor,and texture.Bell pepper is also considered a nutritious food due to its vitamin and antioxidant contents.In Mexico,bell pepper production has a high value because it is grown for the international markets,particularly the United States of America.Nevertheless,the abscission offlowers and fruits is a factor that limits the yield,hinders the planning of activities,and causes a variation in the prices of peppers.Due to the importance of this process,in this work we did a bibliometric analysis and literature review of scientific advances for the understanding of the abscission pro-cess in plants,and in particular for the bell pepper.Finally,we introduce new perspectives that would help direct future research about organ abscission in plants.Likewise,the lack of research that would further clarify abscis-sion process in the bell pepper plant is discussed.

Regulation role of miR-204 on SIRT1/VEGF in metabolic memory induced by high glucose in human retinal pigment epithelial cells

AIM:To examine the regulatory role of microRNA-204(miR-204)on silent information regulator 1(SIRT1)and vascular endothelial growth factor(VEGF)under highglucose-induced metabolic memory in human retinal pigment epithelial(hRPE)cells.METHODS:Cells were cultured with either normal(5 mmol/L)or high D-glucose(25 mmol/L)concentrations for 8d to establish control and high-glucose groups,respectively.To induce metabolic memory,cells were cultured with 25 mmol/L D-glucose for 4d followed by culture with 5 mmol/L D-glucose for 4d.In addition,exposed in 25 mmol/L D-glucose for 4d and then transfected with 100 nmol/L miR-204 control,miR-204 inhibitor or miR-204 mimic in 5 mmol/L D-glucose for 4d.Quantitative reverse transcription-polymerase chain reaction(RT-qPCR)was used to detect miR-204 mRNA levels.SIRT1 and VEGF protein levels were assessed by immunohistochemical and Western blot.Flow cytometry was used to investigate apoptosis rate.RESULTS:It was found that high glucose promoted miR-204 and VEGF expression,and inhibited SIRT1 activity,even after the return to normal glucose culture conditions.Upregulation of miR-204 promoted apoptosis inhibiting SIRT1 and increasing VEGF expression.However,downregulation of miR-204 produced the opposite effects.CONCLUSION:The study identifies that miR-204 is the upstream target of SIRT1and VEGF,and that miR-204 can protect hRPE cells from the damage caused by metabolic memory through increasing SIRT1 and inhibiting VEGF expression.

非小细胞肺癌组织AIP1、EDIL3表达变化观察

目的观察非小细胞肺癌(NSCLC)组织凋亡信号调节激酶1-相互作用蛋白1(AIP1)、表皮生长因子样结构域3(EDIL3)表达变化,分析其与微血管密度(MVD)、临床病理特征及预后的关系,为NSCLC的靶向治疗提供新的干预靶点。方法纳入155例NSCLC患者,免疫组织化学法检测癌组织和癌旁组织中AIP1、EDIL3蛋白,Weidner法检测癌组织MVD。比较不同AIP1、EDIL3表达的NSCLC患者MVD值及不同临床病理特征NSCLC患者癌组织AIP1、EDIL3表达水平。Kaplan-Meier生存曲线分析不同AIP1、EDIL3表达的NSCLC患者生存情况,多因素Cox回归分析NSCLC患者预后的影响因素。结果与癌旁组织比较,NSCLC癌组织中EDIL3阳性表达率高、AIP1阳性表达率低(P均<0.05)。不同分化程度、淋巴结转移、肿瘤直径、TNM分期的NSCLC患者癌组织中AIP1、EDIL3蛋白阳性表达率比较,P均<0.05。AIP1阳性表达的NSCLC患者癌组织MVD值低于AIP1阴性表达者(P<0.05),EDIL3阳性表达的NSCLC患者癌组织MVD值高于EDIL3阴性表达者(P<0.05)。EDIL3阳性表达的NSCLC患者3年总生存(OS)率低于EDIL3阴性表达者(P<0.05),AIP1阳性表达的NSCLC患者3年OS率高于AIP1阴性表达者(P<0.05)。淋巴结转移、TNM分期ⅢA期、EDIL3阳性表达是NSCLC患者预后不良的危险因素(P均<0.05),AIP1阳性表达是保护因素(P<0.05)。结论NSCLC癌组织中AIP1阳性表达率降低,EDIL3阳性表达率升高;癌组织中AIP1、EDIL3阳性表达率与MVD、分化程度、淋巴结转移、肿瘤直径、TNM分期有关,是NSCLC预后不良的影响因素。

血管内皮生长因子C及其受体对动物肠道脂肪消化吸收的调控作用及机制

提高肠道对脂肪的消化吸收效率可以促进动物的生长发育及维持机体健康。脂肪被肠道消化吸收后,在细胞内再合成,包括脂肪酸的摄取、甘油三酯的重新合成、乳糜微粒的合成以及乳糜微粒进入乳糜管等过程,其中乳糜微粒进入乳糜管是影响肠道对脂肪消化吸收的关键因素。血管内皮生长因子C(VEGFC)是一种促血管内皮细胞生长的调控因子,能与血管内皮生长因子受体3(VEGFR3)结合,从而参与调控机体的多项生理过程。最新的研究表明,VEGFC还参与调控乳糜微粒进入乳糜管这一过程,进而影响动物肠道的脂肪消化吸收。本文主要阐述了VEGFC及其受体VEGFR3在动物机体内的分布情况及其对肠道脂肪消化吸收的调控作用,并初步探讨了VEGFC及VEGFR3对乳糜管结构和淋巴内皮细胞(LECs)连接方式的调控机制,以期深入了解VEGFC及其受体在动物肠道脂肪消化吸收中的作用,并为其应用提供参考依据。

慢性心力衰竭患者血清CTGF、SIRT1表达及与心肌重构的相关性研究

目的观察慢性心力衰竭(心衰)患者血清结缔组织生长因子(CTGF)、沉默信息调节因子1(SIRT1)的表达,并分析其与心肌重构的相关性。方法选择2022年1月至2023年5月于青岛市市立医院收治的120例慢性心衰患者作为观察组,美国纽约心脏病协会(NYHA)心功能分级Ⅱ级38例、Ⅲ级57例、Ⅳ级25例,并选择同期体检中心的100例健康志愿者作为对照组。比较两组不同心功能分级患者血清CTGF、SIRT1、心肌重构指标[左室舒张末期内径(LVEDD)、左心房内径(LAD)、左心室后壁厚度(LVPWD)、左心室质量指数(LVMI)、左心室重构指数(LVRI)]的表达,并分析血清CTGF、SIRT1与心肌重构指标的相关性。结果与对照组相比,观察组血清CTGF、LVEDD、LAD、LVPWD、LVMI、LVRI均更高,血清SIRT1更低(P<0.05);随着心功能分级增加,血清CTGF、LVEDD、LAD、LVPWD、LVMI、LVRI均升高,血清SIRT1降低,有统计学意义(P<0.05);Pearson相关性分析显示,血清CTGF、SIRT1与心肌重构指标均具有相关性(P<0.05)。结论慢性心衰患者血清CTGF升高,SIRT1水平降低,且与心肌重构存在密切关系.

miRNA-7-EGFR/ERK通路用于卵巢癌治疗的研究进展

卵巢癌(OC)在女性生殖系统肿瘤中致死率最高,治疗多选择手术切除加辅助化疗,然而易出现耐药性,导致患者预后差。miRNA-7在卵巢癌细胞中低表达,通过靶向表皮生长因子受体(EGFR)/细胞外调节蛋白激酶(ERK)信号通路发挥抗肿瘤作用。本综述介绍miRNA-7-EGFR/ERK通路在卵巢癌治疗中的作用,为卵巢癌的治疗提供新的思路。