<rss version="2.0">
  <channel>
    <title>2022年第4期</title>
    <link>https://jhip.gdpu.edu.cn/2022%E5%B9%B4%E7%AC%AC4%E6%9C%9F</link>
    <description><![CDATA[]]></description>
    <item>
      <title>Motor learning dysfunction and its association with neurotransmitters and gut microbiota dysbiosis in hepatic encephalopathy mice</title>
      <link>https://jhip.gdpu.edu.cn/motor-learning-dysfunction-and-its-association-with-neurotransmitters-and-gut-microbiota-dysbiosis-in-hepatic-encephalopathy-mice</link>
      <description><![CDATA[<p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><span style="font-family: 仿宋_GB2312; font-size: 16pt;">Motor learning dysfunction and its association with neurotransmitters and gut microbiota dysbiosis in hepatic encephalopathy mice(肝性脑病小鼠运动学习功能损伤与脑内神经递质和肠道菌群紊乱的相关关系)</span><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[摘要]目的 </span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">肝性脑病（</font><font face="仿宋_GB2312">HE）临床患者可见认知和运动学习功能障碍。目前认为该疾病的主要发病机制为高血氨症、外周及中枢神经炎症。神经递质和神经环路的功能异常被认为是导致认知和运动学习障碍的重要因素。然而，较少研究开展运动皮层中神经递质的改变及其与肠道菌群的相关性。因此，本研究建立HE小鼠模型，以期从神经递质和肠道菌群关系角度探究肝性脑病的潜在发病机制。</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">方法</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">以</font><font face="仿宋_GB2312">C57 BL/6小鼠腹腔注射硫代乙酰胺建立肝性脑病小鼠模型，ELISA试剂盒检测血清和运动皮层中肿瘤坏死因子（TNF-α）和氨浓度，转棒实验评价HE小鼠运动学习功能，16S rDNA分析HE小鼠肠道菌群种属及丰度变化。运动皮层中的26中神经递质经采用UPLC-TQ-MS进行含量测定，并将其与异常变化的肠道菌属</font></span><i><span style="font-family: 仿宋_GB2312; font-size: 16pt;">Escherichia_Shigella</span></i><span style="font-family: 仿宋_GB2312; font-size: 16pt;">,</span><i><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">Allobaculum</font></span></i><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">和</font><font face="仿宋_GB2312">Muribaculacea做相关分析。</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">结果</font> </span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">LEfSe分析结果表明，HE小鼠与对照组之间的25个种属存在显著差异，且与HE小鼠运动皮层中含量升高的adrenaline hydrochloride、4-aminobytyric acid、L-glutamic acid 4种神经递质和含量减低的 L-histidine and histamine存在显著相关。</span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">结论</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">HE小鼠可见运动皮层中神经递质改变与肠道菌群存在相关性，该相关关系的揭示为HE小鼠认知和运动学习功能障碍的发病机制研究提供依据。</font></span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[关键词]</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">肝性脑病；</font> <font face="仿宋_GB2312">肠道菌群；</font> <font face="仿宋_GB2312">中枢神经系统；</font> <font face="仿宋_GB2312">运动皮层；</font> <font face="仿宋_GB2312">神经递质</font> </span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><br></p>]]></description>
      <pubDate>Mon, 10 Apr 2023 07:52:21 GMT</pubDate>
      <guid isPermaLink="true">https://jhip.gdpu.edu.cn/motor-learning-dysfunction-and-its-association-with-neurotransmitters-and-gut-microbiota-dysbiosis-in-hepatic-encephalopathy-mice</guid>
    </item>
    <item>
      <title>Analysis on the treatment of acne by Sanhuang with network pharmacology and experimental research</title>
      <link>https://jhip.gdpu.edu.cn/analysis-on-the-treatment-of-acne-by-sanhuang-with-network-pharmacology-and-experimental-research</link>
      <description><![CDATA[<p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><span style="font-family: 仿宋_GB2312; font-size: 16pt;">Analysis on the treatment of acne by Sanhuang with network pharmacology and experiment research（基于网络药理学和实验探讨三黄治疗痤疮的机制） &nbsp;&nbsp;&nbsp;</span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoNormal" style="mso-pagination:widow-orphan;line-height:150%;"><b><span style="font-family: 仿宋_GB2312; line-height: 150%; font-size: 16pt;">[摘要]目的</span></b><span style="font-family: 仿宋_GB2312; line-height: 150%; font-size: 16pt;">&nbsp;&nbsp;<font face="仿宋_GB2312">基于网络药理学、分子对接和抑菌、细胞实验探讨</font><font face="仿宋_GB2312">“三黄泻心汤”（简称三黄）治疗痤疮的机制。</font></span></p><p class="MsoNormal" style="mso-pagination:widow-orphan;line-height:150%;"><b><span style="font-family: 仿宋_GB2312; line-height: 150%; font-size: 16pt;">方法</span></b><span style="font-family: 仿宋_GB2312; line-height: 150%; font-size: 16pt;">&nbsp;&nbsp;<font face="仿宋_GB2312">三黄活性成分及靶点通过</font><font face="仿宋_GB2312">TCMSP和SwissTarget数据库获得，痤疮靶点由DisGeNET、OMIM和GeneCards 数据库获得，对交集靶点进行KEGG和GO富集分析，用分子对接、抑菌和细胞实验验证预测结果。</font></span></p><p class="MsoNormal" style="mso-pagination:widow-orphan;line-height:150%;"><b><span style="font-family: 仿宋_GB2312; line-height: 150%; font-size: 16pt;"><font face="仿宋_GB2312">结果</font> </span></b><span style="font-family: 仿宋_GB2312; line-height: 150%; font-size: 16pt;"><font face="仿宋_GB2312">三黄与痤疮交集靶点</font><font face="仿宋_GB2312">123个，主要通过IL-17、MAPK、PI3K-Akt和TNF等信号通路来发挥作用。分子对接结果表明芦荟大黄素和槲皮素与核心靶点TNF、IL-6、INS和AKT1具有较强亲和力。抑菌实验结果显示，质量浓度为0.1 g/mL、0.5 g/mL 的三黄的抑菌圈直径分别为(20.96±0.32) mm和(26.12±0.95) mm，最低抑菌浓度是4 mg/mL，除此之外三黄还能通过破坏细菌细胞形态、提高细胞壁通透性、抑制痤疮丙酸杆菌的生长，治疗痤疮。细胞实验结果表明，三黄可以抑制IL-6的生成。</font></span></p><p class="MsoNormal" style="mso-pagination:widow-orphan;line-height:150%;"><b><span style="font-family: 仿宋_GB2312; line-height: 150%; font-size: 16pt;">结论</span></b><span style="font-family: 仿宋_GB2312; line-height: 150%; font-size: 16pt;">&nbsp;&nbsp;<font face="仿宋_GB2312">三黄可以抑制痤疮丙酸杆菌生长，其治疗痤疮的机制与</font><font face="仿宋_GB2312">TNF、IL-6、INS和AKT1等靶基因密切相关。</font></span><span style="font-family: 仿宋_GB2312; line-height: 150%; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoNormal"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[关键词]</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">三黄；</font> <font face="仿宋_GB2312">痤疮；</font> <font face="仿宋_GB2312">网络药理学；</font> <font face="仿宋_GB2312">分子对接；</font> <font face="仿宋_GB2312">抑菌；</font> <font face="仿宋_GB2312">抗炎</font></span></p><p class="MsoNormal"><br></p>]]></description>
      <pubDate>Mon, 10 Apr 2023 07:52:44 GMT</pubDate>
      <guid isPermaLink="true">https://jhip.gdpu.edu.cn/analysis-on-the-treatment-of-acne-by-sanhuang-with-network-pharmacology-and-experimental-research</guid>
    </item>
    <item>
      <title>Antiseptic property screening for 18 natural plants and efficiency–toxicity research of Coptis chinensis fermentation</title>
      <link>https://jhip.gdpu.edu.cn/antiseptic-property-screening-for-18-natural-plants-and-efficiency-toxicity-research-of-coptis-chinensis-fermentation</link>
      <description><![CDATA[<p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><span style="font-family: 仿宋_GB2312; font-size: 16pt;">Antiseptic property screening for eighteen natural plants and efficiency/toxicity research on Coptis Chinensis fermentation（</span><span style="font-family: 仿宋_GB2312; font-size: 16pt;">18</span><span style="font-family: 仿宋_GB2312; font-size: 16pt;">种天然植物防腐性能筛选及黄连发酵增效减毒研究）</span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[摘要]目的</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">比较</font><font face="仿宋_GB2312">18种天然植物对化妆品中易滋生的6种微生物的抑菌性能大小，筛选出安全低毒、抗菌谱广的最佳天然防腐中药。探究黄连经酵母菌发酵处理后的安全性和抗氧化、美白、抗炎功效。</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">方法</font> </span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">采用牛津杯法对比</font><font face="仿宋_GB2312">18种天然植物醇提液对6种微生物的抑菌效果；MTT法测定黄连提取液及发酵液的细胞存活率；通过DPPH、羟基和ABTS自由基清除率及还原铁能力评价抗氧化功效；通过酪氨酸酶和透明质酸酶活力抑制率分别评价黄连提取及发酵液的美白和抗炎性能｡</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">结果</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">18种天然植物中，黄连对6种微生物的抑菌圈最大，MIC值最小。黄连醇提液经发酵后，对细胞存活率的IC50值明显上升，表现出更低的毒性。经发酵后黄连提取液的自由基清除率、酪氨酸酶抑制率和透明质酸酶抑制率明显上升，表现出比醇提液更好的抗氧化活性、美白活性和抗炎活性｡</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">结论</font> </span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">这</font><font face="仿宋_GB2312">18种天然植物中，黄连抑菌能力最强，是最优异的防腐剂｡黄连经酵母菌发酵后细胞毒性降低，抗氧化、美白和抗炎活性提高，表明微生物发酵对植物防腐剂具有减毒增效的作用｡</font></span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[关键词]</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">发酵；</font> <font face="仿宋_GB2312">抑菌；</font> <font face="仿宋_GB2312">抗氧化；</font> <font face="仿宋_GB2312">美白；</font> <font face="仿宋_GB2312">抗炎；</font> <font face="仿宋_GB2312">黄连</font></span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><br></p>]]></description>
      <pubDate>Mon, 10 Apr 2023 07:53:09 GMT</pubDate>
      <guid isPermaLink="true">https://jhip.gdpu.edu.cn/antiseptic-property-screening-for-18-natural-plants-and-efficiency-toxicity-research-of-coptis-chinensis-fermentation</guid>
    </item>
    <item>
      <title>Molecular mechanism and rule of TCM prescriptions containing Alismatis Rhizoma in the clinical treatment of hyperlipidemia based on data mining and network pharmacology</title>
      <link>https://jhip.gdpu.edu.cn/molecular-mechanism-and-rule-of-tcm-prescriptions-containing-alismatis-rhizoma-in-the-clinical-treatment-of-hyperlipidemia-based-on-data-mining-and-network-pharmacology</link>
      <description><![CDATA[<p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><span style="font-family: 仿宋_GB2312; font-size: 16pt;">Molecular Mechanism and Rule of TCM Prescriptions Containing Alismatis Rhizoma in Clinical Treatment of Hyperlipidemia Based on Data Mining and Network Pharmacology（基于数据挖掘和网络药理学探讨含泽泻组方治疗高脂血症用药规律及作用机制）</span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[摘要]目的 </span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">基于数据挖掘和网络药理学的思路和方法分析含泽泻药方治疗高脂血症的临床用药规律及作用机制。</span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">方法</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">检索中国知网（</font><font face="仿宋_GB2312">CNKI）、万方、Pubmed数据库，收集治疗高脂血症的含泽泻药方，运用Apriori算法挖掘各药方中隐藏的药物配伍规律及药对；利用TCMSP、Pubchem、Swiss Target Prediction数据库分析药对的化学成分和靶点信息，并通过Drugbank数据库筛选疾病的靶点，取二者交集；使用Cytoscape软件获取药方治疗高脂血症的核心靶点，再利用DAVID数据库对交集靶点进行KEGG通路富集及分析；用Autodock对核心化学成分和关键靶点进行分子对接，并将对接结果用Discovery Studio 2016 Client平台进行可视化处理。最后通过体外细胞实验进行验证。</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">结果</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">筛选出支持度最高的药对为山楂</font><font face="仿宋_GB2312">-丹参-泽泻，该药对共包含112种活性成分，与活性成分相关性较高的靶点384个，检索获得高脂血症相关靶点111个，药物与疾病共45个交集靶点；生物功能和靶点通路富集分析发现山楂-丹参-泽泻治疗高脂血症的生物过程主要与类固醇代谢过程、药物反应以及氧化还原过程等相关。体外实验结果表明，泽泻醇A可以降低细胞脂质积累，降低TC、TG水平。上调ABCB1及下调CYP1A2、CYP3A4、SLC6A4的mRNA表达水平。</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">结论</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">基于网络药理学分析得出山楂</font><font face="仿宋_GB2312">-丹参-泽泻药对可通过多靶点、多通路对高脂血症起治疗作用，为进一步研究中医药治疗高脂血症提供基础。</font></span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoNormal"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[关键词]</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">高脂血症；</font> <font face="仿宋_GB2312">数据挖掘；</font> <font face="仿宋_GB2312">网络药理学；</font> <font face="仿宋_GB2312">泽泻；</font> <font face="仿宋_GB2312">药对</font></span></p><p class="MsoNormal"><br></p>]]></description>
      <pubDate>Mon, 10 Apr 2023 07:53:43 GMT</pubDate>
      <guid isPermaLink="true">https://jhip.gdpu.edu.cn/molecular-mechanism-and-rule-of-tcm-prescriptions-containing-alismatis-rhizoma-in-the-clinical-treatment-of-hyperlipidemia-based-on-data-mining-and-network-pharmacology</guid>
    </item>
    <item>
      <title>Oxidative low-density lipoprotein oxLDL induces pyroptosis in trophoblast cells HTR-8|Svneo by downregulating TET2</title>
      <link>https://jhip.gdpu.edu.cn/oxidative-low-density-lipoprotein-oxldl-induces-pyroptosis-in-trophoblast-cells-htr-8-svneo-by-downregulating-tet2</link>
      <description><![CDATA[<p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><span style="font-family: 仿宋_GB2312; font-size: 16pt;">Oxidative low-density lipoprotein oxLDL induces pyroptosis of trophoblast cells HTR-8/Svneo by down-regulating TET2（氧化型低密度脂蛋白oxLDL通过下调TET2诱导滋养层细胞HTR8/Snero的焦亡）</span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[摘要]目的</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">探讨</font><font face="仿宋_GB2312">TET2在氧化型低密度脂蛋白(oxLDL) 诱导滋养层细胞HTR8/Snero的焦亡。</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">方法</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">分别以</font><font face="仿宋_GB2312">0、50 mg/L oxLDL处理 HTR8/Snero 24 h，Western blot检测oxLDL对HTR8/Snero细胞中TET2表达的影响。CCK8检测和克隆实验检测TET2干预对HTR8/Snero增殖的影响；Transwell实验和划痕实验检测TET2干预对HTR8/Snero迁移的影响；Western blot检测TET2干预对焦亡蛋白、GSDMD和Casepase-1的表达。</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">结果</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">oxLDL呈浓度依赖性下调TET2的表达，敲低TET2抑制HTR8/Snero的侵袭和迁移但促进细胞增殖。Western blot结果表明，oxLDL抑制TET2的表达，敲低TET2能上调GSDMD和Casepase-1的表达。</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">结论</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">&nbsp;<font face="仿宋_GB2312">oxLDL可下调TET2的表达，从而诱导HTR8/Snero的焦亡。</font></span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[关键词]</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">氧化型低密度脂蛋白；</font> <font face="仿宋_GB2312">TET2； HTR8/Snero； 细胞焦亡</font></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><br></p>]]></description>
      <pubDate>Mon, 10 Apr 2023 07:54:14 GMT</pubDate>
      <guid isPermaLink="true">https://jhip.gdpu.edu.cn/oxidative-low-density-lipoprotein-oxldl-induces-pyroptosis-in-trophoblast-cells-htr-8-svneo-by-downregulating-tet2</guid>
    </item>
    <item>
      <title>Effect and mechanism of Buyang Huanwu decoction on retinal inflammation in streptozotocin-induced diabetic rats</title>
      <link>https://jhip.gdpu.edu.cn/effect-and-mechanism-of-buyang-huanwu-decoction-on-retinal-inflammation-in-streptozotocin-induced-diabetic-rats</link>
      <description><![CDATA[<p class="MsoPlainText" style="line-height:28.0pt;mso-line-height-rule:exactly"><span lang="EN-US" style="font-size:16.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt">22H041&nbsp; </span><span style="font-size:16.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt">邵晓奇，蔡平东，张越<span lang="EN-US">(</span>广东药科大学<span lang="EN-US">).Infarction or reperfusion-induced cardiac autophagy: role of
microRNAs</span>（梗死或再灌注诱导的心脏自噬：<span lang="EN-US">microRNA</span>的作用）</span><span lang="EN-US" style="font-size:12.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt"><o:p></o:p></span></p><p class="MsoNormal"><b><span lang="EN-US" style="font-size:12.0pt;font-family:
&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:宋体;mso-font-kerning:0pt">[</span></b><b><span style="font-size:12.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt">摘要<span lang="EN-US">]</span>目的 </span></b><span style="font-size:12.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt">观察补阳还五汤对糖尿病大鼠视网膜炎症的保护作用及机制。<b>方法</b> 选取健康雄性<span lang="EN-US">Wistar</span>大鼠作为研究对象，随机分为正常组与模型组。模型组大鼠采用一次性腹腔注射链脲佐菌素（<span lang="EN-US">STZ</span>）建立糖尿病模型，再将造模成功的大鼠随机分为模型组、阳性对照组、补阳还五汤组。各组对应给药<span lang="EN-US">8</span>周后，通过尾静脉注射荧光素标记的右旋糖酐观察大鼠视网膜血管通透性；尾静脉注射伊文思蓝染液定量检测大鼠视网膜的血管渗漏量；灌注荧光素标记的刀豆蛋白检测大鼠视网膜白细胞黏附；蛋白免疫印迹法（<span lang="EN-US">WB</span>）检测大鼠视网膜组织中炎症因子<span lang="EN-US">TNF-</span><i>α</i>、<span lang="EN-US">NF-</span><i>κ</i><span lang="EN-US">Bp65</span>和<i><span lang="EN-US">p</span></i><span lang="EN-US">-NF-</span><i>κ</i><span lang="EN-US">Bp65</span>蛋白的表达水平。<b>结果</b> 与正常组相比，模型组大鼠视网膜血管渗漏和白细胞黏附量以及<span lang="EN-US">TNF-</span><i>α</i>和<i><span lang="EN-US">p</span></i><span lang="EN-US">-NF-</span><i>κ</i><span lang="EN-US">Bp65</span>蛋白表达水平显著升高（<i><span lang="EN-US">P</span></i><span lang="EN-US">&lt;0.05</span>）；与模型组相比，阳性对照组与补阳还五汤组中大鼠视网膜血管渗漏和白细胞黏附量<span lang="EN-US">,</span>以及<span lang="EN-US">TNF-</span><i>α</i>和<i><span lang="EN-US">p</span></i><span lang="EN-US">-NF-</span><i>κ</i><span lang="EN-US">Bp65</span>的表达水平明显降低（<i><span lang="EN-US">P</span></i><span lang="EN-US">&lt;0.05</span>）。<b>结论</b> 补阳还五汤能防治由糖尿病引起的大鼠视网膜炎症反应，其作用机制可能与抑制<span lang="EN-US">TNF-</span><i>α</i>表达及<span lang="EN-US">NF-</span><i>κ</i><span lang="EN-US">B</span>通路激活有关。<span lang="EN-US"><o:p></o:p></span></span></p><p class="MsoNormal">

</p><p class="MsoNormal"><b><span lang="EN-US" style="font-size:12.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt">[</span></b><b><span style="font-size:12.0pt;
font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:宋体;mso-font-kerning:0pt">关键词<span lang="EN-US">]</span></span></b><span style="font-size:12.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;
mso-bidi-font-family:宋体;mso-font-kerning:0pt">糖尿病； 大鼠； 视网膜炎症； 补阳还五汤； 机制<span lang="EN-US"><o:p></o:p></span></span></p><p class="MsoNormal" align="left" style="word-break: break-all;"><b><span lang="EN-US" style="font-size:12.0pt;color:#007A84;
mso-font-kerning:0pt">[Abstract] </span></b><b><span lang="EN-US" style="font-size:12.0pt;color:#231F20;mso-font-kerning:0pt">Objective</span></b><span lang="EN-US" style="font-size:12.0pt;color:#231F20;mso-font-kerning:0pt"> To
observe the protective effect of Buyang Huanwu decoction (BYHWD) against retinal
inflammation in diabetic rats. <b>Methods</b> Healthy male Wistar rats were
randomly divided into normal and diabetic model groups. Diabetic rats were
given a one-time intraperitoneal injection of streptozotocin (STZ) to establish
a diabetic phenotype and were randomly assigned to the negative control
(saline), positive control (calcium dobesilate), and BYHWD treatment groups.
After 8 weeks of treatment, fluorescein-labeled dextran and Evans blue dye were
injected into the tail vein to observe vascular permeability and vascular
leakage in the retina, respectively. Perfusion of fluorescein-labeled
concanavalin was used to detect adhesion in rat retinal leukocytes. Western
blotting was used to quantify the expression levels of the inflammatory factors
TNF-<i>α</i>, NF-<i>κ</i>Bp65, and <i>p</i>-NF-<i>κ</i>Bp65 in retinal tissue. <b>Results</b>
Compared with nondiabetic rats, saline-treated diabetic rats showed</span><span lang="EN-US" style="font-size: 12pt;">&nbsp;</span>significantly increased retinal vascular leakage,
leukocyte adhesion, and protein levels of TNF-<i style="color: rgb(35, 31, 32); font-size: 12pt; background-color: var(--bs-body-bg); font-weight: var(--bs-body-font-weight); text-align: var(--bs-body-text-align);">α</i> and <i style="color: rgb(35, 31, 32); font-size: 12pt; background-color: var(--bs-body-bg); font-weight: var(--bs-body-font-weight); text-align: var(--bs-body-text-align);">p</i>-NF- <i style="color: rgb(35, 31, 32); font-size: 12pt; background-color: var(--bs-body-bg); font-weight: var(--bs-body-font-weight); text-align: var(--bs-body-text-align);">κ</i>Bp65
(<i style="color: rgb(35, 31, 32); font-size: 12pt; background-color: var(--bs-body-bg); font-weight: var(--bs-body-font-weight); text-align: var(--bs-body-text-align);">P</i>&lt;0.05). These effects were significantly reduced in the positive
control and BYHWD groups (<i style="color: rgb(35, 31, 32); font-size: 12pt; background-color: var(--bs-body-bg); font-weight: var(--bs-body-font-weight); text-align: var(--bs-body-text-align);">P</i>&lt;0.05). <b style="color: rgb(35, 31, 32); font-size: 12pt; background-color: var(--bs-body-bg); text-align: var(--bs-body-text-align);">Conclusion</b> Buyang Huanwu
decoction can ameliorate retinal inflammation in STZ-induced diabetic rats. Its
mechanism of action may be related to the inhibition of TNF-<i style="color: rgb(35, 31, 32); font-size: 12pt; background-color: var(--bs-body-bg); font-weight: var(--bs-body-font-weight); text-align: var(--bs-body-text-align);">α</i> expression
and NF-<i style="color: rgb(35, 31, 32); font-size: 12pt; background-color: var(--bs-body-bg); font-weight: var(--bs-body-font-weight); text-align: var(--bs-body-text-align);">κ</i>B pathway activation.</p><p class="MsoNormal" align="left">



</p><p class="MsoNormal" style="line-height:150%;layout-grid-mode:char;mso-layout-grid-align:
none;word-break:break-all"><b><span lang="EN-US" style="font-size:12.0pt;
line-height:150%;color:#007A84;mso-font-kerning:0pt">[Key words] </span></b><span lang="EN-US" style="font-size:12.0pt;line-height:150%;color:#231F20;mso-font-kerning:
0pt">Diabetes; Rats; Retinitis; Buyang Huanwu decoction; Mechanism</span><span lang="EN-US" style="font-size:12.0pt;line-height:150%;mso-font-kerning:0pt"><o:p></o:p></span></p><p class="MsoNormal">



</p>]]></description>
      <pubDate>Tue, 11 Apr 2023 08:00:18 GMT</pubDate>
      <guid isPermaLink="true">https://jhip.gdpu.edu.cn/effect-and-mechanism-of-buyang-huanwu-decoction-on-retinal-inflammation-in-streptozotocin-induced-diabetic-rats</guid>
    </item>
    <item>
      <title>Infarction or reperfusion-induced cardiac autophagy: role of microRNAs </title>
      <link>https://jhip.gdpu.edu.cn/infarction-or-reperfusion-induced-cardiac-autophagy-role-of-micrornas</link>
      <description><![CDATA[<p class="MsoPlainText" style="line-height:28.0pt;mso-line-height-rule:exactly"><span lang="EN-US" style="font-size:16.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt">22H041&nbsp; </span><span style="font-size:16.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt">邵晓奇，蔡平东，张越<span lang="EN-US">(</span>广东药科大学<span lang="EN-US">).Infarction or reperfusion-induced cardiac autophagy: role of
microRNAs</span>（梗死或再灌注诱导的心脏自噬：<span lang="EN-US">microRNA</span>的作用）</span><span lang="EN-US" style="font-size:12.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt"><o:p></o:p></span></p><p class="MsoPlainText" style="line-height:28.0pt;mso-line-height-rule:exactly"><b><span lang="EN-US" style="font-size:12.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt">[</span></b><b><span style="font-size:12.0pt;
font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:宋体;mso-font-kerning:0pt">摘要<span lang="EN-US">]</span></span></b><span style="font-size:12.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;
mso-bidi-font-family:宋体;mso-font-kerning:0pt">心肌梗死（<span lang="EN-US">MI</span>）期间，心肌细胞死亡的过程是由长时间心脏缺血触发的。近年来，非编码<span lang="EN-US">RNA</span>在心血管疾病病理生理学中的作用越来越重要。被称为<span lang="EN-US">microRNA</span>（<span lang="EN-US">miRNA</span>）的<span lang="EN-US">RNA</span>分子是小的非编码<span lang="EN-US">RNA</span>，其表达在不同器官中有所不同。<span lang="EN-US">microRNA</span>在与自噬相关的过程中发挥重要作用，自噬有助于心力衰竭的发展。这些过程包括调节线粒体完整性和功能、抗氧化防御、氧化应激、铁超载、铁死亡和生存途径。<span lang="EN-US">microRNA</span>可以作为治疗心血管疾病的有前途的生物标志物和有用靶点。对于新靶向药物的开发，揭示<span lang="EN-US">microRNA</span>表达如何变化及其如何调节自噬至关重要。为了理解心肌梗死和缺血再灌注损伤的机制，了解这<span lang="EN-US">2</span>个过程之间的相互关系至关重要。这篇综述将简要介绍<span lang="EN-US">microRNA</span>、自噬以及与<span lang="EN-US">microRNA</span>相关的药物。<span lang="EN-US"><o:p></o:p></span></span></p><p class="MsoNormal" align="left" style="word-break: break-all;">

</p><p class="MsoPlainText" style="line-height:28.0pt;mso-line-height-rule:exactly"><b><span lang="EN-US" style="font-size:12.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:
宋体;mso-font-kerning:0pt">[</span></b><b><span style="font-size:12.0pt;
font-family:&quot;微软雅黑&quot;,sans-serif;mso-bidi-font-family:宋体;mso-font-kerning:0pt">关键词<span lang="EN-US">]</span></span></b><span style="font-size:12.0pt;font-family:&quot;微软雅黑&quot;,sans-serif;
mso-bidi-font-family:宋体;mso-font-kerning:0pt">心肌梗死<span lang="EN-US">/</span>再灌注损伤<span lang="EN-US">; </span>自噬<span lang="EN-US">; </span>微小<span lang="EN-US">RNA<o:p></o:p></span></span></p><p class="MsoNormal" align="left" style="word-break: break-all;"><b><span lang="EN-US" style="font-size:12.0pt;color:#007A84;
mso-font-kerning:0pt">[Abstract] </span></b><span lang="EN-US" style="font-size:
12.0pt;color:#231F20;mso-font-kerning:0pt">The process of cardiomyocyte death
is triggered by prolonged ischemia in the heart during myocardial infarction
(MI). And the role of non-coding RNAs in the pathophysiology of cardiovascular
diseases has become increasingly important in recent years. RNA molecules known
as microRNAs (miRNAs) are small non-coding RNAs whose expression varies across
organs. microRNAs play an important role in processes associated with
autophagy, which contribute to the development of heart failure. These
processes include mitochondrial integrity and function, antioxidant defense,
oxidative stress, iron overload, ferroptosis, and survival pathways. microRNAs
may serve as promising biomarkers and useful targets in the treatment of
cardiovascular disease. For the development of new targeted drugs, it is vital
to uncover how microRNA expression changes and how they regulate autophagy. In
order to comprehend the mechanisms of myocardial infarction and ischemic reperfusion
injury, it is crucial to understand how these two processes relate to each
other. In this review, we will provide a brief introduction to microRNAs,
autophagy, and associated medicine to microRNAs. </span><span lang="EN-US" style="font-size:12.0pt;mso-font-kerning:0pt"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;">

</p><p class="MsoPlainText" style="line-height:28.0pt;mso-line-height-rule:exactly;
word-break:break-all"><b><span lang="EN-US" style="font-size:12.0pt;font-family:
&quot;Times New Roman&quot;,serif;color:#007A84;mso-font-kerning:0pt">[Key words] </span></b><span lang="EN-US" style="font-size:12.0pt;font-family:&quot;Times New Roman&quot;,serif;
color:#231F20;mso-font-kerning:0pt">Myocardial infarction/reperfusion injury;
Autophagy; MicroRNA</span><span lang="EN-US" style="font-size:12.0pt;font-family:
&quot;Times New Roman&quot;,serif;mso-fareast-font-family:微软雅黑;mso-font-kerning:0pt"><o:p></o:p></span></p><div><h4 style="margin-top:0cm;margin-right:36.0pt;margin-bottom:0cm;margin-left:
0cm;margin-bottom:.0001pt;word-break:break-all"><p>

</p></h4><h3 style="margin-top:0cm;margin-right:36.0pt;margin-bottom:0cm;margin-left:
0cm;margin-bottom:.0001pt;word-break:break-all">

</h3></div>]]></description>
      <pubDate>Tue, 11 Apr 2023 16:25:39 GMT</pubDate>
      <guid isPermaLink="true">https://jhip.gdpu.edu.cn/infarction-or-reperfusion-induced-cardiac-autophagy-role-of-micrornas</guid>
    </item>
    <item>
      <title>Study on the Molecular mechanisms of RNA m6 A-modifying enzymes in cardiovascular diseases</title>
      <link>https://jhip.gdpu.edu.cn/molecular-mechanisms-of-rna-m6-a-modifying-enzymes-in-cardiovascular-diseases</link>
      <description><![CDATA[<p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><span style="font-family: 仿宋_GB2312; font-size: 16pt;">Study on the molecular mechanism of RNAm6A modifying enzyme in cardiovascular diseases（RNAm</span><sup><span style="font-family: 仿宋_GB2312; font-size: 16pt; vertical-align: super;"><font face="仿宋_GB2312">6</font></span></sup><span style="font-family: 仿宋_GB2312; font-size: 16pt;">A修饰酶在心血管疾病中的分子机制研究）</span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[摘要]</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><font face="仿宋_GB2312">心血管疾病是除传染病外世界上人类的第一死因。其病理机制复杂，至今尚未完全阐明。随着近年对表观遗传学的研究深入，发现</font><font face="仿宋_GB2312">RNA的其中一种表观修饰N6-甲基腺嘌呤 (N6-methyladenosine, m</font></span><sup><span style="font-family: 仿宋_GB2312; font-size: 16pt; vertical-align: super;"><font face="仿宋_GB2312">6</font></span></sup><span style="font-family: 仿宋_GB2312; font-size: 16pt;">A) 修饰在心血管疾病的发生发展中发挥重要作用。并且，m</span><sup><span style="font-family: 仿宋_GB2312; font-size: 16pt; vertical-align: super;"><font face="仿宋_GB2312">6</font></span></sup><span style="font-family: 仿宋_GB2312; font-size: 16pt;">A甲基转移酶、去甲基化酶和识别蛋白可调控RNA 的m</span><sup><span style="font-family: 仿宋_GB2312; font-size: 16pt; vertical-align: super;"><font face="仿宋_GB2312">6</font></span></sup><span style="font-family: 仿宋_GB2312; font-size: 16pt;">A甲基化水平，进而影响RNA剪接、出入核、蛋白质翻译及降解等多种生物学过程。本文围绕m</span><sup><span style="font-family: 仿宋_GB2312; font-size: 16pt; vertical-align: super;"><font face="仿宋_GB2312">6</font></span></sup><span style="font-family: 仿宋_GB2312; font-size: 16pt;">A的生物学功能，研究其在心血管疾病的细胞凋亡、炎症、氧化应激、能量代谢和脂肪代谢等生物学过程中的作用，阐述其在心血管疾病中的作用机制及目前研究现状，并在此基础上讨论了治疗心血管疾病的m</span><sup><span style="font-family: 仿宋_GB2312; font-size: 16pt; vertical-align: super;"><font face="仿宋_GB2312">6</font></span></sup><span style="font-family: 仿宋_GB2312; font-size: 16pt;">A潜在靶向药物。</span><span style="font-family: 仿宋_GB2312; font-size: 16pt;"><o:p></o:p></span></p><p class="MsoPlainText" style="text-autospace:ideograph-numeric;mso-pagination:none;line-height:28.0000pt;
mso-line-height-rule:exactly;"><b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">[关键词]</span></b><span style="font-family: 仿宋_GB2312; font-size: 16pt;">N6-甲基腺嘌呤(m</span><sup><span style="font-family: 仿宋_GB2312; font-size: 16pt; vertical-align: super;"><font face="仿宋_GB2312">6</font></span></sup><span style="font-family: 仿宋_GB2312; font-size: 16pt;">A)； 心血管疾病； 炎症； 细胞凋亡；靶向药物</span></p>]]></description>
      <pubDate>Tue, 11 Apr 2023 16:25:33 GMT</pubDate>
      <guid isPermaLink="true">https://jhip.gdpu.edu.cn/molecular-mechanisms-of-rna-m6-a-modifying-enzymes-in-cardiovascular-diseases</guid>
    </item>
  </channel>
</rss>