大鼠,近交SHR

摘要： 目的 探讨儿茶酚胺抑素(catestatin)在高血压发展过程中的变化规律及其对交感神经活性的作用.方法 以自发性高血压大鼠(SHR)(SHR组)及其相应的正常大鼠(WKY)(WKY组)作为研究对象.在大鼠不同的发育阶段(6、12和16周龄)检测心率、血压及血浆catestatin水平.以心率作为交感神经活性的标志.酶联免疫吸附测定catestatin的浓度,尾套法检测大鼠的血压及心率.结果 SHR组各个周龄的血压、心率均高于相应周龄的WKY组大鼠.SHR组血浆catestatin浓度高于WKY组(P<0.05),随着周龄的增加,SHR组血浆catestatin浓度逐渐升高,6周龄为(1.60±0.54)ng/ml,12周龄为(1.76±0.26)ng/ml,16周龄为(3.03±0.57)ng/ml.而WKY组大鼠则保持不变,6周龄为(1.10±0.28)ng/ml,12周龄为(1.05±0.21)ng/ml,16周龄为(1.17±0.12)ng/ml,两组血浆catestatin的浓度变化趋势有差异(P<0.05).12周SHR组大鼠尾静脉注射catestatin,30 min后心率由(417.6±20.9)次/min降到(378.1±15.6)次/min(P<0.05);但血压未下降.结论catestatin具有抑制心率的作用,可能具有代偿性抑制交感活性的作用.

摘要： 目的 探讨硫化氢H2S对自发性高血压大鼠(SHR)间隙连接蛋白40(Cx40)、43(Cx43)表达的调控作用,以及与心肌重构的关系.方法 取8周龄雄性SHR 16只,随机分为SHR对照组(n=8)、SHR+硫氢化钠NaHS组(n=8);取同周龄的正常Wistar京都(WKY)雄性大鼠8只,设为WKY组.SHR+NaHS组腹腔注射NaHS 56μmol/(kg·d),SHR对照组和WKY组每日腹腔注射等量生理盐水,持续8周.用分光光度计检测各组大鼠外周血和心肌组织中H2S含量;通过HE染色及Masson三色染色观察H2S对心肌的病理学改变;通过免疫组织化学检测3组大鼠心脏组织中Cx40、Cx43表达位置的变化;运用Western blotting检测3组大鼠心脏组织中Cx40、Cx43及 α-平滑肌肌动蛋白(α-SMA)、骨桥蛋白(OPN)表达量的变化.结果 与WKY组大鼠比较,SHR组大鼠外周血及心肌组织中H2S含量减少(P<0.05),NaHS干预后SHR外周血及心肌组织中H2S含量增加(P<0.05);与WKY组大鼠比较,SHR组大鼠心肌纤维结构排列较为紊乱,NaHS干预后SHR心肌纤维排列较为整齐;SHR组大鼠心肌中的Cx40、Cx43表达增加且分布紊乱,SHR+NaHS组大鼠心肌中的Cx40、Cx43分布较规整;且SHR组大鼠心肌中Cx40、Cx43、α-SMA、OPN表达升高(P<0.05),SHR+NaHS组大鼠心肌中Cx40、Cx43、α-SMA、OPN表达降低(P<0.05).结论 H2S可能通过调控Cx40、Cx43的表达来改善SHR心肌重构.

摘要： 目的 探讨拉西地平对自发性高血压大鼠模型血管内皮功能的保护作用,并分析其可能的作用机制.方法 选取50只Wistar大鼠为WKY组,分为WKY对照组和WKY研究组,每组25只;50只自发性高血压大鼠为SHR组,分为SHR对照组和SHR研究组,每组25只.WKY研究组和SHR研究组大鼠给予拉西地平,WKY对照组和SHR对照组大鼠给予等体积的生理盐水,持续8周.各组大鼠分别于干预前后测量尾动脉收缩压.采用肠系膜上动脉血管舒张试验检测肠系膜动脉舒张度,Western blot检测主动脉Cx37蛋白表达水平,硝酸还原法检测血清NO水平,ELISA检测血浆ET水平及血清TNF-α水平.结果 SHR研究组和SHR对照组大鼠平均动脉压明显高于WKY研究组和WKY对照组(P<0.05);与干预前比较,干预后的SHR研究组大鼠平均动脉压明显降低,且明显低于SHR对照组,差异有统计学意义(P<0.05).与WKY研究组和WKY对照组相比较,SHR研究组和SHR对照组大鼠肠系膜上动脉舒张度、主动脉Cx37蛋白表达水平、血清NO水平明显降低(P<0.05),而SHR研究组明显高于SHR对照组(P<0.05);血浆ET水平、血清TNF-α水平明显升高(P<0.05),而SHR研究组明显低于SHR对照组(P<0.05).结论 拉西地平能够改善血管内皮功能,其可能通过调节血管舒张因子NO、收缩因子ET的表达,保证细胞间缝隙连接通讯正常,抑制炎症反应,从而保护血管内皮.

摘要： 目的探讨钙激活氯通道ANO1抑制剂T16A（inh）-A01（A01）对自发性高血压大鼠血管平滑肌细胞（SHR-VSMC）增殖的影响。方法取SHR-VSMC及其对照WKY大鼠的血管平滑肌细胞（WKY-VSMC）,均分为对照组（加入体积分数为0.001的DMSO）和A01处理组（分别加入浓度为1、5、10、20μmol/L的A01）。采用MTT法检测各组细胞存活率,Western blot法检测各组增殖细胞核抗原（PCNA）表达,观察A01对细胞增殖能力的影响。结果 MTT结果显示,与WKY-VSMC对照组比较,SHR-VSMC对照组的生长速度明显加快（t=3.702,P〈0.01）。与SHR-VSMC对照组比较,A01处理组的细胞存活率呈剂量依赖性下降,其中10、20μmol/L A01的抑制作用比较差异有统计学意义（F=9.916,q=4.468-7.483,P〈0.01）。Western blot结果显示,与WKY-VSMC对照组相比,SHR-VSMC对照组的PCNA表达水平显著升高（t=2.871,P〈0.01）,A01（20μmol/L）处理24h后,SHR-VSMC的PCNA表达部分被抑制（t=2.064,P〈0.01）。结论 ANO1抑制剂能明显抑制SHR-VSMC的异常增殖。

摘要： 目的 探讨镇肝熄风汤对自发性高血压大鼠(SHR)酪酪肽(PYY)表达的影响.方法 2012年6月—2015年4月选取14周龄雄性SHR 75只,随机分为模型组(n=15)、贝那普利组(盐酸贝那普利灌服0.90 mg·kg-1·d-1,n=15)、镇肝熄风汤低、中、高剂量组(镇肝熄风汤分别灌服15、30、60 g·kg-1·d-1,n=15),以WKY大鼠15只作为WKY组,模型组及WKY组每日灌服同体积的蒸馏水.干预8周后,实验过程中WKY组大鼠死亡6只,模型组大鼠死亡6只,贝那普利组大鼠死亡7只,镇肝熄风汤高剂量组大鼠死亡6只,镇肝熄风汤中剂量组大鼠死亡6只,镇肝熄风汤低剂量组大鼠死亡6只应用酶联免疫实验法检测各组大鼠血清PYY水平,采用免疫组化法检测结肠组织PYY水平,RT-PCR法检测结肠组织PYY mRNA水平.结果 模型组血清PYY水平高于WKY组(P<0.05);镇肝熄风汤高剂量组血清PYY水平低于模型组(P<0.05).模型组结肠组织PYY水平高于WKY组(P<0.05);贝那普利组和镇肝熄风汤高、中、低剂量组结肠组织PYY水平低于模型组(P<0.05);镇肝熄风汤高剂量组结肠组织PYY水平低于贝那普利组(P<0.05).模型组结肠组织PYY mRNA水平高于WKY组(P<0.05);贝那普利组和镇肝熄风汤高、中剂量组结肠组织PYY mRNA水平低于模型组(P<0.05);镇肝熄风汤高剂量组结肠组织PYY mRNA水平低于贝那普利组(P<0.05).结论 SHR结肠组织PYY调节失衡,镇肝熄风汤可能通过调节PYY的表达而达到降压目的.%Objective To investigate the influence of Zhengan Xifeng decoction on the expression of peptide tyrosine tyrosine (PYY)in spontaneously hypertensive rats (SHRs). Methods We randomly assigned 75 SHRs (14 weeks old, male)into model group (n = 15),Benazepril group (n = 15),Zhengan Xifeng decoction high,medium,and low dose groups (15 SHRs in each group),and set 15 WKY rats as the WKY group between June 2012 and April 2015. During the intervention period of 8 weeks,six rats died in model group,WKY group,Zhengan Xifeng decoction high,medium,and low dose group, seven rats died in Benazepril group. The rats in model group and WKY group were given the same volume of distilled water every day,Benazepril group were fed with Benazepril 0. 90 mg·kg - 1 ·d - 1 ,Zhengan Xifeng decoction high,medium,and low dose groups were fed with Zhengan Xifeng decoction 15,30,60 g·kg - 1 ·d - 1 ,respectively. At the end of intervention,the level of PYY in serum was detected by ELISA,the expression of PYY and its mRNA in colon was detected by immunohistochemistry and RT - PCR. Results The serum PYY levels in model group were significant higher than those in WKY group (P < 0. 05). Zhengan Xifeng decoction high dose group had lower serum PYY levels than model group (P < 0. 05). Compared with the model group,the expression of PYY in colon was lower in the WKY group (P < 0. 05)as well as in Benazepril group,and Zhengan Xifeng decoction high,medium,and low dose groups (P < 0. 05). The expression of PYY in colon in Zhengan Xifeng decoction high dose group was lower than that in Benazepril group (P < 0. 05). WKY group had lower expression of PYY mRNA in colon than model group (P < 0. 05 ),likewise,Benazepril group,and Zhengan Xifeng decoction high,medium dose groups possessed lower expression of PYY mRNA in colon than model group (P < 0. 05). Zhengan Xifeng decoction high dose group displayed a lower expression of PYY mRNA in colon in comparison to Benazepril group (P < 0. 05). Conclusion SHRs have regulation disorder of PYY in colon. The antihypertensive effect of Zhengan Xifeng decoction may be realized by regulating the expression of PYY.

摘要： 目的 探讨MicroRNA-124 (miR-124)对大鼠血管平滑肌细胞增殖的作用及可能的调控机制.方法 选择10只11周龄雄性SPF级自发性高血压大鼠(SHR)作为实验组及同龄的10只SPF级Wistar大鼠(WKY)为对照组.采用组织贴片法原代培养SHR和WKY主动脉平滑肌细胞.通过实时荧光定量PCR(qRT-PCR)技术检测miR-124在两组主动脉平滑肌细胞间的表达差异.将miR-124模拟物或模拟物阴性对照转染SHR主动脉平滑肌细胞,分析过表达miR-124对血管平滑肌细胞增殖的影响.通过数据库及生物信息学软件预测miR-124的靶基因,并利用双荧光素酶报告基因系统进行验证.通过qRT-PCR和Western blot检测靶基因Meox2 mRNA及蛋白表达变化.采用RNA干扰技术,观察敲低Meox2表达对血管平滑肌细胞增殖的影响.结果 MiR-124在SHR主动脉平滑肌细胞中的表达为WKY主动脉平滑肌细胞的0.22倍(P＜0.01).体外过表达miR-124可明显抑制SHR主动脉平滑肌细胞的增殖.经生物信息学分析及体外双荧光素酶报告基因系统检测,证实Meox2是miR-124的靶基因.过表达miR-124后SHR主动脉平滑肌细胞中Meox2 mRNA的表达为阴性对照组的0.29倍(P＜0.01);Western blot结果显示,Meox2蛋白表达水平亦明显降低.干扰Meox2的表达亦可降低SHR主动脉平滑肌细胞的增殖.结论 MiR-124在SHR中表达下调,其可能通过介导Meox2调控主动脉平滑肌细胞的增殖进而抑制高血压病变的发生过程.

摘要： Objective: To explore the effects of fosinopril on oxidative stress and vascular function in experimental rats with spontaneous hypertension. Methods: The rats were divided into 3 groups: Control group, with normal healthy rats (n=15), Spontaneous hypertension (SH) group (n=15), SH rats received intragastric administration of normal saline and Treatment group (n=15), SH rats received intragastric administration of fosinopril 10mg/(kg•d). All animals were treated for 7 weeks. Caudal artery systolic blood pressure (SBP) was measured at each week. blood levels of superoxide dismutase (SOD), reactive oxygen species (ROS), malonaldehyde (MDA) and NO2-/NO3- were determined in different groups respectively after 7 weeks. Moreover, thoracic aorta was taken to examine its diastolic reactive rate by acetylcholine (Ach)/sodium nitroprusside (SNP) induction. Results: From the 1st week until the end of experiment, compared with SH group, Treatment group had decreased SBP,P<0.05. With 7 weeks treatment, compared with Control group, SH group had decreased SOD activity, while increased protein levels of MDA and ROS, allP<0.05; compared with SH group, Treatment group showed elevated SOD activity (P=0.010), while reduced protein levels of MDA (P=0.021) and ROS (P=0.009). Compared with Control group, SH group had the lower content of NO2-/NO3-(P<0.001); both SH group and Treatment group had decreased diastolic rates by Ach/SNP induction,P<0.05. Compared with SH group, Treatment group presented the higher content of NO2-/NO3- and higher diastolic rate by Ach induction, allP<0.001. Conclusion: Fosinopril could improve vascular diastolic function via anti-oxidative stress in experimental SH rats, which might be one of its anti-hypertensive mechanisms.%目的：探讨福辛普利对自发性高血压大鼠氧化应激水平及血管功能的影响。方法：大鼠分3组：正常对照组(n=15)、自发性高血压组（高血压组，n=15）、自发性高血压福辛普利治疗组（治疗组， n=15）。治疗组每日予灌胃福辛普利[10 mg/（kg·d）]，高血压组则予灌胃等体积生理盐水，每周测量尾动脉收缩压（SBP）。7周后检测血浆氧化物歧化酶（SOD）、血清活性氧（ROS）、丙二醛（MDA）、一氧化氮代谢产物（NO2-/NO3-）水平；并取胸主动脉，检测其对乙酰胆碱（Ach）/硝普钠（SNP）的舒张率。结果：自第1周末开始至结束，治疗组的SBP较高血压组均显著下降（P<0.05）。7周后，高血压组的血浆SOD活性较正常对照组明显下降（P<0.05），而血清MDA及ROS水平则显著上升（P<0.05）；但经福辛普利治疗后，治疗组大鼠的血浆SOD活性较高血压组有所上升（P=0.010），且MDA、ROS水平下降（MDA：P=0.021；ROS：P=0.009），差异均有统计学意义。高血压组NO2-/NO3-含量较正常对照组显著下降（P<0.001），高血压组和治疗组对Ach/SNP诱导的血管舒张率均较正常对照组显著下降（P<0.05）。治疗组血清NO2-/NO3-含量显著高于高血压组（P<0.001）；对比高血压组，治疗组对Ach（P<0.001）诱导的血管舒张率有明显上升。结论：福辛普利通过抗氧化应激改善血管舒张功能，可能是其发挥降压作用的机制之一。

摘要： Objective This study aims to explore antihypertension and heart protective effect of acupuncture on SHR rats through the observation of blood pressure, cardiac ultrasound and pathology examination of SHR rats after needling the Zusanli (ST 36) and Taichong (LR 3). Methods A total of 14 SHR rats (10 weeks) were randomly divided into two groups:6 for model group and 8 for acupuncture group, another 6 SD rats (10 weeks) were used as the control group. SHR rats in the acupuncture group were fixed in the holder, and then they exposed both lower limbs for needling both sides Zusanli (ST 36) and Taichong (LR 3), and then they retained needles for 20 minutes per time with four weeks. The other two groups were fixed in the holder without needling. Blood pressure was examined each week. LVSs, LVDd, LVPWs, LVPWd were measured and recorded by cardiac ultrasound in the day after the whole course of acupuncture. LVM, LVMI, RWT were calculated. The hearts of rats were dissected and fixed in formalin for heart pathology detection after doing the cardiac ultrasound. Results After acupuncture treatment, compared with model group, the systolic blood pressure (SBP) of the third week (178.38 ± 9.47 mmHg vs. 190.00 ± 13.90 mmHg) and the fourth week (167.96 ± 23.47 mmHg vs. 195.47 ± 11.36 mmHg) of acupuncture group significantly decreased (P<0.01). The diastolic pressure (DBP) of the third week (139.33 ± 13.20 mmHg vs. 159.56 ± 12.89 mmHg) and the fourth week (132.92 ± 18.02 mmHg vs. 165.61 ± 13.36 mmHg) of acupuncture group significantly decreased (P<0.01). The LVSs (0.96 ± 0.07 vs. 1.28 ± 0.24), LVPWs (1.15 ± 0.08 vs. 1.68 ± 0.19) of the acupuncture group were significantly lower than those of the model group (P<0.01). The LVM (0.51 ± 0.12 vs. 0.84 ± 0.17) and LVMI (14.96 ± 1.53 vs. 23.65 ± 5.04) of acupuncture group were significantly lower than those of the model group (P<0.01). Histopathologic examination of the heart of the model group showed chronic inflammatory granulation tissue hyperplasia and fibrosis in myocardial outer membrane, but the acupuncture group showed no obvious changes in the heart tissue. Conclusions Acupuncture treatment on Zusanli (ST 36) and Taichong (LR 3) could effectively control the left ventricular hypertrophy by decreasing the SBP and DBP , prevent cardiac remodeling, and protect myocardial cells.%目的：观察针刺“足三里”“太冲”对自发性高血压大鼠(spontaneously hypertensive rat， SHR)血压指标、心脏超声指标及病理学检测的影响，探讨其作用机制。方法14只10周龄SHR大鼠按随机数字表法分为模型组6只、针刺组8只，6只同周龄SD大鼠为空白对照组。针刺组大鼠针刺双侧“足三里”“太冲”，留针20 min/次，连续4周，模型组及空白对照组无针刺干预。每周检测血压，连续5周。在针刺干预结束次日，使用彩色超声心动仪测量并记录各组大鼠左室舒张末期室间隔厚度、舒张末期左室内径、收缩末期左室后壁厚度、左室舒张末期后壁厚度。计算左室质量、左室质量指数、相对室壁厚度。采用HE染色法观察各组大鼠心脏病理学改变。结果与模型组比较，针刺干预第3、4周，针刺组大鼠收缩压[第3周：(178.38±9.47)mmHg比(190.00±13.90)mmHg；第4周：(167.96±23.47)mmHg比(195.47±11.36)mmHg]、舒张压[第3周：(139.33±13.20)mmHg比(159.56±12.89)mmHg；第4周：(132.92±18.02)mmHg比(165.61±13.36)mmHg]降低(P＜0.01或P＜0.05)；针刺组大鼠左室舒张末期室间隔厚度[(0.96±0.07)mm 比(1.28±0.24)mm]、收缩末期左室后壁厚度[(1.15±0.08)mm 比(1.68±0.19)mm]、左室质量[(0.51±0.12)g 比(0.84±0.17)g]、左室质量指数[(14.96±1.53)比(23.65±5.04)]降低(P＜0.01)。HE 染色显示，模型组大鼠心肌外膜有慢性炎症伴肉芽组织增生及纤维化；针刺组大鼠心脏组织未见明显变化。结论针刺“足三里”“太冲”可有效降低 SHR 大鼠收缩压及舒张压，控制左室肥厚和心脏重构，对心肌细胞有保护作用。

摘要： 目的：探讨当归挥发油对自发性高血压大鼠（SHRs）心肌组织中微小 RNA （miRNA）表达谱的影响，阐明当归挥发油发挥作用的可能机制。方法：将 SHRs 分为模型组、卡托普利组和当归组，取同周龄的正常 Wistar 大鼠作为对照组，采用无创套尾法测定大鼠尾动脉收缩压，给药4周后，采用 Affymetrix miRNA 4.0芯片测定心肌组织中 miRNA 表达谱，采用京东基因与基因组百科全书（KEGG）富集法分析差异表达的miRNA 靶基因。结果：给药前模型组大鼠收缩压明显高于对照组（P ＜0.05），连续服药1～4周后，卡托普利组和当归组大鼠收缩压明显低于模型组（P ＜0.05）。与模型组比较，当归组大鼠差异表达的 miRNA 29个，其中表达上调的 miRNA 13个（Ratio＞2.0，P ＜0.05），表达下调的 miRNA 16个（Ratio ＜0.5，P ＜0.05）。KEGG 富集分析，miR-19a、let-7i 和 miR-181c 与胰岛素信号通路有关联（P ＜0.05），let-7i 、miR-181a 和miR-455与血管内皮生长因子（VEGF）信号通路调控有关联（P ＜0.05），miR-122、miR-181a、miR-200b、miR-181c、let-7i 和 miR-19a 与细胞凋亡有关联（P ＜0.05）。结论：当归挥发油可降低 SHRs 血压，对 SHRs 心肌组织中 miRNA 表达谱产生影响，可能通过调节胰岛素信号通路及 VEGF 信号通路相关 miRNA 发挥血压调节作用。%Objective:To explore the effect of Angelica Sinensis Volatile Oil on the mi RNA expression profiling in myocardium tissue of the spontaneously hypertensive rats (SHRs),and to clarify the possible mechanism of Angelica Sinensis Volatile Oil.Methods:All the SHRs were divided into Angelica group,model group and captopril group,and other Wistar rats with the same age were selected as control group.The non-invasive systolic blood pressure was detected;after 4 weeks of administration,the changes of miRNA expression profiling in myocardium tissue were measured by Affymetrix miRNA 4.0 Array.KEGG analysis was used to identify the target genes. Results:Compared with control group,the systolic blood pressure of the rats in model group was significantly decreased (P < 0.05)before treatment.4 weeks after administration,compared with model group,the systolic blood pressure of the rats in Angelica group was significantly decreased (P <0.05).Compared with model group, 29 differential miRNAs of rats in Angelica group were found (P < 0.05 ), with 13 up-regulated miRNAs and 16 down-regulated miRNAs.The KEGG analysis results showed that miR-19a,let-7i,and miR-181c were related to insulin signaling pathways; let-7i, miR-181a, and miR-455 were related to VEGF signaling pathways;miR-122,miR-181a, miR-200b, miR-181c, let-7i, and miR-19a were related to apoptosis (P < 0.05 ). Conclusion:Angelica Sinensis Volatile Oil can decrease the blood pressure in SHRs and it can regulate the blood pressure by regulating the miRNA related to insulin signaling pathways and VEGF signaling pathways.

摘要： Objective To investigate the effects of candesartan on the expression of Nrf2 and insulin sensi-tivity of the spontaneously hypertensive rats(SHR)and its possible mechanism.Methods 30 SHR were randomly di-vided into model group,low dose group and high dose group.10 WKY rats served as control group.All the rats fed with fructose,while the low and high dose group rats accepted candesartan consecutive treatment with the dose of 0.4 mg/kg and 0.8 mg/kg respectively.At the 8th weekend,the insulin resistance index(HOMA-IR),the level of reactive oxygen species(ROS)and the expression of Nrf2 were detected.Results Compared with the control group,the HO-MA-IR was significantly increased in the model group(P <0.05),the protein expression of Nrf2 in model group sig-nificantly decreased(P <0.01)at the same time while the level of ROS increased significantly(P <0.01).Compared with the model group,the HOMA-IR decreased obviously in the high dose group (P <0.01).The protein expression of Nrf2 in the low dose and high dose group increased significantly (P <0.01,P <0.05)compared with model group,and the level of ROS significantly decreased compared with the model group(P <0.05).Conclusion Candesartan could improve the insulin resistance and oxidative stress by the antagnism effect of AngⅡin the skeletal muscle cells.%目的：研究坎地沙坦对自发性高血压大鼠骨骼肌核转录因子-2（Nrf2）表达和胰岛素敏感性的影响。方法30只自发性高血压大鼠随机分为对照组（C 组）、模型组（M组）、坎地沙坦低剂量组（Can1组）、坎地沙坦高剂量组（Can2组），10只 WKY 大鼠作为对照组，均给予果糖喂养，Can1组及 Can2组分别给予坎地沙坦（0．4 mg／kg、0．8 mg／kg）灌胃干预。实验第8周末，检测各组大鼠胰岛素抵抗指数（HOMA-IR）、血管紧张素Ⅱ（AngⅡ）、活性氧（ROS）以及 Nrf2的表达水平。结果与 C 组相比，M组 HOMA-IR 水平及 ROS 表达显著升高，而 Nrf2表达降低，差异有统计学意义（P ＜0．05、P ＜0．01）；与 M组相比，Can2组的 ROS 生成减少，HOMA-IR 下降，差异有统计学意义（P ＜0．05、P ＜0．01）；Can1及 Can2组的 Nrf2表达均较 M组显著增加，差异有统计学意义（P ＜0．05、P ＜0．01）。结论坎地沙坦可以通过拮抗 AngⅡ减轻 AngⅡ诱导的骨骼肌胰岛素抵抗和氧化应激。

摘要： 本发明为一种Klotho腺相关病毒在制备治疗SHR大鼠高血压心脏病药物中的应用。通过实验研究结果显示，通过Klotho基因转导可以控制SHR大鼠血压进一步升高，减轻高血压心脏病心脏损害即可以保护SHR大鼠心脏，至少可以持续12周，Klotho腺相关病毒完全可以作为制备治疗SHR大鼠高血压心脏病药物对高血压及相关心血管疾病进行治疗。

摘要： 一种基于SHR的污泥干燥系统及其干燥方法，系统包括污泥干化装置、废气洗涤装置、废气增压装置和废气膨胀装置。湿污泥与载湿气体一同进入间接加热的污泥干化装置干燥。排出的高含湿废气经增压后，返回至干化装置循环加热。加热后的高压不凝气经膨胀装置回收能量，并脱水后，部分作为载湿气体返回污泥干化装置循环载湿，其余排入废气处理系统。加热冷凝后的凝结水返回至洗涤装置除尘除酸后排出。该系统在保留原有载湿气体的基础上，充分利用了蒸发水分的热量，系统高效节能，适合于大部分的间接干化机，具有较强的普适性。

摘要： 本申请公开了一种成功切换报告SHR的处理、管理、控制方法及装置，属于通信领域，本申请实施例的成功切换报告SHR的处理方法包括：终端从网络侧设备获取目标信息；终端基于目标信息，执行目标操作；其中，目标操作包括：不生成SHR或删除已生成的SHR。

摘要： 本公开实施例公开了一种成功切换报告SHR的记录上报方法和装置，可应用于通信技术领域，其中，由终端设备执行的方法包括：接收网络侧设备在源小区上发送的切换命令，其中，切换命令用于指示终端设备由源小区切换至目标小区，源小区为长期演进LTE小区，目标小区为新无线NR小区，切换命令包括SHR配置，在成功由LTE小区切换至NR小区的情况下，根据SHR配置记录成功切换报告。由此，终端设备支持在LTE小区接收网络侧设备配置的SHR配置，支持由LTE小区切换至NR小区的场景下，记录成功切换报告。

摘要： 本发明涉及一种CDK4/6激酶抑制剂SHR6390的制备方法。本发明通过6步化学反应，能够快速、有效地制备获得SHR6390。本发明第一步反应充分利用了嘧啶4位反应活性高的优势，温和条件就能很好的得到目标产物化合物3，第四步反应得到化合物8的合成反应的后处理简单，基本上靠过滤、洗涤就可以得到很好的白色固体产物，不需要纯化，适合放大和工艺生产。

摘要： 本发明属于生物技术和植物学领域；涉及细胞属性改造，调节根瘤共生的方法，特别是基于SHR‑SCR构成的植物体内新机制在改造皮层细胞分裂潜能中的应用。本发明还提供了新型的用于鉴定植物的性状的途径，从而为植物的有效鉴定提供了可行的方法，为植物的育种筛选提供了有力的工具。

摘要： 本发明公开了一种基于虚拟现实技术防控与改善视力的人机互动远近交替智能训练方法，其包括VR一体机头盔及植入其内的应用控制程序，通过应用控制程序建立虚拟现实空间、登录系统、远近交替训练走向及起停时长、语音提示、动画引导等可随时随地进行人机互动智能训练视力的方法。本发明能够使眼部睫状肌等眼肌得到训练，提升睫状肌等眼肌力量及伸拉弹性，促进眼部血液循环，从而防控与改善视力，对青少年儿童效果更明显。

摘要： 本发明公开一种适用于配电网产消者就近交易的新能源就地消纳系统，其特征在于，所述新能源就地消纳系统包括以下步骤：拥有常规负荷、空调、分布式光伏发电的产消者市场准入；获准进入市场的产消者电量电价投标决策；基于产消者电量电价投标的多轮出清方法，形成市场交易结果；基于交易结果执行偏差的偏差惩罚方法；基于第一轮偏差校核的市场结算；促进偏差就地平衡的共享储能机制；基于共享储能交易结果与第二轮偏差校核的第二轮市场结算。本发明新能源就地消纳系统实现了配电网产消者在分布式交易市场中的自动报量电量电价投标决策，促进了能量的就近交易和新能源的就地消纳，实现了个体效益和系统效益的激励相容。

摘要： 本申请涉及小鼠品系鉴定的技术领域，具体公开了一种SNP标记在近交系小鼠品系鉴定中的应用、引物序列。具体地，SNP标记在近交系小鼠品系鉴定中的应用，所述SNP标记包括15个SNP位点；所述近交系小鼠品系选自C57BL/6J、C57BL/6N、BALB/c、FVB、DBA/2、CBA/CaJ和C3H。以及用于合成上述SNP位点的引物序列在近交系小鼠品系鉴定中的应用。本申请能够同时鉴别出C57BL/6J、C57BL/6N、BALB/c、FVB、DBA/2、CBA/CaJ和C3H 7种近交系小鼠品系，提高了近交系小鼠品系鉴定结果的准确性。

摘要： 本发明涉及灌溉技术领域，尤其是涉及一种实现远近交替喷灌的节水灌溉装置，包括往复式液压阀，所述往复式液压阀从外向内依次设有空腔外壳和液压阀外壳，所述液压阀外壳与所述空腔外壳之间形成用于水流通过的夹层，所述往复式液压阀的底部设有与所述液压阀外壳内壁螺纹连接的入水底盖，所述入水底盖上设有与所述往复式液压阀的相通的入水口，所述液压阀外壳内壁的顶部固定设有导向柱，所述导向柱上活动套设有活塞，所述活塞的上端与所述液压阀外壳内壁的顶部之间相互抵接有复位弹簧，所述液压阀外壳上设有连通所述夹层与所述液压阀外壳内侧的通孔，所述往复式液压阀的顶部连接有与所述夹层相通的出水喉管，所述出水喉管的出水端连接有喷头主体。