Effects of electroacupuncture at Taichong(LR 3) and Baihui(DU 20)on cardiac hypertrophy in rats with spontaneous hypertension

OBJECTIVE: To investigate the effects of electroacupuncture(EA) at Taichong(LR 3) and Baihui(DU 20)on myocardial hypertrophy in spontaneously hypertensive rats(SHRs).METHODS: Thirty-six SHRs were randomly assigned to model, EA, and Losartan groups, with twelve rats per group. Twelve Wistar Kyoto rats were selected as the normal control group. Systolic blood pressure(SBP) and cardiac function were measured in all rats.Expression levels of factors associated with the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR) pathway were evaluated by Western blotting and real-time PCR.Pathological changes of the heart tissue were observed by hematoxylin-eosin staining.RESULTS: After treatment, enhanced SBP was significantly decreased in the EA and Losartan groups compared with the model group(P < 0.01). Echocardiographic and morphological analyses revealed that enhanced end-diastolic interventricular septal thickness and left ventricular posterior wall thickness, as well as ratio of left ventricular weight to body weight were markedly diminished in the EA and Losartan groups(P < 0.01 or P < 0.05), while reduced left ventricular end-diastolic dimension and left ventricular ejection fraction were significantly ameliorated(P < 0.01). Real-time PCR and western blotting analyses showed that the expression levels of PI3K,Akt, and mT OR in SHRs were significantly up-regulated by EA and Losartan(P < 0.01), while the expression levels of PTEN and ANP were down-regulated(P < 0.01).CONCLUSION: EA at Taichong(LR 3) and Baihui(DU20) inhibited the development of cardiac hypertrophy and improved the cardiac function in SHRs, possibly through regulation of the PI3K/Akt/mTOR signalling pathway.

Endothelin-1, an important mitogen of smooth muscle cells of spontaneously hypertensive rats

OBJECTIVE: To study the features of vascular smooth muscle cell (VSMC) proliferation induced by endothelin-1 (ET-1). METHODS: VSMCs of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats were cultured and treated with ET-1. Basic fibroblast growth factor (bFGF) gene expression was measured using both Northern blot and an enzyme-linked immunoassay. RESULTS: ET-1 resulted in an increase in bFGF transcripts at 8 - 24 h; bFGF levels were significantly higher in VSMCs treated with ET-1 than in those not treated. However, VSMCs growth responses in SHR and WKY were different. Smooth muscle cells of SHR were hyper-responsive to ET-1. Maximal bFGF mRNA levels were elevated 3.5-fold at 4 h of stimulation in WKY and 8-fold at 8h in SHR4. Moreover, the proliferation of VSMCs induced by ET-1 was inhibited by antisense phosphorothioate oligodeoxynucleotides (10 micromol/L AS-bFGF) but not sense bFGF oligomers at the same concentrations, being reduced by 80% in SHR and 40% in WKY vs control, respectively. Furthermore, the effect of AS-bFGF oligomers on SHR SMC proliferation is significantly greater than on WKY SMC proliferation. CONCLUSION: ET-1 may be required for exaggerated vascular growth responses in SHR and bFGF may be involved.

Influence of Valsartan on myocardial apoptosis in spontaneously hypertensive rats

OBJECTIVE: To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. METHODS: Thirty spontaneously hypertensive rats (SHRs) were divided into two groups: 15 treated with Valsartan (20 mg x kg(-1) x d(-1)) (SHR + Valsartan group), the others with placebo (SHR + placebo group), with 15 normal Wistar rats as control. Systolic blood pressure was measured by the tail-cuff method. The observation period was from 8 to 16 weeks of age. Cardiac apoptosis was evaluated by a Terminal Deoxynucleotidyl Transferase-Mediated dUTP-biotin Nick End Labeling (TUNEL) assay. RESULTS: Mean blood pressure values were 127 +/- 2 mm Hg in controls, 163 +/- 6 mm Hg in the SHR + Valsartan group and 193 +/- 7 mm Hg in the SHR + placebo group at 16 weeks of age, whereas the blood pressure in 8-week-old SHR and Wistar rats were 175 +/- 3 mm Hg and 125 +/- 5 mm Hg, respectively. The ratio of the heart weight over body weight declined in Wistar (3.07 +/- 0.03 mg/g) and SHR + Valsartan groups (3.22 +/- 0.19 mg/g) compared with the SHR + placebo group (4.02 +/- 0.31 mg/g) (P

Endothelin receptor antagonist combined with a calcium channel blocker attenuates renal injury in spontaneous hypertensive rats with diabetes

OBJECTIVE: To investigate the effects of the mixed endothelin receptor antagonist, bosentan, combined with the long-acting calcium channel blocker, amlodipine, compared to the angiotensin-converting enzyme inhibitor, cilazapril, on the progressive renal injury in spontaneous hypertensive rats (SHR) with diabetes. METHODS: Diabetic hypertensive rats (SHR-DM) were induced by streptozotozin injected in male SHR (7-week-old),and divided into an untreated and three treated groups: 1) cilazapril treated group; 2) bosentan+amlodipine treated group; and 3) amlodipine treated group. Wistar Kyoto rats (WKY) and SHR rats served as normotensive and hypertensive control, respectively. The mean arterial blood pressure, renal function, endothelin and angiotensin II levels as well as the protein expression of renal extracellular matrix components and transforming growth factor (TGF)-beta1 were determined at the end of the 4th week. RESULTS: Mean arterial blood pressure significantly increased in SHR and SHR-DM rats compared to WKY rats. All the therapies reduced the blood pressure to normal levels. However, the enhanced urinary protein excretion, the decreased creatinine clearance as well as the increased plasma and intrarenal endothelin and angiotens in II levels were found in the untreated SHR-DM and prevented by treatment with bosentan+amlodipine and cilazapril. Similarly, these two kinds of therapies in SHR-DM abolished the overexpression of renal TGF-beta1 by Western blot analysis and reduced the accumulation of collagen type IV, laminin and fibronectin proteins by an immunochemical approach. Amlodipine monotherapy had no detectable effects on the above parameters. CONCLUSION: Bosentan combined with amlodipine can offer similar renoprotective effects on that of cilazapril and may be a potent therapy to attenuate renal injury by reducing renal protein levels of TGF-beta1 in diabetes with a hypertensive state.

Ventricular remodeling by Scutellarein treatment in spontaneously hypertensive rats

OBJECTIVE: To observe reversal of ventricular remodeling by the protein kinase C inhibitor Scutellarein in spontaneously hypertensive rats (SHRs). METHODS: Twelve SHRs were randomly divided into two groups. Scutellarein and saline (10 mg x kg(-1) x d(-1)) were given by intraperitoneal injection to two groups of rats separately. Systolic blood pressure (SBP) and ventricular weight index (LVW/BW, RVW/BW) were measured. A polarization microscope and an image analyzer system (IAS) were used to observe changes in cardiovascular structure and to count the content of cardiac muscle interstitial collagen. RESULTS: The pathologic changes in the left ventricle in the Scutellarein group rats (SHR(D)) improved to varying degrees, including hypertrophy of the cardiac muscle and collagen volume fraction. CONCLUSION: Scutellarein can reverse ventricular remodeling, improve myocardial stiffness and protect heart cardiac muscle.

Phosphorylation and biosynthesis of high molecular weight proteins of tumor nuclear matrix

Our previous studies showed a predominance of high molecular weight protein group in tumor nuclear matrices. Contrary to normal cells, proteins of this group are preferentially phosphorylated. Phosphoproteins of hepatoma nuclear matrix are selectively subjected to rapid proteolysis. By alkali treatment and a monoclonal antibody against phosphotyrosyl residue the presence of two high molecular weight bands of phosphotyrosyl-containing proteins was detected in nuclear matrices of tumor but not of normal liver cells. High molecular weight protein group of tumor nuclear matrices revealed also a rapid turnover and preferential incorporation of labeled amino acids selectively inhibited by chloramphenicol.

Five novel monoclonal antibodies to thymic epithelial cell surface antigens in rats

OBJECTIVE: To establish monoclonal antibodies (mAbs) against thymic epithelial cells and study the function of epithelial cells during T-cell differentiation in the thymus. METHODS: Hybridomas secreting mAbs against thymic epithelial cells were derived by immunization of Balb/c mice with two thymic epithelial cell lines, TaD3 and FTE. The distribution of antigens recognized by these mAbs was detected by immunochemical staining and cytofluorographic analysis, and the molecular weight of the antigens by immunoblotting. RESULTS: Five specific monoclonal antibodies (mAb) were obtained. On the basis of their distribution in the thymus determined by immunochemical staining, mAb RE-4D8 was regarded as clusters of thymic epithelium staining (CTES) type IIA: mAb RE-12B2, which showed a unique distribution pattern only in the medulla, was CTES type V: mAb RE-5C6 was CTES type IV: mAb RE-6D6 might be CTES type IIB: and mAb RE-1D4 was classified as type V. The molecular weight (MW) of antigen RE-4D8, RE-6D6 and RE-12B2 were 120 kDa, 220 kDa and 35 kDa, respectively. Antigen RE-1D4 is a novel marker of cortical epithelium, several established thymic epithelial cell lines were classified and their original intrathymic locations were determined by these mAbs. Thymic cell lines, TuD3 and FTE were cortical phenotypes whereas TaD3 had a medullar phenotype. CONCLUSIONS: These mAbs clearly demonstrate the heterogeneity of the thymic epithelium; they could detect antigens not only in the cytoplasm but also on the surface of thymic epithelial cells. Our data suggest that these newly established mAbs may help elucidate the interaction between thymocytes and epithelial cells during T cell maturation.

PVG大鼠生化标记基因的测定

目的 对PVG大鼠进行生化标记基因的测定。方法 依据国家标准GB/T 14927.1—2008《实验动物近交系小鼠、大鼠生化标记检测法》测定,随机抽取4只PVG大鼠,取(肺、肾、小肠、睾丸)组织器官进行样品制备,用醋酸纤维薄膜电泳法检测11个生化位点(Hbb、Cs1、Alp1、Akp1、Esl、Es3、Es4、Es6、Es8、Es9和Esl0)。结果 PVG大鼠11个位点的基因型分别是Hbb为b型,Cs1为b型,Alp1为b型,Akp1为a型,Esl为a型,Es3为d型,Es4为b型,Es6为b型,Es8为b型,Es9为a型和Esl0为a型,且均为纯合。结论 PVG大鼠遗传生化标记结果符合近交系特征。

Effect of Taichong(LR 3) acupuncture in spontaneously hypertensive rats

OBJECTIVE: To evaluate the effects of Taichong(LR3) acupuncture points(acupoints) on the expression of glucose transporter protein 1(GLUT1) in the hypothalamus of spontaneously hypertensive rats(SHRs) as measured by combined positron emission tomography and computed tomography(PETCT).METHODS: Spontaneously hypertensive rats(SHR)were divided into model, Taichong(LR 3) acupuncture, and sham groups. Additionally, Tokyo Wistar rats were used as the control group. Changes in blood pressure were recorded in different groups of rats before and after the corresponding treatment. Hematoxylin and eosin(HE) staining was used to study basic morphological changes, and immunohistochemistry was used to determine GLUT1 expression in the hypothalamus. Further,PET-CT was utilized to elucidate the antihypertensive mechanism after acupuncture at the Taichong(LR 3) acupoints.RESULTS: PET-CT indicated activation of the hypothalamus. Measurement of blood pressure showed that acupuncture at the Taichong(LR 3) acupoints lowered blood pressure. HE staining did not show any significant pathological changes, although differences in cell number were observed. Immunohistochemical analysis indicated a GLUT1 downregulation in the SHRs of the Taichong(LR 3) acupuncture group after the treatment.CONCLUSION: Acupuncture at Taichong(LR 3) acupoints lowered blood pressure in SHRs, with possible mechanisms being changes in cell number and GLUT1 expression in the hypothalamus.

Mechanism and effect of Shijueming (Concha Haliotidis) on serum calcium in spontaneously hypertensive rats

OBJECTIVE： To observe the impact of Shijueming （Concha Haliotidis） on spontaneously hypertensive rats via blood pressure, serum calcium, vascular smooth muscle membrane L-type calcium channel α1 C subunit （CaL-α1C）, plasma membrane calci- um-ATPase （PMCA） mRNA expression, and the L-type calcium channel in vascular smooth muscle cells. METHODS： Twelve-week-old male rats with sponta- neous hypertension were divided into three groups： a Shijueming （Concha Haliotidis） group （group 1）, a nifedipine group （group 2）, and a dis- tilled water group （group 3）. All were given a four-week treatment. Blood pressure and dissocia- tive serum calcium were examined before treat- ment. Blood pressure was taken every week during treatment. Atomic absorption spectrometry was used to examine dissociative serum calcium. Re-verse transcription-polymerase chain reaction was used to examine the expression of CaL-α1C and PM- CA1 mRNA. The patch clamp technique was used to examine the electrophysiological characteristics of the vascular smooth muscle cell calcium chan- nels. RESULTS： After treatment, blood pressure of the Shijueming （Concha Halioticlis） group lowered but not significantly （P〉0.05）. Blood pressure of the nifedipine group lowered significantly （P〈0.05）. Blood pressure of the distilled water group re- mained high. The concentration of serum calcium in the Shijueming （Concha Haliotidis） and the dis- tilled water groups lowered （P〈0.05）. Expression of CaL-α1C mRNA in the nifedipine group decreased compared with the distilled water group （P〈0.01）. There was the decreasing trend in the Shijueming （Concha Haliotidis） group, but it was not statistically significant. Shijueming （Concha Haliotidis） also had effects on the expression of PMCA1 mRNA but with- out statistical significance. However, there was a significant decreasing effect on vascular smooth muscle cell Ica-L flow. CONCLUSION： This study indicated that Shijuem- ing （Concha Haliotidis） could increase serum calci- um and decrease blood pressure. It may work by in- fluencing calcium channels, expression of PMCA1 mRNA, and regulating ion calcium channels and calcium-ATPase.

人ATP7B基因对Wilson病动物模型LEC大鼠暴发性肝炎的治疗

目的 探讨人ATP7B基因对Wilson病动物模型LEC大鼠暴发性肝炎的治疗效果。 方法 将构建的 7.1kb含有鸡 β肌动蛋白启动子的人正常ATP7BcDNA ,经显微注射法导入人Wilson病动物模型LEC(long EvansCinnamon)大鼠受精卵 ,建立转基因功能恢复大鼠模型。以Westernbolt检测人ATP7B在转基因大鼠肝内的表达 ,用同窝无转基因大鼠及正常野生型LEA大鼠作对照 ,对 6～ 16周龄的转基因大鼠的血清AST、ALT和总胆红素水平进行连续测定 ,同时取 13周龄转基因大鼠的肝组织进行病理学和组织化学分析。 结果 人ATP7B基因在转基因大鼠的肝组织中获得正确和完整的表达 :12周龄前后 ,与同窝无转基因大鼠相比 ,转基因大鼠的血清AST、ALT和总胆红素水平明显降低 ,肝组织的炎性病变显著减轻 ,肝细胞内铜的蓄积减少 ;至 16周龄 ,转基因大鼠的临床表型未见异常 ,存活率达 10 0 %。说明人ATP7B的导入 ,成功地抑制了Wilson病动物模型LEC大鼠的暴发性肝炎的发生。结论 Wilson病肝炎的发生与ATP7B基因功能缺陷引起的铜蓄积有直接关系。基因转移有可能是一种有效的治疗Wilson病的方法。

Proliferation of aortic smooth muscle cells and renin-angiotensin system in SHR rats

目的：探讨ＳＨＲ大鼠主动脉平滑肌细胞（ＡＳＭＣ）异常增殖和肾素血管紧张素系统（ＲＡＳ）的关系．方法：测定血管紧张素Ｉ（Ａｎｇ）、卡托普利（Ｃａｐ）、沙拉新（Ｓａｒ）对培养的ＳＨＲ、ＷＫＹＡＳＭＣ增殖和Ａｎｇ、血管紧张素转化酶（ＡＣＥ）的影响．结果：Ａｎｇ在２％血清培养基中可刺激ＳＨＲＡＳＭＣ增生．ＳＨＲＡＳＭＣ分裂增殖能力比ＷＫＹ强，ＳＨＲＡＳＭＣＲＡＳ处于高功能状态．Ｃａｐ长期（４周）干预显著抑制ＳＨＲＡＳＭＣ异常增殖和Ａｎｇ、ＡＣＥ活性，Ｓａｒ长期干预同样抑制ＳＨＲＡＳＭＣ的增殖和ＡＣＥ活性，但Ａｎｇ水平反而升高．Ｃａｐ短期（２４小时）干预不影响两种大鼠ＡＳＭＣＲＡＳ．结论：Ｃａｐ和Ｓａｒ长期干预通过减少ＳＨＲＡＳＭＣＡｎｇ生成或阻断Ａｎｇ和特异受体结合，抑制其异常增殖．

Upregulation of the angiotensin-converting enzyme 2-angiotensin-(1-7)-Mas receptor axis by a combination of Yinyanghuo(Herba Epimedii Brevicornus) and Cheqianzi(Semen Plantaginis) improves erectile function in spontaneously hypertensive rats

OBJECTIVE:To evaluate the effects of a combination of Yinyanghuo(Herba Epimedii Brevicornus)(HEB)and Cheqianzi(Semen Plantaginis)(SP)on erectile dysfunction caused by essential hypertension in spontaneously hypertensive rats(SHRs),and to elucidate the role of the angiotensin-converting enzyme 2-angiotensin-(1-7)-Mas receptor(ACE2/Ang[1-7]/Mas receptor)axis in this process.METHODS:A total of 24 SHRs were randomly assigned to three groups:SHR-control,low-dose(12.5 g/kg)and high-dose(25 g/kg)HEB+SP(HEBSP).Eight Wistar-Kyoto rats were used as normal controls.HEBSP was administered by oral gavage for 28 d.Erectile function was measured once a week using the Heaton test.After 4 weeks of treatment,the corpus cavernosum was harvested from each rat to measure nitric oxide(NO),nitric oxide synthase(e NOS)and Ang(1-7)levels,as well as ACE2,Mas receptor and neuronal nitric oxide synthase(n NOS)protein expression.RESULTS:After 4 weeks of treatment,HEBSP significantly increased erectile function in the treated group compared with SHR-control group(P<0.01).Additionally,HEBSP treatment significantly increased cavernosal levels of Ang(1-7),e NOS and NO.Moreover,HEBSP significantly elevated the expression levels of ACE2,Mas receptor and n NOS.These beneficial effects were elevated in the high-dose HEBSP group.CONCLUSION:HEBSP improved erectile function in SHRs by upregulating the ACE2/Ang(1-7)/Mas receptor axis,e NOS and n NOS pathways.

用镭射激光捕获技术研究LEC鼠P53基因突变和肝癌发生的关系

目的研究P53基因突变与原发性肝癌发生发展的关系。方法利用LEC鼠(long evan cinnamon)作为肝癌的动物模型。选取15周,37周,101周的LEC鼠15,14和10只,正常对照SD大鼠15只,取出肝脏组织进行切片。切片一部份用于GST-P免疫组化(immunohistochemistry,IHC)染色,另一部份利用镭射激光捕获技术(laser capture microdissection,LCM)定位切割,进行P53基因外显子5,6/7,8突变的分析。结果37周龄LEC鼠和101周龄LEC鼠GST-P阳性率高于对照组(P<0.005),15周龄LEC鼠GST-P阳性率与对照组相比差异无统计学意义(P>0.05)。P53基因在GST-P表达阳性肝炎组有3例突变(3/11),GST-P表达阳性肝癌组有10例发生突变(10/15),肝癌组显著高于肝炎组(P<0.05)。结论P53的突变发生在肝癌形成的早期阶段,随着发展过程,突变率明显增高。GST-P虽然特异性不强,但是不失为一种灵敏的判断肝损伤的指标。

人ATP7B基因对Wilson病动物模型LEC大鼠肝硬化及肝癌的治疗

目的 探讨人ATP7B基因对Wilson病动物模型LEC(Long EvansCinnamon)大鼠肝硬化及肝癌的治疗效果。 方法 将 7 1kb含有鸡 β肌动蛋白启动子的人正常ATP7BcDNA ,经显微注射法导入Wilson病动物模型LEC大鼠受精卵 ,建立转基因功能恢复大鼠模型。以无转基因大鼠及正常野生型LEA大鼠为对照 ,对 17～ 30周龄的转基因大鼠的血清AST、ALT水平进行连续测定 ,同时取 30和 6 0周龄转基因大鼠的肝脏进行病理组织学和组织化学分析。 结果 17～ 30周龄 ,转基因大鼠的血清丙氨酸氨基转移酶 (AST)、天门冬氨酸氨基转移酶 (ALT)保持在较低的水平。至 6 0周龄 ,雄性转基因大鼠肝组织未见胆管纤维化。在所有被检的转基因大鼠个体未见肝细胞癌性病变。转基因大鼠的存活率达 95 7%。此外 ,30和 6 0周龄的转基因大鼠肝细胞内铜着色颗粒的分布及数量无明显变化。 结论 人ATP7B的导入有效的延缓了Wilson病动物模型LEC大鼠肝硬化的形成、抑制了肝癌的发生。Wilson病的肝硬化及肝癌的发生可能与铜的蓄积无直接关系。

建立6种近交系大鼠遗传质量检测及品系鉴别的单核苷酸多态性组合

目的 筛选出均匀分布在大鼠染色体上的单核苷酸多态性(SNP)位点,建立常用近交系大鼠遗传质量检测及品系鉴别方法。方法 在文献中获得SNP共141个,利用Ensembl数据库中获取的信息筛选出在BN、F344、GK、LEW、SHR和WKY 6种大鼠品系中呈现多态性的SNP位点,并从中优化出均匀分布各染色体且包含品系特异性SNP的最佳位点组合。通过PCR扩增技术和Sanger测序方法对组合位点用于常用近交系大鼠遗传质量检测和品系鉴别的效果进行验证。结果 优化出了在各品系内表现单态性、品系间呈多态性的40个SNP标记。其中包含可以用于品系鉴别的特异性位点:4个BN大鼠特异性位点,3个F344大鼠特异性位点,2个GK大鼠特异性位点,2个LEW大鼠特异性位点和1个SHR大鼠特异性位点。分别利用BN、F344、LEW、SHR和WKY大鼠的DNA混合样本对优化出的40个位点进行验证,结果与网站数据一致。结论 成功建立了常用近交系大鼠遗传质量检测及品系鉴别的SNP组合。

LEC鼠自发性肝癌谷胱甘肽S-转移酶表达的意义

目的 :观察 L EC大鼠自发性肝癌谷胱甘肽 S-转移酶 (GST- P)的蛋白表达 ,探讨 GST- P对原发性肝癌早期诊断的价值。方法 :采用免疫组织化学方法检测 L EC大鼠肝脏 GST- P的表达。结果 :6 7周龄 L EC鼠即肝癌组 GST- P的表达率 (96 .97% )明显高于 4～ 6个月龄 L EC鼠即肝炎组 (37.5 % )及 SD大鼠组 (9.38% )的表达率 (P<0 .0 1) ,4～ 6个月龄 L EC鼠 GST- P的表达率高于 SD大鼠组 (P<0 .0 5 )。结论 :GST- P可作为大鼠原发性肝癌早期诊断的肿瘤标志物。

Tong-xin-luo capsule inhibits left ventricular remodeling in spontaneously hypertensive rats by enhancing PPAR-γ expression and suppressing NF-κB activity

Background Tong-xin-luo capsule （TXL）, used as a traditional Chinese herb, offeres a therapeutic potential for treatment of cardiovascular diseases. It has been shown to exert a variety of pharmacological effects, including antihypertensive effects, and is able to improve ventricular remodeling. However, the mechanisms of its action are not completely understood. The aim of this study was to evaluate the molecular mechanisms of Tong-xin-luo capsule on left ventricular remodeling in spontaneously hypertensive rats （SHR）. Methods Sixteen eight-week-old SHRs were randomized into an SHR group （n=8） and a TXL group （n=8） that were given Tong-xin-luo capsule （1.5 mg·kg^-1·d^-1）. Eight Wistar Kyoto （WKY） rats fed with 0.9% NaCl served as the control group （WKY group）. Systolic blood pressure （BP）, body weight and heart rate were monitored once every two weeks. Ventricular remodeling was detected by histopathological examination. Nuclear factor kappa B P65 （NF-κB P65） and peroxisome proliferators activated receptor y （PPAR-γ） protein and phosphorylated inhibitor kappa a （IκBα） protein were detected by immunohistochemistry and western blot respectively. The physical interaction of the P65-P50 heterodimer with IκBα and NF-κB were measured by co-immunoprecipitation. PPAR-γ mRNA, collagen Ⅰ mRNA and collagen Ⅲ mHNA were measured by real-time PCR.Results TXL inhibited NF-κB P65 expression and ventricular remodeling and suppressed the activation of NF-κB compared with the SHR group （P〈0.01, P〈0.05）. TXL reduced IκBα phosphorylation, increased expression of PPAR-γ protein and enhanced the physical interaction of the P65-P50 heterodimer with IκBα. The mRNA expression of PPAR-γ was enhanced but the mRNA expression of collagen Ⅰ mRNA and collagen Ⅲ mRNA were suppressed by TXL. Conclusions In spontaneously hypertensive rats, TXL could inhibit ventricular remodeling induced by hypertension, and the inhibitory effect might be associated with the process of TXL increasing the expression of PPAR-γ that could result in the inhibition of the activation of NF-κB.

Inhibitory effect of antisense basic fibroblast growth factor oligonucleotides on proliferation of cultured aortic smooth muscle cells induced by angiotensin Ⅱ in SHR rats

目的：研究转染反义碱性成纤维细胞生长因子（ｂＦＧＦ）寡核苷酸（ＯＤＮ）对培养的自发性高血压大鼠（ＳＨＲ）主动脉平滑肌细胞（ＳＭＣ）生长的影响．方法：用脂质体介导法将反义ｂＦＧＦＯＤＮ转入ＳＭＣ内，用Ｎｏｒｔｈｅｒｎ杂交检测ｂＦＧＦ基因表达，并测定［３Ｈ］ｔｈｙｍｉｄｉｎｅ掺入和细胞计数．结果：转染反义ｂＦＧＦＯＤＮ（５μｍｏｌ·Ｌ－１）几乎完全抑制血管紧张素Ⅱ（ＡｎｇⅡ，１μｍｏｌ·Ｌ－１）诱导增高的ｂＦＧＦｍＲＮＡ表达和明显抑制ＳＭＣ增殖，在基础状态和ＡｎｇⅡ刺激条件下，［３Ｈ］ｔｈｙｍｉｄｉｎｅ掺入分别被抑制２６５％（Ｐ＜００１）和４２０％（Ｐ＜００１），细胞数分别被抑制１７３％（Ｐ＜００１）和２２２％（Ｐ＜００１）．结论：反义ｂＦＧＦＯＤＮ能有效抑制ＡｎｇⅡ诱导的ｂＦＧＦ基因表达和ＳＭＣ增殖．

蓝光致棕色挪威大鼠慢性视网膜光损伤的实验研究

目的通过构建蓝光致棕色挪威(Brown Norway,BN)大鼠慢性视网膜光损伤的模型,探究大鼠光感受器细胞及视网膜色素上皮细胞(RPEc)损伤的特点及可能损伤机制。方法根据随机数字表法将大鼠分组为光照0 d(正常对照组)和光照1、3、7及14 d组,每组8只。正常对照组不进行光照;余各组每日暴露于光照强度为(1000±100)Lux的LED蓝光光源环境中3 h,连续1、3、7及14 d,观察大鼠的行为活动;视网膜电流图(ERG)记录最大混合反应的a、b波振幅和潜伏期;进行眼底照相;HE染色观察视网膜组织;酶联免疫吸附试验(ELISA)检测大鼠视网膜组织的活性氧(ROS)含量。结果与正常对照组比较,光照3 d组对光声刺激的反应迟钝,光照7 d及14 d组精神较萎靡,行动稍迟缓,对光声刺激反应更为迟钝;光照3 d组偶见视网膜出血点,RPEc层基底部色素颗粒增多,外核层可见轻度细胞核固缩;光照7 d组视网膜上见散在点状出血点、黄白色点状颗粒物,视网膜静脉迂曲扩张;光照14 d组视网膜上见大量黄白色点状渗出,视网膜动脉呈铜丝样甚至银丝样外观,视网膜静脉迂曲扩张;光照7、14 d组视网膜光感受器内节/外节结构排列紊乱,外核层细胞核固缩,RPEc层基底部色素颗粒沉积。与正常对照组比较,光照3、7、14 d组大鼠视网膜变薄(P<0.05);光照3、7及14 d组ERG b波潜伏期逐渐延长、a波、b波振幅逐渐降低,视网膜组织ROS逐渐升高(P<0.05)。结论蓝光持续照射BN大鼠可产生氧化应激反应,导致慢性视网膜光损伤,且照射时间越长,视网膜光损伤越重。