丙烯腈染毒双大鼠肝脏钙稳态某此指标的影响

本研究观察了丙烯腈对大鼠肝脏Ｃａ＾２＋－ＡＴＰａｓｅ、Ｍｇ＾２＋－ＡＴＰａｓｅ、ＮＡ＾＋／Ｋ＾＋－ＡＴＰａｓｅ和磷酸化酶ａ（Ｐ－ａ）活性的影响,探讨其对大鼠肝脏钙稳态的影响。结果表明,随着染毒剂量的增大和染毒时间的延长,各ＡＴＰａｓｅ活性均逐渐降低,而Ｐ－ａ的活性却逐渐升高（Ｐ〈０．０１）。其中高剂量（５０ｍｇ／ｋｇ）组的各观察时段和染毒４２天时各染毒组酶活性的变化均具有显著性意义（Ｐ〈０．０５）     

间硝苯地平对老龄肾性高血压大鼠心肌和脑微粒体Na~＋，K~＋－ATP酶，Ca~

间硝苯地平（ｍ－Ｎｉｆ，ｉｇ２０ｍｇ·ｋｇ－１·ｄ１持续给药９周）可显著降低老龄肾性高血压大鼠（ＲＶＨＲ）血压和左室重量（Ｐ＜０．０１），增高心、脑微粒体Ｎａ＋，Ｋ＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性（Ｐ＜０．０１），降低Ｍｇ２＋－ＡＴＰ酶活性，体外量效关系研究发现，ｍ－Ｎｉｆ在较高剂量（１０～１０００μｍｏｌ·Ｌ－１）时可增高ＲＶＨＲ心脑微粒体Ｎａ＋，Ｋ＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性，且随剂量增加而增高。上述结果表明，ｍ－Ｎｉｆ可改善老龄ＲＶＨＲ心脑微粒体Ｎａ＋，Ｋ＋泵和Ｃａ２＋泵功能。     

白术水煎剂对老龄大鼠心肌Na~+,K~+-ATPase和血清TAA的影响

目的：探讨白术对老年大鼠心肌细胞膜钠钾ＡＴＰ酶（Ｎａ＋,Ｋ＋－ＡＴＰａｓｅ）活性和总抗氧化能力（ＴＡＡ）的影响,及产生显著影响的时间．方法：给老年Ｗｉｓｔａｒ大鼠灌服白术水煎制,制备血清、心肌匀浆和心肌细胞膜,分别测定血清ＴＡＡ和Ｎａ＋, Ｋ＋－ＡＴＰａｓｅ活性,并与对照组进行比较．结果：老年大鼠心肌 Ｎａ＋, Ｋ＋－ＡＴＰａｓｅ活性和ＴＡＡ明显低于青年对照组（Ｐ＜０．０５, Ｐ＜０．０１）．灌服白术后３０天心肌Ｎａ＋, Ｋ＋－ＡＴＰａｓｅ明显高于老年时照组,分别为（０． ９１± ０． ０５）、（０． ６２ ± ０． ０９）μ　ｍｏｌＰｉ．ｍｇ－１Ｐｒ．ｈ－１;而血清ＴＡＡ在２０天时明显高于老年对照组,分别为（６．６６±０．９０）、（５．３８±０．５８）Ｕ．ｍｌ－１;两组各项比较差异均有显著性（Ｐ＜０．０１）;血清ＴＡＡ和Ｎａ＋,Ｋ＋－ＡＴＰａｓｅ呈显著的正相关。结论：白术能明显增强心肌Ｎａ＋,Ｋ＋－ＡＴＰａｓｅ活性,其机理可能与血清ＴＡＡ的提高有关,白术的显效时间为 ３０天．     

四氯化碳引起大鼠肝微粒体钙泵抑制途径的初步探讨

四氯化碳引起大鼠肝微粒体钙泵抑制途径的初步探讨符立梧，周炯亮，汤丽芬，何玉莺细胞内钙稳态失调在细胞中毒性肝损害过程中起着十分重要的作用。毒物对钙泵（Ｃａ２＋－Ｍｇ２＋－ＡＴＰａｓｅ）的抑制是导致细胞内钙稳态失调的主要原因之一。我们用体外动物实验对ＣＣ...     

牛磺酸对缺血大鼠心肌腺苷三磷酸酶的影响

目的观测牛磺酸（ｔａｕｒｉｎｅ，Ｔａｕ）对心肌缺血损伤时心肌肌膜和线粒体ＡＴＰ酶活性的影响。方法以异丙肾上腺素（Ｉｓｏ，５ｍｇ·ｋｇ－１）诱导心肌缺血损伤模型，用定磷法分别测定Ｃａ２＋－ＡＴＰ酶、Ｍｇ２＋－ＡＴＰ酶及Ｎａ＋，Ｋ＋－ＡＴＰ酶活性。结果与对照组比较，缺血组心肌肌膜和线粒体Ｃａ２＋－ＡＴＰ酶、Ｍｇ２＋－ＡＴＰ酶及Ｎａ＋，Ｋ＋－ＡＴＰ酶活性均降低，在注射ＩＳＰ前３０ｍｉｎ腹腔注射Ｔａｕ（２００ｍｇ·ｋｇ－１），则上述酶活性未见显著性变化。结论Ｔａｕ具有拮抗缺血大鼠心肌肌膜及线粒体Ｃａ２＋－ＡＴＰ酶、Ｍｇ２＋－ＡＴＰ酶及Ｎａ＋，Ｋ＋－ＡＴＰ酶活性降低的细胞保护作用     

肾虚骨质疏松症病理机制及补肾方药对其防治作用的实验研究

本实验研究通过复制肾虚骨质疏松症大鼠动物模型，探讨该病证的病理机制以及补肾方药对其的防治作用。结果表明：肾虚骨质疏松症难性大鼠血清Ｅ２、ＰＴＨ含量均明显低于正常对照组（Ｐ〈０．０１）；该病证ＰＫＣ、Ｃａ＾２＋－Ｍｇ＾２＋ＡＴＰａｓｅ、Ｍｇ＾２＋ＡＴＰａｓｅ活性明显降低（Ｐ均〈０．０５）。提示该病证病理机制与较公认的内分泌相关，同时具有细胞膜结构和功能以及受体介导的磷脂－Ｃａ＾２＋系统信息传递的改变     

实验性颅脑损伤家兔线粒体Ca^2＋—ATPase活性的变化

测定家兔急性外伤性脑水肿后,脑细胞线粒体Ｃａ＾２＋－ＡＴＰａｓｅ活性及ＭＤＡ含量,探讨其在继发性脑损伤中的作用。方法利用家兔自由落体损伤模型在伤后４,８,２４,４８ｈ测定脑细胞线粒体Ｃａ＾２＋－ＡＴＰａｓｅ活必一粒体Ｃａ＾２＋－ＡＴＰａｓｅ活性在伤后４ｈ即开始下降,至４８ｈ降到最低,ＭＤＡ含量显著增加,随时间延长增加更明显,ＭＤＡ与Ｃａ＾２＋－ＡＴＰａｓｅ之间呈负相关,脑损伤后脑水含量增多,与Ｃａ     

丹参酮ⅡA磺酸钠对大鼠心，脑微粒体Na~＋，K~＋－ATP酶的抑制作用

丹参酮ⅡＡ磺酸钠（ＤＳ－２０１）体外可逆性抑制大鼠心，脑微粒体Ｎａ＋，Ｋ＋ＡＴＰ酶。并具有浓度依赖性，且对心微粒体Ｎａ＋，Ｋ＋－ＡＴＰ酶的抑制作用较扯降低Ｎａ＋或ＡＴＰ浓度则增强或减弱其抑酶作用，动力学分析表明ＤＳ－２０１对脑微粒体Ｎａ＋，Ｋ＋－ＡＴＰ酶的作用近似Ｎａ＋的竞争性拮抗剂，ＡＴＰ的反竞争性拮抗剂，有Ｋ＋及Ｍｇ２＋存在时则表现为非竞争性或混合型抑制，但对心肌微粒体Ｎａ＋，Ｋ＋－ＡＴＰ酶的作用则略有差别。     

The Effects of Etimicin and Gentamicin on Renal Endoplasmic Reticulum ~(45)Ca~(2 )-Uptake and Ca~(2 )-Mg~(2 )-ATPase Activity

目的：研究爱大霉素和庆大霉素对大鼠肾皮质内质网４５Ｃａ２＋摄取以及对内质网膜上Ｃａ２＋Ｍｇ２＋ＡＴＰａｓｅ活性的影响。方法：４５Ｃａ２＋示踪技术和孔雀蓝分光光度法。结果：爱大霉素和庆大霉素在大于或等于３．４×１０４ｍｏｌ·Ｌ１时，能抑制内质网４５Ｃａ２＋摄取（抑制率分别大于或等于１７．４％和２５．５％）；在３．４×１０２ｍｏｌ·Ｌ１时，对内质网膜上Ｃａ２＋Ｍｇ２＋ＡＴＰａｓｅ活性有抑制作用（抑制率分别为２４．１７％和２９．１９％）。结论：爱大霉素和庆大霉素在较高浓度时可使胞浆钙升高，这可能与其产生肾毒性有关     

丹参酮ⅡA磺酸钠对大鼠心,脑微粒体Na^＋,K^＋—ATP酶的…

丹参酮ⅡＡ磺酸钠（ＤＳ－２０１）体外可逆性抑制大鼠心，脑微粒体Ｎａ＾＋，Ｋ＾＋－ＡＴＰ酶，并具有浓度依赖性，且对心微粒体Ｎａ＾＋，Ｋ＾＋－ＡＴＰ酶的抑制作用较强，降低Ｎａ＾＋或ＡＴＰ浓度则增强或减弱其抑酶作用。动力学分析表明ＤＳ－２０１对脑微粒体Ｎａ＾＋，Ｋ＾＋－ＡＴＰ酶的作用近似Ｎａ＾＋的竞争性拮抗剂，ＡＴＰ的反竞争性拮抗剂，有Ｋ＾＋及Ｍｇ＾２＾＋存在时则表现为非竞争性或混合型抑制，但对心肌微粒     

Study of renovascular hypertension in rats: I. The role of the contralateral, non-clipped kidney in two-kidney, one-clip hypertension in rats

We attempted to produce two-kidney one-clip renovascular hypertension in SD rats, using hemoclips 0.2mm in diameter. After 12 weeks, 10 of the 16 rats were hypertensive. At this point, one-kidney, one-clip models were prepared by contralateral nephrectomy in five of the 10 hypertensive rats and in all six normotensive rats. Postoperatively, these 11 rats developed hypertension. Four to 6 weeks later, the clip was removed from the renal artery in five two-kidney and 11 one-kidney hypertensive rats. After unclipping, all the rats became normotensive although the extent of the fall in blood pressure in the one-kidney model was significantly greater than in the two-kidney model. The roles of the contralateral non-clipped kidney in the evolution of two-kidney, one-clip Goldblatt hypertension appear to be dual; sometimes depressing elevated blood pressure and sometimes maintaining it. Thus, it is postulated that in the six initially normotensive rats, its action was predominantly antihypertensive, while in the other 10 hypertensive rats, the presence of a contralateral non-clipped kidney served to develop and maintain hypertension even after unclipping.     

黄芪提取物对局灶性脑缺血再灌注损伤的抗氧化及线粒体保护作用

目的　研究黄芪提取物 (Extractofastragalus,EA)对局灶性脑缺血再灌注损伤大鼠的抗氧化及线粒体保护作用。方法　采用栓线法复制局灶性脑缺血 (MCAO)再灌注损伤模型,观察EA对大鼠脑组织匀浆中超氧化物歧化酶(SOD)、丙二醛(MDA)和乳酸 (LD)的影响;检测脑组织线粒体组分中的SOD、MDA含量及ATP酶活性的变化 ;电镜观察缺血再灌注后脑组织神经元超微结构的改变。结果　EA对大鼠MCAO2h再灌注 24h后脑组织及其线粒体组分中SOD活性的降低有明显的抑制作用,能抑制大鼠脑组织和脑组织线粒体组分中MDA含量的增加,能抑制大鼠脑组织LD含量的增加; EA可明显提高脑组织线粒体组分中Na+,K+ ATPase,Ca2+,Mg2+ ATPase活性;电镜照片显示EA组能改善脑组织神经元在脑缺血再灌注后的结构破坏情况。结论　EA对局灶性脑缺血再灌注损伤大鼠的保护作用的机制可能与其抗脂质过氧化和保护线粒体的作用有关。     

粉防己碱对肾型高血压左室肥厚大鼠心肌ATP酶活性的影响

目的　观察粉防己碱对肾型高血压左室肥厚大鼠心肌 Ａ Ｔ Ｐ 酶活性的影响。方法　采用二肾一夹肾型高血压形成大鼠左室肥厚,用光电比色、无机磷显色法测定心肌细胞膜 Ｎａ＋ , Ｋ＋ Ａ Ｔ Ｐ 酶及线粒体 Ｎａ＋ , Ｋ＋ Ａ Ｔ Ｐ 酶、 Ｃａ２ ＋ Ａ Ｔ Ｐ酶活性。结果　左室肥厚组大鼠心肌细胞 Ａ Ｔ Ｐ 酶活性明显降低,粉防己碱５０ ｍｇ·ｋｇ － １·ｄ － １ｉｇ 连续给药８ ｗｋ 可逆转左室肥厚,显著增加心肌细胞膜 Ｎａ ＋ , Ｋ＋ Ａ Ｔ Ｐ 酶及线粒体 Ｃａ２ ＋ Ａ Ｔ Ｐ酶活性。结论　粉防己碱因其钙拮抗作用,在降低血压、逆转左室肥厚的同时,可使细胞膜钠泵活性、线粒体钙泵活性恢复     

Inhibition by chlorpromazine, metals and I-ascorbic acid of calcium-ATPase and magnesium-ATPase in bovine adrenal medullary microsomes

Effects of chlorpromazine, metals and I-ascorbic acid (AA) on Ca2+-ATPase and Mg2+-ATPase in microsomal and granular fractions obtained from the bovine adrenal medulla were studied. Marker enzyme analysis on microsomal subfractions in a discontinuous sucrose density gradient showed a correlation of distribution between ATPase activities and plasma membrane. The two ATPase activities in such plasma membrane-rich microsomes were reduced by chlorpromazine, Hg2+ and Cu2+ (0.3 mM of each), and their effects were greater on the Mg2+-ATPase activity. Zn2+ (0.3 mM) also reduced only the Mg2+-ATPase activity. AA (3 mM) reduced the two ATPase activities to an equal extent. Nevertheless, the inhibitions of ATPases by Hg2+, Cu2+ and Zn2+ were decreased, unaltered and additively enhanced in combination with AA, respectively. We also observed high Mg2+-ATPase activity in the granule-rich fraction, but this ATPase activity was unaffected by all of the above agents. These results indicate that Mg2+-ATPase in the plasma membrane-rich microsome of adrenal medulla is inhibited by chlorpromazine, Hg2+, Cu2+ and Zn2+ more significantly than Ca2+-ATPase, but Mg2+-ATPase in the granular fraction is unaffected, and that AA changes the potency of inhibition by some metals of ATPases diversely.     

牛磺酸对2型糖尿病大鼠胰腺线粒体氧化应激的影响

目的探讨牛磺酸对糖尿病大鼠胰腺线粒体氧化应激的影响。方法将30只Wistar大鼠随机分为正常对照组、糖尿病组(DM组)和牛磺酸治疗组(Tau组,采用20g.L-1牛磺酸生理盐水溶液治疗,200mg·kg-1),前两组注射等体积的生理盐水溶液。8wk后,测3组大鼠血浆葡萄糖、胰岛素、丙二醛(MDA),胰腺线粒体MDA、Ca2+、超氧化物歧化酶(SOD)及Na+,K+-ATP酶(Na+,K+-ATPase)和Ca2+,Mg2+-ATP酶(Ca2+,Mg2+-ATPase)的活性。结果①DM组大鼠血糖、MDA和胰腺线粒体MDA、Ca2+含量明显高于对照组(P<0.01),而血浆胰岛素水平、SOD、Na+,K+-AT-Pase和Ca2+,Mg2+-ATPase活性明显降低(P<0.05)。②Tau组大鼠血糖、MDA及胰腺线粒体Ca2+、MDA含量较DM组明显降低(P<0.05),血浆胰岛素水平、SOD、Na+,K+-ATPase和Ca2+,Mg2+-ATPase活性明显升高(P<0.05)。结论牛磺酸可减轻2型糖尿病大鼠胰腺线粒体氧化应激水平。     

红景天苷对大鼠局灶性脑缺血/再灌注损伤的保护作用

目的研究红景天苷对大鼠局灶性脑缺血/再灌注损伤的保护作用。方法制作大鼠大脑中动脉闭塞(middlecerebral artery occlusion,MCAO)模型,观察大鼠行为学改变;取大脑并用红四氮唑(tetrazolium chloride,TTC)染色后测定梗死百分比和含水量;进行大脑组织学的检查以及制作脑匀浆测定SOD、MDA、GSH、Na+,K+-ATP酶、Ca2+-ATP酶、LD和NO的含量。结果红景天苷高、中、低剂量组(24、12、6mg.kg-1)均能使动物的行为学评分、脑梗死百分比、脑含水量明显降低;改善脑组织学损伤;并能够明显增加SOD、GSH的含量并降低MDA、NO、LD的含量,其中24、12mg.kg-1组还能明显提高缺血/再灌注后脑匀浆内Na+,K+-ATP酶、Ca2+-ATP酶的活力。结论红景天苷对脑缺血/再灌注有一定的保护作用。     

ATPase activities in kidney basolateral plasma membranes of young and old rats

The present work studied the turnover rate of (Na+ + K+)-ATPase as well as Mg2+- and Na+- ATPase activities in basolateral plasma membranes from kidney cortex cells of young and old rats. It was found that, as for the homogenates, the turnover rate of the (Na+ + K+)-ATPase was diminished by aging in about 40%. The Mg2+-ATPase activities on the other hand, were similar for the rat kidneys of young and old, in both the homogenates as well as the basolateral plasma membrane fractions.     

粉防己碱对高血压心肌肥厚大鼠心肌胶原含量和肌球蛋白ATP酶活性的影响(英文)

观察粉防己碱对高血压心肌肥厚大鼠心肌胶原含量和肌球蛋白ATP酶活性的影响 .采用二肾一夹肾血管性高血压造成大鼠左心室肥厚模型 ,自术后第 9周起按粉防己碱 50mg·kg- 1,依那普利 6mg·g- 1灌胃给药 ,每日 1次 ,连续 8周 .用分光光度法测定心肌羟脯氨酸含量及肌球蛋白ATP酶活性 .结果表明左心室肥厚组心肌羟脯氨酸为 (5.9± 0 .3)mg·g- 1干重 ,明显高于假手术对照组〔(3.6± 0 .4 )mg·g- 1干重〕 ,粉防己碱组和依那普利组心肌羟脯氨酸含量分别较左心室肥厚组低 2 8.2 %和 39.0 % .左心室肥厚组肌球蛋白ATP酶活性仅为 (0 .4 3± 0 .0 9)mmolPi·min- 1·g- 1蛋白质 ,较假手术对照组〔(0 .97±0 .0 6 )mmolPi·min- 1·g- 1蛋白质〕明显降低 ,而粉防己碱组和依那普利组则分别比左心室肥厚组高 6 0 .5%和 118.6 % .实验结果表明粉防己碱可部分逆转肾血管性高血压所致的大鼠左心室肥厚 ,降低心肌胶原含量 ,升高肌球蛋白ATP酶活性     

前列腺素E_1对脑缺血再灌注损伤的保护作用

目的　探讨前列腺素E1 (PGE1 )在脑缺血再灌注损伤中对脑组织过氧化的影响、对脑细胞膜ATP酶的保护、对血浆炎性细胞因子及内皮素的干预作用。方法　采用线栓法阻断大鼠左侧大脑中动脉 ,造成局灶性脑缺血再灌注模型 ,用药组于缺血前 5minivgttPGE1 (1 2 ,2 4 ,48μg·kg- 1 ) ,模型组及假手术组给予等容积NS。各组在大脑中动脉阻塞(MCAO) 60min ,再灌注 60min后 ,断头、取脑匀浆 ,测定其丙二醛 (MDA)含量 ,总超氧化物歧化酶 (SOD)活性 ,谷胱甘肽过氧化物酶 (GSH Px)活性及Na+ ,K+ ATP酶 ,Ca2 + ATP酶 ,Mg2 + ATP酶活性。心脏取血分离血浆测定其肿瘤坏死因子 (TNFα)的浓度及白介素 (IL 1 β、IL 6)和血浆内皮素 (ET 1 )的含量。结果　缺血再灌注模型组与假手术组相比 ,MDA含量升高 (P <0 0 5)、SOD及GSH Px活力降低 (P<0 0 5) ,Na+ ,K+ ATP酶、Ca2 + ATP酶、Mg2 + ATP酶活性降低 (P <0 0 5) ,TNFα、IL 1 β、ET 1含量升高 (P <0 0 5)。PGE1 3剂量组与模型组相比 ,MDA含量降低 (P <0 0 5) ,SOD及GSH Px活力升高 (P <0 0 5) ,Na+ ,K+ ATP酶、Ca2 + ATP酶、Mg2 + ATP酶活性升高 (P <0 0 5 ) ,Mg2 + ATP酶活性亦升高 ,TNFα、IL 1 β、ET 1含量降低 (P<0 0 5)。结论　PGE1 对缺血再灌注?