血管内皮生长因子在尾悬吊模拟失重大鼠肺组织中表达的研究

目的：研究尾悬吊模拟失重大鼠肺组织血管内皮生长因子的变化。方法：采用尾悬吊模拟失重，分为悬吊7 d和21 d及相应对照4组，每组10只健康雄性SD大鼠，共40只大鼠。并采用免疫组织化学技术检测肺组织的血管内皮生长因子表达情况。结果：7 d尾悬吊模拟失重大鼠肺组织血管内皮生长因子的表达水平明显高于正常对照组（P<0.05），且21 d悬吊组模拟失重大鼠肺组织血管内皮生长因子的表达水平仍较高（P<0.05），但增高程度已明显低于7 d悬吊组。结论：在模拟失重条件下肺组织血管内皮生长因子的表达水平增高，并且随着时间延长增高程度会有所降低.     

尾悬吊模拟失重大鼠胃黏膜超微结构改变及氧化应激损伤

目的 探讨尾悬吊模拟失重对大鼠胃黏膜组织超微结构和氧化应激的影响.方法 健康雄性Wistar大鼠88只,按随机数字表分为11组(n=8),采用尾悬吊法建立模拟失重大鼠动物模型,各组大鼠分别尾悬吊0h(正常对照组)、6h、12h、1d、2d、3d、5d、7d、14d、21 d、28 d.实验结束后观察各组大鼠胃黏膜组织病理改变,检测胃黏膜组织超氧化物歧化酶(SOD)、丙二醛(MDA)和一氧化氮(NO)含量,免疫组化法检测胃黏膜组织诱生型一氧化氮合酶(NOS2)和环氧化酶2(COX2)的表达.结果 透射电镜下可见尾悬吊模拟失重大鼠胃黏膜部分腺细胞核皱缩畸形,染色质浓缩边聚,线粒体肿胀,嵴断裂、溶解,空泡变性,粗面内质网扩张.上述改变在尾悬吊14d、21d、28 d比较明显.与正常对照组比较,尾悬吊1d、5d、14 d、21 d、28 d组大鼠胃黏膜组织SOD含量明显升高(均P＜0.05);尾悬吊12h、14d、21 d、28 d组大鼠胃黏膜组织MDA含量明显升高(均P＜0.05);尾悬吊12h、2d、3d、5d、14d、28d组大鼠胃黏膜组织NO含量明显升高(均P＜0.05).免疫组化显示,尾悬吊6h、12h、1d、2d大鼠胃黏膜组织NOS2和COX2表达明显增强,随后表达减弱;尾悬吊14d、21 d、28 d表达再度增强.结论 尾悬吊模拟失重可导致大鼠胃黏膜组织超微结构改变和NOS2、COX2表达变化.     

胆道外引流对大鼠肝再生的影响及其细胞周期调控机制

目的: 观察胆道外引流(ED)对大鼠肝再生及肝细胞周期的影响。方法: 采用大鼠70％肝切除模型,SD大鼠随机分成6组,每组8只,分别为正常切肝24 h组、48 h组,阻塞性黄疸(OJ)切肝24 h组、48 h组,OJ后ED 3 d切肝24 h组、48 h组。采用增殖细胞核抗原(PCNA)标记和Feulgen染色测定肝再生能力;采用RT-PCR 测定肝组织肝细胞生长因子(HGF)、p27和cyclin D1 mRNA水平变化;免疫组化法测定HGF、转化生长因子β₁(TGF-β₁)和p21在肝细胞的表达。结果: OJ切肝后PCNA标记指数较对照组低(P<0.05),ED后PCNA标记指数更低,与OJ组对比差异显著(P<0.05)。DNA含量变化与PCNA标记指数相似。与正常切肝组比较,OJ后切肝组HGF mRNA下降(P<0.05),ED后切肝组进一步下降并较OJ组低(P<0.05)。与正常组相比,OJ后切肝24 h和48 h cyclin D1 mRNA均下降(P<0.05,P<0.01),ED后切肝组进一步下降,但差异不显著。与正常切肝组相比,48 h时OJ后切肝组高于正常切肝组(P<0.05),ED后p27 mRNA水平较OJ进一步升高(P<0.05)。与正常切肝组比较,OJ后切肝组肝细胞HGF表达在24 h下降(P<0.05),ED后切肝组进一步下降并较OJ组低(P<0.05)。p21表达各组间无显著差异。与正常切肝组相比,24 h时OJ后切肝组TGF-β₁表达上调,差异显著(P<0.05),ED后切肝组上调,但差异不显著。结论: OJ可造成大鼠肝再生能力下降,ED后其肝再生能力进一步降低。ED后肝再生能力下降可能和HGF、p27密切相关,与TGF-β₁、p21、cyclin D1无关。     

甲状腺功能减退对新生仔鼠心肌肌浆网钙转运蛋白表达的影响

目的: 探讨甲状腺功能减退(甲减)对新生仔鼠心肌肌浆网钙转运蛋白肌浆网Ca²⁺-ATP酶(SERCA2a)、磷酸受纳蛋白(PLB) mRNA表达以及肌浆网Ca²⁺-ATP酶活性的影响,并观察左旋甲状腺素(L-T₄)替代治疗后以上指标的改变。方法: SD孕鼠自孕15 d起每天予丙基硫氧嘧啶(PTU)(50mg/d)灌胃至仔鼠出生并持续整个哺乳期,制成围生期甲减模型,并对部分甲减仔鼠自出生当天起每天腹腔注射L-T₄(20 μg /kg)。收集甲减、治疗及对照组出生3、5、7日龄的仔鼠心室肌组织(每组10只),应用实时荧光定量PCR方法检测SERCA2a及PLB mRNA含量,并同时采用荧光分光光度计法测定心肌细胞内游离钙(MyoCa²⁺)浓度,无机磷酸根法检测心肌肌浆网钙泵活性。结果: 实时荧光定量PCR结果显示甲减组新生仔鼠心肌SERCA2a mRNA水平下降(P<0.05),PLB mRNA水平升高(P<0.01),SERCA2a/PLB下降(P<0.01);L-T₄治疗组仔鼠SERCA2a mRNA水平较甲减组上升(P<0.05),PLB mRNA水平下降(P<0.05),SERCA2a/PLB上升(P<0.01)。心肌细胞内游离钙浓度检测结果显示甲减组心肌细胞MyoCa²⁺浓度较同日龄对照组升高(P<0.01);L-T₄治疗组仔鼠心肌细胞MyoCa²⁺浓度低于同日龄甲减组仔鼠(P<0.05)。酶活性检测结果显示甲减组仔鼠肌浆网Ca²⁺-ATP酶活性低于同日龄对照组(P<0.01);L-T₄治疗组仔鼠肌浆网Ca²⁺-ATP酶活性较同日龄甲减组仔鼠升高(P<0.05)。结论: 甲状腺激素缺乏可使新生大鼠肌浆网Ca²⁺-ATP酶活性降低,并下调SERCA2a表达,上调PLB表达;肌浆网钙转运蛋白SERCA2a与PLB参与调控围生期甲减诱发的新生仔鼠心功能下降。     

人端粒酶反转录酶过表达抑制低氧/复氧大鼠心肌细胞的凋亡

目的探讨人端粒酶反转录酶(TERT)在大鼠心肌低氧/复氧(Hypo/Ro)损伤中的保护作用。方法利用腺病毒将端粒酶催化亚基转染至大鼠心肌细胞;利用慢病毒介导小干扰核糖核酸(siRNA)沉默心肌细胞TERT基因;研究TERT过表达和沉默后对大鼠心肌细胞Hypo/Ro诱导的细胞凋亡的影响。结果 Hypo/Ro组细胞凋亡率显著高于对照组;TERT过表达组可显著降低Hypo/Ro心肌细胞的凋亡率;过表达的TERT可降低心肌细胞CytC的表达并增强P21的表达(P<0.05)。结论过表达的TERT可抑制Hypo/Ro诱导的心肌细胞凋亡,其机制可能与调控p21及CytC基因表达有关。     

中药何首乌饮抗大鼠卵巢组织衰老的机理

目的探讨何首乌饮抗大鼠卵巢组织衰老的机理。方法36只SD大鼠随机分为3组:正常组、模型组、预防组。采用D-半乳糖连续腹腔注射法制造雌性大鼠亚急性衰老模型,预防组在造模的同时以中药方剂何首乌饮灌胃。应用逆转录聚合酶连反应(RT-PCR)方法检测各组大鼠卵巢组织p53、p19ARF、Rb及p16基因的表达,用Western blotting方法检测各组大鼠卵巢组织Rb及p16蛋白的表达情况。结果何首乌饮明显抑制了衰老大鼠卵巢组织中p53、p19ARF、Rb以及p16基因表达的上调趋势(P<0.05),且明显降低了衰老大鼠卵巢组织中Rb及p16蛋白的表达(P<0.05)。结论何首乌饮抑制衰老途径中关键的调节因子p53、p19ARF、Rb及p16的表达,从而起到抗大鼠性腺衰老的作用。     

下调EZH2表达促进卵巢癌细胞衰老的机制研究

目的:探讨下调EZH2表达促进卵巢癌细胞衰老的分子机制。方法:采用real-time PCR、Western blot及免疫组化检测卵巢癌组织和正常组织及4种卵巢癌细胞和人正常卵巢上皮细胞IOSE80中EZH2的表达水平;运用脂质体2000转染法将EZH2小干扰RNA转染,或将GSK126作用于卵巢癌细胞和IOSE80细胞,siRNA转染的IOSE80细胞经5 Gy电离辐射照射,以阴性对照siRNA为对照。MTT法、集落形成实验、流式细胞术和SA-β-Gal染色法检测细胞增殖、凋亡率和细胞衰老情况;Western blot检测EZH2、p53、p21、p16、caspase-3、cleaved caspase-3、PARP、cleaved PARP、H3K27me3、H3K27me2和H3K27me1的蛋白水平。结果:EZH2在卵巢癌组织和4种卵巢癌细胞中的表达水平均显著高于正常组织和IOSE80细胞(P0.01);敲减EZH2表达显著抑制卵巢癌细胞的增殖,促进电离辐射诱导的细胞衰老,其作用与GSK126处理的细胞表型相一致。Western blot检测发现敲减EZH2表达明显抑制H3K27me3的表达,促进p53、p21和p16的表达(P0.01),但对细胞凋亡通路关键蛋白的水平无影响。结论:EZH2在卵巢癌组织和卵巢癌细胞中高表达。敲减EZH2表达通过降低H3K27me3水平促进卵巢癌细胞衰老,从而抑制细胞增殖。     

雌激素通过KATP通道影响大鼠肠系膜动脉的反应性

目的: 观察雌激素对大鼠肠系膜动脉平滑肌ATP敏感性钾离子通道 (K_ATP 通道)mRNA表达的影响,探讨K_ATP通道在雌激素调节大鼠肠系膜血管反应性中的作用。方法: 雌性SD大鼠48只,体重(100±10) g,随机分为假手术组(sham)、卵巢切除组(Ovx)和卵巢切除后补充雌激素组(Ovx +E)。采取实时荧光定量PCR检测大鼠肠系膜动脉中K_ATP通道mRNA的表达;观察各组大鼠肠系膜动脉对去甲肾上腺素(NE)升压效应的反应性。结果: 与sham组相比,Ovx组大鼠肠系膜动脉K_ATP 通道的Kir6.1及SUR2B亚单位mRNA表达减少(P<0.05),而Ovx+E组则表达增加(P<0.05)。与sham组相比,Ovx组大鼠的血管反应性明显增加(P<0.05),Ovx+E组无明显差异。给予K_ATP通道阻滞剂格列本脲后,sham组和Ovx+E组的动脉反应性增加(P<0.05),Ovx组无明显变化(P>0.05),此时3组间比较无明显差异(P>0.05)。结论: 雌激素可能通过上调肠系膜动脉平滑肌细胞K_ATP通道的表达来降低动脉对去甲肾上腺素升压效应的反应性。     

模拟失重大鼠肺组织显微结构和一氧化氮合酶表达的动态变化

目的 观察模拟失重对大鼠肺组织显微结构及其一氧化氮合酶(NOS)表达的影响,为模拟失重时肺组织的适应机制研究积累资料.方法 采用Wistar雄性大鼠-30°尾部悬吊模拟失重生理效应.常规光镜和免疫组织化学方法 观察悬吊7 d组(TS7)、14 d组(TS14)及对照组(Con)肺组织显微结构和结构型NOS(cNOS)、诱导型NOS(iNOS)表达.结果 TS7组大鼠出现肺实变、肺水肿、支气管黏膜内淋巴细胞浸润、肺泡内有红细胞及肺泡融合.TS14组大鼠肺病变较TS7组大鼠明显加重,表现为肺泡融合增多、肺泡内更多红细胞和肺泡壁增厚.各组大鼠肺组织cNOS表达区域主要为支气管上皮细胞、血管内皮细胞和平滑肌细胞,各组间表达水平无统计学差异.iNOS表达在TS7、TS14组血管内皮细胞和平滑肌细胞表达显著增多,其中TS14组血管内皮细胞表达量高于TS7组.结论 模拟失重大鼠肺组织形态学变化可能与肺循环iNOS表达增加有关.     

超排卵对大鼠卵巢组织结构及生殖内分泌的影响

目的: 探讨超排卵对大鼠卵巢组织结构和生殖内分泌功能的影响,为临床合理使用超排卵提供理论依据。方法: 30只雌性SD大鼠随机分为3组: 实验A组接受孕马血清和人绒毛膜促性腺激素重复6次超排卵,实验B组 给予3次生理盐水注射及孕马血清和人绒毛膜促性腺激素重复3次超排卵,对照组接受6次生理盐水注射。15 d及30 d后分别处死各组一半大鼠,观察卵巢组织形态学变化,采用放射免疫法检测血清雌二醇(E₂)、卵泡刺激素(FSH)、黄体生成素(LH)水平,并计算FSH/LH水平,比较各组间的差异。结果: 实验A和B组大鼠卵巢始基卵泡和初级卵泡计数明显低于对照组(P<0.05),但各组大鼠体内血清基础激素水平无显著差异(P>0.05)。结论: 超排卵会引起大鼠卵巢的卵泡发育受限,且随着超排卵次数的增加而加重,但尚未导致生殖内分泌激素水平的显著改变。     

短程与长程去卵巢大鼠骨计量学的实验研究

目的:探讨3月龄SD大鼠去卵巢短程和长程骨量的变化,以指导临床用药。方法:30只3月龄SD雌性大鼠,随机分为基础对照组、年龄对照(30天和90天)组、去卵巢(30天和90天)组,切除双侧卵巢建立骨质疏松症模型,实验结束,取胫骨近端行不脱钙骨制片进行骨组织形态计量学分析。结果:实验30天去卵巢大鼠与年龄对照,骨形成的参数值(荧光标记周长百分率、骨矿化沉积率、骨形成率)和骨吸收的参数值(破骨细胞数目)都明显增加。但骨吸收大于骨形成,造成骨量丢失(骨小梁面积百分率明显减少),骨结构变差(骨小梁数目减少,分离度增加),90天去卵巢大鼠组与对照组比较,荧光标记周长百分率减少,骨矿化沉积率增加,破骨细胞数目显著增加,骨吸收增强,骨质丢失,出现骨质疏松。结论:30天去卵巢大鼠呈骨高转化,但90天去卵巢大鼠表现为骨形成参数有下降趋势,同时骨吸收增加,骨量丢失,造成骨质疏松。     

碘过量对仔鼠垂体促甲状腺激素细胞的形态学影响

目的探讨碘过量时60日龄大鼠仔鼠垂体TSH细胞的形态学变化。方法将断乳1个月的Wistar大鼠,雌雄各半随机分为NI组、10HI组、50HI组和100HI。饲养3个月的雌雄鼠1:1合笼交配产生仔鼠,断乳后的仔鼠喂养同上述大鼠。测定60日龄仔鼠的血清甲状腺激素水平及垂体TSH细胞的体密度和强阳性细胞百分比。结果与NI组比较,50HI组、100HI组60日龄仔鼠的体密度和强阳性细胞百分比明显增高,而10HI组无明显改变;50HI组、100HI组的血清甲状腺素高于NI组。结论碘过量可导致仔鼠TSH细胞体积增大,强阳性细胞数据多并呈剂量依赖性,可能是由于T4升高抑制TSH细胞释放TSH,使TSH颗粒贮积在细胞内造成的。     

缺血性急性肾功能衰竭下丘脑精氨酸加压素表达的变化

目的：探讨精氨酸加压素(AVP)在急性肾功能衰竭发病过程中的作用。方法：将SD大鼠随机分成对照组、术后2d和术后4d急性肾功能衰竭模型组,取脑,行精氨酸加压素的免疫组织化学反应,比较下丘脑阳性区域的灰度值。结果：急性肾功能衰竭模型组的下丘脑阳性区域的灰度值低于对照组,术后4d急性肾功能衰竭模型组的灰度值最小。结论：在急性肾功能衰竭的发生发展中,下丘脑精氨酸加压素分泌增加并参与了缺血性肾功能损伤。     

禁止交配下调成年雌性大鼠乳腺组织雌二醇水平及雌激素受体α的表达

目的 研究禁止交配对成年雌性大鼠乳腺组织雌二醇(E2)水平、雌激素受体α(ERα)表达的影响.方法 12只成年雌性SD大鼠随机分为对照组(交配组)和禁止交配组,实验第61天终止实验后在间情期采集标本,光镜下观察各组大鼠乳腺组织结构,透射电镜下观察乳腺组织超微结构;采用放射免疫法检测外周血及乳腺组织E2浓度;采用免疫组织化学染色和Western blotting技术检测乳腺组织ERα的表达变化. 结果禁止交配60d后,成年雌性大鼠乳腺组织E2水平下降,与对照组比较P<0.05;同时乳腺组织上皮细胞、基质细胞细胞核ERα表达下调,与对照组比较P<0.05;光镜、电镜下各组大鼠乳腺组织未见明显异常. 结论禁止交配可下调雌性大鼠乳腺组织E2水平和ERα的表达.     

The effect of supplemental copper on osteopenia induced by ovariectomy in rats

OBJECTIVE: The effect of a copper supplement on preventing bone mass loss induced by ovariectomy in rats was investigated. DESIGN: Three groups of fifteen 100-day-old female Wistar rats, each with a mean initial weight of approximately 260 g per animal, were selected for a 30-day experiment. One group of 15 ovariectomized rats was fed a diet supplemented with 15 mg of copper per kilogram of feed. The other two groups: 15 ovariectomized and 15 Sham- ovariectomized rats did not receive the supplement. Morphometric (weight and length) and densitometric studies with dual-energy x-ray absorptiometry were performed on the whole femur and the fifth lumbar vertebra of each animal at the end of the 30-day period. RESULTS: The ovariectomized rat group fed a diet supplemented with copper did not show the bone mass loss at the axial (fifth lumbar vertebra) or peripheral (femur) level that was evidenced in the ovariectomized group. CONCLUSIONS: The results of the measurement of axial and peripheral bones show that a supplement of copper may have a potential therapeutic application in the treatment and prevention of involutional osteoporosis.     

Energy intake of rats fed a cafeteria diet

The proportion of lipid, carbohydrate and protein energy self-selected by male and female rats from a cafeteria diet has been studied for a 48-day period (36-day in female rats). The diet consisted in 12 different items and was offered daily, in excess and under otherwise standard conditions, to rats--caged in groups of three--from weaning to adulthood. Groups of control animals were studied in parallel and compared with the cafeteria groups. Cafeteria diet fed groups of rats ingested more energy and lowered their metabolic efficiency with age. Male rats ate more than females and increased their body weight even after female practically stopped growing. There was a wide variation in the aliments consumed each day by the cafeteria-fed rats. However, the proportion of lipid, protein and carbohydrate the rats ate remained constant. Male rats ingested more lipid than females. Carbohydrate consumption was constant in control and cafeteria fed groups of rats independently of sex. Protein consumption was higher in cafeteria rats than in controls, but the differences were not so important as with liquid. Fiber content of the cafeteria diet was lower than that of the control diet. The cafeteria diet selected by the rats was, thus, hypercaloric and hyperlipidic, with practically the same amount of carbohydrate than the control diet, slightly hyperproteic and, nevertheless, remarkably constant in its composition with respect to time. Cafeteria rats had a higher water intake than controls. All these trends were maintained despite the observed changes in the animals' tastes and their differential consumption of the ailments of the diet.     

无创性延迟肢体缺血预适应对大鼠缺血再灌注损伤心肌持续保护效应

 目的：探讨连续不同天数的无创性肢体缺血预适应对大鼠缺血再灌注损伤心肌的延迟保护持续时间的差别。方法：雄性Wistar 大鼠随机分为：（1）对照组：包括假手术组、缺血再灌注组、心肌缺血预适应组和股动脉缺血预适应组;（2）无创性延迟肢体缺血预适应组：包括1 d远端肢体缺血预适应间隔1 d组、3 d组和5 d组,3 d远端肢体缺血预适应间隔1 d组、3 d组和5 d组,7 d远端肢体缺血预适应间隔1 d组、3 d组和5 d组。每组分别在间隔末期进行缺血再灌注损伤,监测缺血再灌注期间左心室功能、心律失常情况和S-T段升高幅度,并检测再灌注结束时心型脂肪酸结合蛋白(heart fatty acid binding protein, H-FABP)、糖原磷酸化酶BB (glycogen phosphorylase BB,GPBB)及心肌梗死面积。结果：与缺血再灌注组相比,心肌缺血预适应组、股动脉缺血预适应组、3 d和7 d远端肢体缺血预适应间隔1 d组明显改善左心室功能,减少心律失常,降低S-T段抬高幅度,降低H-FABP和GPBB活性,减少心肌梗死面积。结论：远端肢体缺血预适应3 d与7 d可获得相似的心肌持续保护效应。     

Persistence of attention to a novel conspecific: Some developmental variables in laboratory rats

Persistence of social attention by male and female laboratory rats was examined following exposure to novel conspecifics. In Experiment I we compared performance of castrate females treated with a 10-day regimen of testosterone propionate to that of intact males and castrate female controls. Testosterone significantly prolonged mean social investigation time. Castrate females treated with a relatively high dosage of testosterone failed to differ from intact males. In Experiment II we compared neonatally andorganized female castrates with castrate male and castrate female controls. Postnatal exposure to testosterone increased sensitivity of females to exogenous testosterone in maturity as measured by persistence of social investigation. In Experiment III we compared investigation time of intact and castrated males and females at 10-day intervals from 40 to 80 days of age. Intact males investigated novel conspecifics significantly longer than other groups, with longest investigation times at 60 and 70 days of age. In Experiment IV we compared investigation times of 30-day, 60-day, and 200-day-old males. Sixty-day-old males investigated significantly longer than 30-day-old or 200-day-old groups, which failed to differ from each other. The combined results demonstrate a gender and aggregated effect of testosterone on persistence of social investigation.     

Uterotrophic assay,Hershberger assay,and repeated 28-day oral toxicity study of flumorph based on the Organization for Economic Co-operation and Development draft protocols

To evaluate the endocrine-mediated effects of flumorph, we performed the uterotrophic assay, the Hershberger assay, and the repeated 28-day oral toxicity study based on the OECD draft protocols. In the uterotrophic assay, female ovariectomized SD rats were subcutaneously injected with flumorph at doses of 0, 50, 150, and 500 mg/kg on each of 3 days, and no changes were observed. In the Hershberger assay, castrated male SD rats were administered with flumorph by oral gavage at doses of 0, 50, 150, and 500 mg/kg/day for 10 consecutive days, and no abnormal changes were observed. However, in the repeated 28-day oral toxicity study , flumorph was orally administered at doses 0, 30, 100, and 300 mg/kg/day for at least 28 days, a significantly increase in T₄ value in male rats and TSH value in female rats were detected in the highest dosage group, respectively. Besides, the flumorph administration increase liver weights, produce hepatocellular diffuse fatty degeneration, and effect biochemical parameters related to liver function in male and/or female rats in dosed groups. Therefore, flumorph is concluded to have thyroid disruption effects and is likely a thyroid disrupter, but the further studies are needed for hazard identification.     

疲劳型亚健康大鼠模型的构建*

背景：有研究用复合因素构建了亚健康及慢性疲劳大鼠模型,但疲劳型亚健康大鼠模型的构建较罕见。 目的：采用力竭游泳复合睡眠剥夺构建疲劳型亚健康大鼠模型,探讨最佳的疲劳型亚健康大鼠模型制备方法。 方法：将大鼠负重5%力竭游泳并睡眠剥夺20 h建立疲劳型亚健康模型,记录力竭游泳时间,各组实验结束禁食1 d,行血液生化检查。 结果与结论：建模后4,5 d大鼠末次力竭游泳时间显著减少(P < 0.05)。建模后5 d,大鼠血α-羟丁酸脱氢酶、尿素氮、血肌酸激酶升高(P < 0.05)、总胆固醇降低,门冬氨酸氨基转移酶、丙氨酸氨基转移酶、血清肌酐、三酰甘油水平均降低        (P < 0.05)。结果证实,负重5%的力竭游泳复合20 h睡眠剥夺持续4 d即可成功制备疲劳型亚健康大鼠模型。