人参三醇组皂苷对大鼠坐骨神经急性损伤保护作用的研究

目的研究人参三醇组皂苷(Panaxtrol Saponin,PTS)对大鼠坐骨神经急性损伤病理学改变的影响。方法建立大鼠坐骨神经挤压损伤模型,随机分为PTS组,模型对照组及空白对照组,每组各10只大鼠;各组均经腹腔注射给药,PTS组损伤后注射PTS;模型对照组损伤后注射同剂量生理盐水;空白对照组,不损伤坐骨神经,注射同剂量生理盐水。坐骨神经损伤术后30 d,观察大鼠健侧、损伤侧腓肠肌湿重及恢复率,大鼠坐骨神经急性损伤及腓肠肌损伤病理学改变。结果 PTS处理组的损伤侧腓肠肌湿重及腓肠肌恢复率(1.28±0.36、83.82±9.21)与模型对照组(0.90±0.44、55.43±22.02)比较差异有统计学意义(P0.05);PTS处理组坐骨神经与模型对照组比较,神经纤维排列更整齐,轴索更清晰,雪旺细胞基本保持正常。PTS处理组腓肠肌与模型对照组比较,肌细胞直径更均匀,胞核更清晰,数量增多,但少于模型对照组,肌纤维萎缩程度较轻。结论人参三醇组皂苷对大鼠坐骨神经急性病理损伤有一定的修复作用。     

人参皂苷Rg1对大鼠视神经损伤病理改变的实验研究

目的研究人参皂苷Rg1对大鼠视神经损伤的影响。方法制作大鼠视神经损伤模型,设置实验组和对照组,腹腔注射人参皂苷Rg1,10mg／kg,连续注射20d,取视神经损伤眼和对照眼球及球后视神经,HE染色、SABC法免疫组织化学染色：Bcl-2、Neurocan表达情况。结果HE染色显示健康大鼠视神经组织细胞和视神经损伤组形态学有差异。免疫化学提示视神经损伤后神经细胞凋亡明显增多,人参皂苷Rg1腹腔注射能够明显改善细胞凋亡情况。视神经损伤后神经纤维蛋白表达明显增多,可能部分与其改善细胞凋亡情况有关,但机制尚不清楚。结论人参皂苷Rg1对大鼠视神经损有保护作用。     

人参皂苷Rg1对局灶性脑缺血大鼠PARP-1和TNFR1表达的影响

目的探讨人参皂苷Rg1对局灶性脑缺血大脑皮质多聚二磷酸腺苷核糖聚合酶(PARP)-1和肿瘤坏死因子受体(TNFR)1表达的影响。方法 90只健康SD大鼠随机均分为假手术组,单纯缺血组,人参皂苷Rg1低、中、高组,阳性对照组。于术前5 d至取材当日,假手术组与单纯缺血组分别腹腔注射生理盐水45 mg/kg,人参皂苷Rg1分别给10、20、40 mg/kg,阳性对照组尼莫地平1 mg/kg。采用大脑中动脉栓塞法制备局灶性脑缺血模型,神经功能缺损评分和TTC染色验证模型是否成功;采用免疫组织化学法和蛋白免疫印迹法检测大脑皮质缺血后PARP-1、TNFR1的表达。结果单纯缺血组较假手术组可见明显神经功能缺陷症状及大面积苍白色梗死区域;人参皂苷Rg1各组和阳性对照组神经功能评分和脑梗死体积百分比高于假手术组,低于单纯缺血组(P<0.05);人参皂苷Rg1各组与阳性对照组差异无统计学意义。人参皂苷Rg1低组每高倍视野PARP-1、TNFR1阳性细胞数高于假手术组和阳性对照组;中、高组高于假手术组,低于单纯缺血组(P<0.05)。单纯缺血组皮质PARP-1、TNFR1较假手术组阳性表达条带显著增强;人参皂苷Rg1低组PARP-1、TNFR1阳性表达高于假手术组;中组高于假手术组,低于单纯缺血组;高组低于单纯缺血组(P<0.05)。结论人参皂苷Rg1对大鼠局灶性脑缺血具有保护作用,其机制可能与下调大脑组织PARP-1、TNFR1的表达,对抗脑细胞坏死有关。     

阿霉素中毒大鼠膈肌骨架蛋白和肌浆网钙泵的表达变化及意义

目的观察不同剂量阿霉素诱导大鼠膈肌急性损伤时膈肌收缩特性的变化与大鼠膈肌细胞骨架蛋白和肌浆网钙泵表达变化的关系。方法一次性腹腔注射阿霉素制备急性膈肌损伤动物模型,♂SD大鼠随机分成:阿霉素低剂量组(10mg·kg-1)、中剂量组(20mg·kg-1)和高剂量组(40mg·kg-1)及对照组,每组10只。对照组用生理盐水腹腔注射。3d后剖胸取膈肌,应用体外灌流大鼠膈肌肌条方法,分别测量其单收缩张力(Pt)、最大强直张力(Po)、峰值收缩时间(CT)、半舒张时间(1/2RT),张力最大上升速度(+dt/dtmax)及张力最大下降速度(-dt/dtmax)。应用逆转录聚合酶链反应(RT-PCR)测定膈肌骨架蛋白肌联蛋白(titin)、伴肌动蛋白(nebulin)和肌浆网钙泵(sarcoplasmic reticulum Ca2+-ATPase,SERCA)mRNA的表达。结果与对照组相比,阿霉素中、高剂量模型组大鼠膈肌Pt,Po,±dt/dtmax下降(P<0.01),CT、1/2RT延长(P<0.01)。阿霉素中毒大鼠膈肌各基因表达较对照组相比分别降低(P<0.01)。结论阿霉素中毒大鼠膈肌细胞膈肌骨架蛋白titin、nebulin和SERCA mRNA表达下调,并可能与膈肌张力改变有关。     

神经对大鼠骨骼肌小电导钙激活钾通道(SK3)表达的影响

目的小电导钙激活的钾通道(SK3)介导了动作电位后的后超极化电位的产生,在调节可兴奋细胞的膜电位中起关键作用。使去神经支配和肌强直营养不良患者骨骼肌SK3表达显著上调。本实验拟观察神经对骨骼肌SK3钾通道表达的调节作用。方法在Wistar大鼠,分别通过切断坐骨神经和局部注射河豚毒素(TTX)建立比目鱼肌去神经支配模型,和通过钳夹损伤比目鱼肌神经建立比目鱼肌去神经后神经再支配模型。在体给予去神经比目鱼肌频率为30Hz的电刺激(100脉冲/100 s)。实验结束后,免疫荧光法测定比目鱼肌中SK3钾通道的表达和定位;提取比目鱼肌组织总mRNA和蛋白,逆转录PCR和Western Blot分别检测SK3 mRNA和蛋白水平。结果切断坐骨神经能显著上调比目鱼肌SK3 mRNA和蛋白表达,且分别在术后第6 d和第9 d到达稳定。TTX诱导肌肉瘫痪也能显著上调比目鱼肌SK3 mRNA和蛋白表达。钳夹比目鱼肌神经所造成的暂时神经损伤能诱导SK3蛋白表达上调,而随着神经功能的恢复SK3蛋白表达也随之显著下调。在切断除坐骨神经术后6 d,在体给予电刺激6 d能显著下调比目鱼肌SK3的高表达;而且,在去除坐骨神经的同时给予电刺激则能阻止比目鱼肌SK3表达的上调。结论神经对骨骼肌SK3钾通道表达具有抑制作用,其作用与唤起肌肉活性密切相关。在体电刺激能抑制和防止去神经诱导的骨骼肌SK3蛋白表达上调,可能是改善神经损伤后或相关疾病所致的肌强直症状的有效手段之一。     

人参皂苷Rg1对Aβ_(25-35)诱导大鼠海马神经元tau蛋白异常磷酸化的影响

目的探讨人参皂苷Rg1对Aβ2535所致大鼠海马神经tau蛋白异常磷酸化的抑制作用及其可能机制。方法应用脑立体定向技术向成年大鼠海马背侧注射凝聚态Aβ25355nmol制备AD样大鼠模型,术后分别给予腹腔内注射不同浓度的人参皂苷Rg1(625、125、25μmol·kg-1)处理,14d后处死,采用镀银染色方法观察海马组织神经元病理改变;免疫组织化学染色方法和免疫蛋白印迹技术显示大鼠脑内[pS396]tau、[pSpS199/202]tau、[pT231]tau的表达水平情况,以及总tau蛋白的水平(tau5);免疫蛋白印迹技术检测海马组织中GSK3β和磷酸化GSK3β的水平变化。结果凝聚态Aβ2535注射组神经元纤维走行紊乱,增粗、肿胀密集成宽带状,轴突深染;而人参皂苷Rg1对神经元具有明显的保护作用,脑内总tau的水平下降,[pS396]tau、[pSpS199/202]tau、[pT231]tau的表达明显低于Aβ2535注射组(P<001),以25μmol·kg-1保护作用最明显;GSK3β和磷酸化GSK3β的水平亦明显低于Aβ2535注射组,与正常和假注射组差异无显著性(P>005),以25μmol·kg-1作用最明显。结论人参皂苷Rg1对Aβ2535诱导的AD样大鼠海马神经元具有保护作用,其机制可能是通过阻断GSK3β的活性而降低磷酸化tau蛋白的表达而实现的。     

耐力运动8周对大鼠骨骼肌收缩功能和线粒体生物合成的影响及机制

目的探讨8周耐力运动对不同类型骨骼肌收缩功能及线粒体能量代谢能力的影响及其机制。方法分离经8周平台跑步训练的♂SD大鼠的比目鱼肌和趾长伸肌,观测给予不同方式电刺激后两种类型骨骼肌收缩能力和抗疲劳能力的变化以及ATP含量和线粒体生物合成相关指标的改变。结果耐力运动8周可一定程度提高比目鱼肌和趾长伸肌在单次电刺激和强直电刺激下的收缩力,明显改善比目鱼肌的抗疲劳能力。ATP含量在两类肌肉中均明显升高,但只有比目鱼肌线粒体DNA、PGC-1α、NRF基因的转录及PGC-1α蛋白明显上调,并伴随p-AMPK/AMPK蛋白比值明显增加。结论耐力运动8周改善骨骼肌的收缩能力,但仅增加富含氧化型肌纤维的比目鱼肌的抗疲劳能力,这可能与耐力运动激活氧化型肌纤维的AMPK,上调PGC-1α转录和表达,增加线粒体生物合成有关。     

人参皂苷Rb1后处理对大鼠全脑缺血再灌注后认知功能的影响

目的 探讨人参皂苷Rb1后处理对大鼠全脑缺血再灌注后认知功能的影响及其可能机制.方法 90只SD雄性大鼠随机分为假手术组、模型组和治疗组.治疗组大鼠造模后连续7d给予腹腔注射20mg/(kg·d)人参皂苷Rb1.模型采用四血管阻断全脑缺血模型.最后一次人参皂苷Rb1腹腔注射后24h每组各取5只,左侧大脑取海马检测髓过氧化物酶(MPO)活力和NF-κB的DNA结合活力.其余每组各25只大鼠分别于再灌注后第7日开始进行Morris水迷宫实验.结果 模型组MPO活力、NF-κB的DNA结合活力、平均潜伏期及探索实验中在第2象限时间比与假手术组比较差异有统计学意义(WTBXP<0.05);治疗组与模型组比较,MPO活力和NF-κB的DNA结合活力下降,平均潜伏期缩短,第2象限时间比增高(P<0.05).结论 HT6K 人参皂苷Rb1后处理可减轻大鼠全脑缺血再灌注后海马区炎症反应,改善认知功能.     

人参皂苷Rh2对高脂膳食大鼠心肌缺血再灌注时内皮祖细胞的影响

目的观察人参皂苷Rh2对高脂膳食大鼠心肌缺血再灌注(IR)时内皮祖细胞数量的影响。方法健康成年雄性SD大鼠,体重180~240 g,高脂饲料喂养24周后,随机分为缺血再灌注组(GIR组)、人参皂苷Rh2组(Rh2组)、假手术组(GS组),另设正常对照组(N组),给予基础饲料喂养24周。每组6只,记录各组大鼠体重。在高脂饲养基础上,采用结扎冠状动脉左前降支30 min,再灌注120 min的方法建立心肌缺血再灌注模型,GS组只穿线不结扎。Rh2组大鼠于缺血再灌注前30 min腹腔注射人参皂苷Rh2 10 mg/kg,GS组、GIR组大鼠于术前30 min腹腔注射等体积生理盐水。于再灌注120 min后处死大鼠,测定血脂水平以及血清血管内皮生长因子(VEGF)水平,流式细胞仪计数大鼠外周血内皮祖细胞(Endothelial progenitor cells,EPCs)的数量。结果喂养24周后,与正常对照组比较,其余组大鼠体重与血脂水平均升高(P<0.05),假手术组大鼠外周血EPCs数量与血清VEGF水平较正常对照组稍有下降,差异有统计学意义(P<0.05);与假手术组比较,缺血再灌注组与人参皂苷Rh2组大鼠外周血内皮祖细胞数量及血清VEGF水平均有升高,且人参皂苷Rh2组升高更为显著(P<0.05)。结论人参皂苷Rh2可增加高脂膳食大鼠心肌缺血再灌注后外周血内皮祖细胞数量,从而减轻心肌缺血再灌注损伤,可能与提高血清VEGF水平相关。     

人参皂苷 Rg1减轻大鼠离体心脏缺血再灌注损伤的作用研究

目的：探讨人参皂苷 Rg1对大鼠离体心脏缺血再灌注损伤的减轻作用及机制。方法制备大鼠离体心脏 I/ R 模型,将18只大鼠随机分为正常对照组、I/ R 组、人参皂苷 Rg1组。100μmol/ L 人参皂苷 Rg1进行预处理10 min,观察血流动力学指标左心室内压最大上升/下降速率和心率压力乘积的变化,检测灌流液中肌酸激酶（CK）、乳酸脱氢酶（LDH）活性。Western blotting 检测心肌组织 PI3K 下游激酶 Akt、ERK1/2及其磷酸化水平的变化,磷酸化GSK-3β的蛋白表达。结果与 I/ R 组比较,人参皂苷 Rg1预处理显著改善心脏功能,降低灌流液中 CK、LDH 活性（ P ﹤0.05）;升高 p-Akt 和 p-GSK-3β的蛋白表达（ P ﹤0.05）。结论人参皂苷 Rg1对大鼠离体心脏缺血再灌注损伤有减轻作用,其机制与激活 PI3K-Akt 通路有关。     

绝经后女性盆底功能障碍患者肛提肌中抗肌营养不良蛋白和结蛋白表达及意义

目的探讨抗肌营养不良蛋白和结蛋白mRNA的表达与绝经后女性盆底功能障碍(PFD)的关系。方法选择30例压力性尿失禁患者(SUI组)、30例盆底组织膨出患者(POP组)及6例无SUI和POP的直肠癌患者(对照组),术中行肛提肌活组织检查(活检),应用实时荧光定量聚合酶链反应(PCR)的方法检测肛提肌中抗肌营养不良蛋白和结蛋白的表达。结果 POP组和SUI组肛提肌中肌营养不良蛋白和结蛋白mRNA表达较对照组均降低(P<0.01)。POP组和SUI组比较,肛提肌中抗肌营养不良蛋白和结蛋白mRNA表达差异无统计学意义(P>0.05)。结论绝经后女性盆底功能障碍性疾病的发生与女性肛提肌中抗肌营养不良蛋白及结蛋白的表达降低有关。     

Roles of exercise and pharmacokinetics in cerivastatin-induced skeletal muscle toxicity.

Three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are associated with adverse skeletal muscle effects, but the underlying mechanisms remain unclear. To determine whether toxicity involves the level of drug exposure in muscle tissue and to test the effect of exercise on cerivastatin (CVA)-induced skeletal muscle damage, female rats were administered vehicle or CVA at 0.1, 0.5, and 1.0 mg/kg/day by gavage for two weeks and exercised or not on treadmills for 20 min/day. Clinical chemistry and plasma and tissue pharmacokinetics were evaluated; light and transmission electron microscopy (TEM) of Type I and Type II fiber-predominant skeletal muscles were performed. Serum levels of AST, ALT, CK, and plasma lactic acid were significantly elevated dose-dependently. CVA treatment decreased psoas and quadriceps weights. At 1 mg/kg all muscles except soleus demonstrated degeneration. Exercise-exacerbated severity of CVA-induced degeneration was evident in all muscles sampled except soleus and quadriceps. Early mitochondrial involvement in toxicity is suggested by the numerous membranous whorls and degenerate mitochondria observed in muscles at 0.5 mg/kg. No significant differences in CVA concentrations between either EDL and soleus or plasma and muscle were found. We found that CVA had no effect on cleaved caspase 3. In summary, we found that treadmill exercise exacerbated the incidence and severity of CVA-induced damage in Type II fiber-predominant muscles. Tissue exposure is likely not the key factor mediating CVA-induced skeletal muscle toxicity.     

Effect of Exercise Intensity on Unfolded Protein Response in Skeletal Muscle of Rat

Endoplasmic reticulum (ER) stress, unfolded protein response (UPR), and mitochondrial biogenesis were assessed following varying intensities of exercise training. The animals were randomly assigned to receive either low- (LIT, n=7) or high intensity training (HIT, n=7), or were assigned to a control group (n=7). Over 5 weeks, the animals in the LIT were exercised on a treadmill with a 10° incline for 60 min at a speed of 20 m/min group, and in the HIT group at a speed of 34 m/min for 5 days a week. No statistically significant differences were found in the body weight, plasma triglyceride, and total cholesterol levels across the three groups, but fasting glucose and insulin levels were significantly lower in the exercise-trained groups. Additionally, no statistically significant differences were observed in the levels of PERK phosphorylation in skeletal muscles between the three groups. However, compared to the control and LIT groups, the level of BiP was lower in the HIT group. Compared to the control group, the levels of ATF4 in skeletal muscles and CHOP were significantly lower in the HIT group. The HIT group also showed increased PGC-1α mRNA expression in comparison with the control group. Furthermore, both of the trained groups showed higher levels of mitochondrial UCP3 than the control group. In summary, we found that a 5-week high-intensity exercise training routine resulted in increased mitochondrial biogenesis and decreased ER stress and apoptotic signaling in the skeletal muscle tissue of rats.     

吡格列酮对高脂喂养大鼠骨骼肌组织脂质异位沉积的影响

目的:观察吡格列酮(Pio)对高脂喂养大鼠骨骼肌组织脂质异位沉积的影响。方法:30只Wistar大鼠平均分为对照组、胰岛素抵抗组和吡格列酮干预组,对照组给予基础饲料,其余2组均给予高脂饲料喂养,其中吡格列酮干预组同时给予吡格列酮20 mg·kg^-1·d^-1灌胃,各组均喂养16周后检测各组大鼠血游离脂肪酸(FFA)水平及骨骼肌组织中三酰甘油(TG)含量,同时应用蛋白免疫印迹法检测骨骼肌组织一磷酸腺苷活化蛋白激酶α(AMPKα)磷酸化水平。结果:与对照组比较,胰岛素抵抗组大鼠胰岛素敏感性显著降低,血FFA水平及骨骼肌组织TG含量增高,骨骼肌组织中AMPKα磷酸化水平降至对照组水平的52.9%;与胰岛素抵抗组比较,吡格列酮干预组大鼠胰岛素敏感性明显提高,血FFA水平及骨骼肌组织TG含量显著下降,骨骼肌组织中AMPKα磷酸化水平显著提高至对照组的81.3%。但是与对照组比较,吡格列酮干预组大鼠血FFA水平及骨骼肌组织TG含量仍然较高,而且胰岛素敏感性及骨骼肌组织中AMPKα磷酸化水平仍然显著降低。结论:高脂饮食诱导胰岛素抵抗,吡格列酮干预可以通过降低血FFA水平及减轻骨骼肌组织脂质异位沉积改善其胰岛素抵抗。     

Endurance training adaptations modulate the redox-force relationship of rat isolated slow-twitch skeletal muscles

1. Studies have shown that, in isolated skeletal muscles, maximum isometric force production (Po) is dependent on muscle redox state. Endurance training increases the anti-oxidant capacity of skeletal muscles, a factor that could impact on the force-producing capacity following exogenous exposure to an oxidant. We tested the hypothesis that 12 weeks treadmill training would increase anti-oxidant capacity in rat skeletal muscles and alter their response to exogenous oxidant exposure. 2. At the conclusion of the 12 week endurance-training programme, soleus (slow-twitch) muscles from trained rats had greater citrate synthase (CS) and catalase (CAT) activity compared with soleus muscles from untrained rats (P < 0.05). In contrast, CAT activity of extensor digitorum longus (EDL; fast-twitch) muscles from trained rats was not different to EDL muscles of untrained rats. The CS activity was lower in EDL muscles from trained compared with untrained rats (P < 0.05). 3. Equilibration with exogenous hydrogen peroxide (H2O2, 5 mmol/L) increased the Po of soleus muscles from untrained rats for the duration of treatment (30 min), whereas the Po of EDL muscles was affected biphasically, with a small increase initially (after 5 min), followed by a more marked decrease in Po (after 30 min). The H2O2-induced increase in Po of soleus muscles from trained rats was less than that in untrained rats (P < 0.05), but no differences were observed in the Po of EDL muscles following training. 4. The results indicate that 12 weeks endurance running training conferred adaptations in soleus but not EDL muscles. These adaptations were associated with an attenuation of the oxidant-induced increase in Po of soleus muscles from trained compared with untrained rats. We conclude that endurance training-adapted soleus muscles have a slightly altered redox-force relationship.     

人参皂苷Rg1对大鼠肠缺血/再灌注损伤的影响

目的观察人参皂苷Rg1(ginsenoside Rg1)对大鼠肠缺血/再灌注后肠组织损伤的影响,并探讨其机制。方法制备SD大鼠肠缺血/再灌注损伤模型。实验分为3组(n=10):假手术组、缺血/再灌注组(对照组)、人参皂苷Rg1干预组(治疗组)。比较各组大鼠肠黏膜肿瘤坏死因子α(TNF-α)水平、白细胞介素6(IL-6)水平、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性的变化;用Chiu氏评分法观察肠黏膜的损伤情况。结果与假手术组相比,对照组TNF-α、IL-6水平明显升高,MDA含量明显增高,SOD活性明显降低,小肠损伤评分明显升高;与对照组相比,治疗组TNF-α、IL-6水平明显降低,MDA含量明显降低,SOD活性明显升高,小肠损伤评分明显降低。结论人参皂苷Rg1对大鼠肠缺血/再灌注后的肠道有保护作用,该保护作用可能与减少TNF-α、IL-6、MDA含量,提高SOD活性有关。     

人参皂苷Rg3对大鼠子宫内膜异位症异位囊肿抑制作用的观察

目的观察人参皂苷Rg3对大鼠子宫内膜异位症(EMs)异位囊肿的抑制作用。方法参照Jones方法建立Wistar大鼠EMs动物模型,3周后将建模成功的大鼠随机分为空白对照组、人参皂苷Rg3组和孕三烯酮组,各组又分为2、4、6、8周共12组,观察子宫内膜异位囊肿形态和体积的变化。结果肉眼观察:Rg3治疗前移植灶体积透明、囊状增大,有新生血管形成,Rg3治疗后血管消失、移植灶体积缩小(P<0.05);Rg3与孕三烯酮治疗后相比,移植物体积亦有明显缩小(P<0.05)。结论Rg3能明显缩小EMs大鼠模型的子宫内膜移植物体积,其作用机制可能是早期抑制了子宫内膜异位囊肿的血液供应。     

Changes in lactate dehydrogenase and 3-hydroxyacetyl-CoA dehydrogenase activities in rat skeletal muscle by the administration of Eucommia ulmoides OLIVER leaf with spontaneous running-training.

We examined the effect of Eucommia ulmoides OLIVER leaf on rat skeletal muscles together with spontaneous running-training in terms of the isozyme profile and specific activity of lactate dehydrogenase (LDH; EC 1.1.1.27) and 3-hydroxyacetyl-CoA dehydrogenase (HAD; EC 1.1.1.35). On the twenty-ninth day of the experimental period, a mandatory endurance running exercise (treadmill, 7 degrees grade) was conducted. Twenty-four hours later, the rats were sacrificed and the skeletal muscles and other organs were dissected. Due to the training, the HAD specific activity in the skeletal muscles had increased and a more oxidative metabolism had developed, which was further enhanced by the administration of the leaf. In soleus (SOL) muscle in the Eucommia leaf treated running-training group (ET), the LDH specific activity in the skeletal muscle was significantly higher than in the sedentary control group (SC). The isozyme profile of the group ET was significantly different when compared with the group SC. The changes in the LDH isozyme profile were larger in the SOL than that in extensor digitorum longus (EDL) muscle. The results show that mechanical training and the use of the leaf cooperatively increase the ability to avoid lactate accumulation in skeletal muscle. This effect is supported by the group where 67% of rats accomplished the endurance running exercise. Theses results suggest that the administration of Eucommia ulmoides OLIVER leaf along with light intensity training enhances the ability of a muscle to resist fatigue.     

Effects of high-fat mixed-lipid diet and exercise on the antioxidant system in skeletal and cardiac muscles of rats with colon carcinoma

Epidemiological and experimental studies suggest that eating habits and a sedentary lifestyle play a critical role in the incidence of colon carcinoma. In order to investigate the effects of high-fat mixed-lipid (HFML) diet in conjunction with long-term swimming, the antioxidant capacity of skeletal and cardiac muscles were observed in rats with 1,2-dimethylhydrazine (DMH)-induced colon carcinoma. Male Wistar rats were randomly divided into one control group and four cancer groups: sedentary and swimming groups fed low fat corn oil diet and sedentary and swimming groups, fed a HFML diet. After 6 months of swimming, rats were sacrificed and the blood, cardiac and soleus muscle were taken for analysis. Serum cholesterol, triglyceride and glucose concentrations were measured and the activity of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase as well as levels of malondialdehyde and glutathione were determined.The results showed that endurance swimming prevented lipid peroxidation in the soleus muscle of HFML diet rats due to elevated activities of antioxidant enzymes. On the other hand, increased lipid peroxidation in the hearts of all cancer groups indicated that DMH-induced colon carcinoma impaired the antioxidant status of the heart. This failure in heart tissue indicated that enhanced antioxidant capacity after regular physical activity is not sufficient to offset oxidative stress caused by DMH-induced colon carcinoma.     

糖尿病大鼠早期骨骼肌改变与血清炎症介质SOD及P物质变化

目的 观察檐尿病(diabetes mellitus,DM)大鼠早期骨骼肌损害的组织病理特点与血清炎症介质及SOD、P物质(S-P)的变化.方法 将26只10周龄雄性Wistar大鼠分为正常对照组(C组,n=13)、DM组(n=13);13只用链脲佐菌素(STZ)建立DM大鼠模型.于第16周末抽取两组大鼠的心脏血,测定肿瘤坏死因子-α(TN F-α)、白细胞介素-6(IL-6)、超敏C反应蛋白(hs-CRP)、超氧化物歧化酶(SOD)、S-P等的水平;并处死取股二头肌,进行病理学观察.结果 16周末DM组TNF-α( 1.45±0.67)ng/mL,IL-6(135.05±43.39)pg/mL,hs-CRP( 3.51±0.62) mg/L,较正常对照组[分别为(0.86±0.60)ng/mL、(99.92±32.36)pg/mL、(2.54±1.31)mg/L]明显增高(P＜0.05);DM组SOD(70.71±37.52)U/mL,S-P(22.22±7.93 )pg/mL,较正常对照组[分别为(137.00±27.60)U/mL、(29.57±3.74)pg/mL]显著降低(P＜0.01).组织学观察显示:DM组骨骼肌普遍萎缩,肌纤维横截面积明显缩小;部分肌纤维变性,间质水肿,炎症细胞浸润.结论 DM大鼠早期骨骼肌损害表现为骨骼肌普遍萎缩,部分肌纤维变性,间质水肿,炎症细胞浸润;血清炎性细胞因子明显增高;超氧化物歧化酶、S-P降低.