病毒性心肌炎小鼠心肌细胞凋亡的检测及意义

目的 研究病毒性心肌炎(VMC)小鼠心肌细胞凋亡及其意义。方法 实验用TUNEL法结合电镜观察小鼠接种VMC病毒后3、5、7、9、15、35天心肌细胞凋亡情况。结果 发现小鼠在接种VMC病毒后的3、5、7、9、15、35天各时点凋亡心肌细胞数目较正常对照组明显增加(P<0.01)。小鼠在接种病毒后7～9天,电镜下心肌细胞可见凋亡。结论VMC中存在异常的心肌细胞凋亡现象,心肌细胞凋亡可能参与了VMC的发病。     

Protective effects of quercetin on testicular torsion/detorsion-induced ischaemia-reperfusion injury in rats

The aim of this study was to investigate the protective effect of quercetin (QE) on testicular torsion/detorsion-induced ischaemia-reperfusion (I/R) injury. A total of 24 male Wistar albino rats were divided into three groups: control, I/R and I/R treated with QE; each group contain eight animals. Testicular torsion was created by rotating the left testis 720° in a clockwise direction. The ischaemia period was 5 h and orchiectomy was performed after 5 h of detorsion. QE (15 mg kg(-1) , i.p.) was administered only once, 40 min prior to detorsion. Left orchiectomy was performed in all I/R groups. To date, no histopathological changes on testicular torsion/detorsion-induced I/R injury in rats by QE treatment have been reported. Spermatogenesis and mean seminiferous tubule diameter were significantly decreased in I/R groups were compared with the control group. Furthermore, QE treated animals showed an improved histological appearance in I/R group. Our data indicate a significant reduction in the activity of TUNEL, endothelial nitric oxide synthase and a rise in the expression of testosterone in testes tissue of I/R treated with QE therapy. We believe that further preclinical research into the utility of QE may indicate its usefulness as a potential treatment on testes injury after I/R in rats.     

Edible wild vegetable, Gymnaster koraiensis protects retinal ganglion cells against oxidative stress

This study was conducted to determine whether Gymnaster koraiensis is effective at blunting the negative influence of N-methyl-d-aspartate (NMDA) on the retinas of rats and on oxidative stress induced cell death in transformed retinal ganglion cells (RGC-5).The ethyl acetate fraction of G. koraiensis (EAGK) and the isolated compound, 3,5-di-O-caffeoylquinic acid (3,5-DCQA), were shown to significantly attenuate the negative effect of H₂O₂ on the RGC-5 cells tested by various procedures.The inclusion of EAGK or 3,5-DCQA in the culture reduced the reactive oxygen species (ROS) and replenished the reduced glutathione levels caused by various radical species such as H₂O_2, O₂⁻ or OH. Moreover, EAGK or 3,5-DCQA inhibited lipid peroxidation caused by sodium nitroprusside (SNP) in rat brain homogenates.From in vivo experiments, the presence of NMDA in the retina affected the thickness of the inner plexiform layer (IPL) and the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) in positive ganglion cells. EAGK or 3,5-DCQA protected the thinning of the IPL and increased TUNEL positive cells in the ganglion cell layer (GCL).Our results clearly demonstrate the neuroprotective effect of EAGK both in vitro and in vivo. Moreover, 3,5-DCQA is suggested to be the active compound of EAGK.     

亚低温对大鼠脑缺血再灌注损伤后热休克蛋白70表达及细胞凋亡的影响

[目的]观察亚低温对大鼠局灶脑缺血再灌注损伤后热休克蛋白70(HSP70)表达的影响,探讨亚低温对脑神经细胞保护作用的机制。[方法]将SD大鼠随机分为正常组、假手术组、常温缺血组和亚低温缺血组。应用大脑中动脉线栓法(MCAO)建立大鼠局灶脑缺血再灌注模型,于缺血2 h再灌注,再灌注后3、6、12、24、72 h和7 d处死。其中亚低温组大鼠于缺血后30 min实施病灶侧脑亚低温并持续4 h。采用HE染色观察神经细胞形态学改变,免疫组化法检测脑组织HSP70表达,TUNEL法检测凋亡细胞。[结果]正常组及假手术组均未见明显病理改变;常温缺血组梗死灶明显,大量神经元坏死消失;亚低温缺血组未见明显梗死灶,但可见神经元固缩。正常组及假手术组未见或偶见HSP70阳性细胞;常温缺血组HSP70阳性细胞较多;与常温缺血组相比亚低温缺血组在相应时间点均明显减少(P<0.05)。常温缺血组TUNEL阳性细胞数随再灌注时间的延长而逐渐增多,至72 h达高峰;与常温缺血组相比,亚低温缺血组各时间点均明显减少(P<0.05)。[结论]亚低温对大鼠缺血再灌注损伤脑有保护作用,通过降低HSP70的表达和减少细胞凋亡可能是其保护机制之一。     

Pyruvate protects against kainate-induced epileptic brain damage in rats

Although the majority of epileptic seizures can be effectively controlled with antiepileptic drugs and/or surgery, a significant number progress to status epilepticus of sufficient duration to cause permanent brain damage. Combined treatment with antiepileptic drugs and neuroprotective agents, however, may help protect these individuals from permanent brain damage. Since toxicity induced by endogenous zinc contributes to epileptic brain injury, and since pyruvate is effective in reducing zinc-triggered neuronal death in cortical culture as well as ischemic neuronal death in vivo, we examined whether systemic pyruvate administration reduces seizure-induced brain damage. Na pyruvate (500 mg/kg) or osmolarity-matched saline (265 mg/kg NaCl, i.p.) were given to adult SD rats 30 or 150 min after 10 mg/kg kainite injection (i.p.), and there was no significant difference in the time course or severity of seizures between these groups. Zinc accumulation in neuronal cell bodies in the hippocampus, however, was much lower in the pyruvate than in the saline group. There was a close correlation between zinc accumulation and cell death, as assessed by acid-fuchsin and TUNEL staining. Pyruvate treatment markedly reduced neuronal death in the hippocampus, neocortex and thalamus. Pyruvate increased HSP-70 expression in hippocampal neurons. These results suggest that pyruvate, a natural glucose metabolite, may be useful as adjunct treatment in status epilepticus to reduce permanent brain damage.