CAJ | 학술논문

目的:通过观察白花丹参对局灶性脑缺血再灌注损伤大鼠脑细胞线粒体超微结构、氧化应激功能及脑细胞凋亡的影响,探讨白花丹参对抗脑缺血再灌注损伤的作用及其机制.方法:采用大脑中动脉内线栓阻断法(MCAO)造成局灶性脑缺血再灌注模型,将SD大鼠随机分为:假手术组、单纯脑缺血再灌注组、白花丹参组及丁苯酞治疗对照组,按照6.5 g/kg BW白花丹参生药及15 mg丁苯酞的剂量灌胃给药,每天1次,分别于再灌注后12 h、24 h及48 h取损伤侧大脑,应用电镜观察脑细胞超微结构的改变、比色法检测脑组织线粒体丙二醛(MDA)含量及谷胱甘肽过氧化物酶(GSH-Px)活性的变化、流式细胞技术检测脑细胞凋亡率的变化.结果:脑缺血再灌注后大鼠脑细胞内出现大量高电子密度中毒颗粒及空泡,线粒体膜崩解、内嵴消失;MDA含量明显增高(P＜0.05);GSH-Px酶活性显著降低(P＜0.05);脑细胞大量凋亡.与脑缺血再灌注组比较,白花丹参能够减少细胞内高电子密度中毒颗粒及空泡,增强线粒体膜的稳定性,显著降低MDA含量(P＜0.05),延缓GSH-Px酶活性的下降并保护其活性(P＜0.05),显著降低脑细胞凋亡率(再灌注后24 h及48 h组,P＜0.05).结论:白花丹参可减轻大鼠脑缺血再灌注所致线粒体损伤、延缓GSH-Px酶活性下降,抑制细胞凋亡,从而发挥脑保护作用.
목적:통과관찰백화단삼대국조성뇌결혈재관주손상대서뇌세포선립체초미결구、양화응격공능급뇌세포조망적영향,탐토백화단삼대항뇌결혈재관주손상적작용급기궤제.방법:채용대뇌중동맥내선전조단법(MCAO)조성국조성뇌결혈재관주모형,장SD대서수궤분위:가수술조、단순뇌결혈재관주조、백화단삼조급정분태치료대조조,안조6.5 g/kg BW백화단삼생약급15 mg정분태적제량관위급약,매천1차,분별우재관주후12 h、24 h급48 h취손상측대뇌,응용전경관찰뇌세포초미결구적개변、비색법검측뇌조직선립체병이철(MDA)함량급곡광감태과양화물매(GSH-Px)활성적변화、류식세포기술검측뇌세포조망솔적변화.결과:뇌결혈재관주후대서뇌세포내출현대량고전자밀도중독과립급공포,선립체막붕해、내척소실;MDA함량명현증고(P＜0.05);GSH-Px매활성현저강저(P＜0.05);뇌세포대량조망.여뇌결혈재관주조비교,백화단삼능구감소세포내고전자밀도중독과립급공포,증강선립체막적은정성,현저강저MDA함량(P＜0.05),연완GSH-Px매활성적하강병보호기활성(P＜0.05),현저강저뇌세포조망솔(재관주후24 h급48 h조,P＜0.05).결론:백화단삼가감경대서뇌결혈재관주소치선립체손상、연완GSH-Px매활성하강,억제세포조망,종이발휘뇌보호작용.
AIM: To observe the effects of Salvia miltiorrhiza Bunge.f.alba. (Sal) on the mitochondrial ultra-structure, oxidative stress and apoptosis induced by ischemia injury in a rat model of focal cerebral ischemia and reperfusion.METHODS: The middle cerebral artery occlusion/reperfusion (MCAO/R) rat model was established by a modified Longa occlusion method. Adult male SD rats were randomly divided into control group, simple ischemia reperfusion group, Sal with ischemia reperfusion group and butylphthalide with ischemia reperfusion group. To study the protective effects of Sal and its mechanism, the intervention of Sal was given and the ultra-structure of mitochondria, functions of mitochondria under oxidative stress and the incidence of apoptosis of brain cells were determined.RESULTS: Many electron dense toxic granulation and vacuolus in mitochondria were observed in the rat brain of focal cerebral ischemia and reperfusion. Under the condition of ischemia and reperfusion, the mitochondria membrane was disaggregative, and the tubular cristae of mitochondrion disappeared. MDA content was obviously increased and the activity of glutathione peroxidase decreased significantly. The apoptosis of brain cells were observed in a great quantity. The changes of ultra-structure of mitochondria and the activity of GSH-Pxase were significantly improved by the treatment of Sal. Furthermore, treatment with Sal delayed the decrease of GSH-Pxase activity, and inhibited the increase in MDA content in brain tissue after ischemia and reperfusion. The incidence of apoptosis of brain cells was also decreased.CONCLUSION: Sal protects the brain tissue from ischemia injury.