中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2009年
3期
243-246
,共4页
郭妍%卢妙%钱进%程蕴琳
郭妍%盧妙%錢進%程蘊琳
곽연%로묘%전진%정온림
银杏内酯类,糖基化终产物%氧化性应激
銀杏內酯類,糖基化終產物%氧化性應激
은행내지류,당기화종산물%양화성응격
Biloba lides%Glycosylation end products%Oxidative stress
目的 探讨银杏叶提取物对老龄大鼠心肌的保护作用.方法 选择20月龄大鼠,分别给予银杏叶提取物(EGB)和非酶糖基化产物(AGEs)交联结裂解剂(ALT-711)灌胃,经16周治疗后,观察心肌内AGEs、血清内抗氧化活性物质超氧化物歧化酶(SOD)和谷胱甘肽过氧化酶(GSH-Px)及氧化代谢产物丙二醛(MDA)的含量,观察心肌细胞内线粒体DNA的缺失率及心肌超微结构的改变.结果 老龄对照组大鼠和成年对照组比较.心肌细胞间质增生、肿大,线粒体和内质网膜受损,心肌组织内AGEs含量减少[分别为(33.5±1.3)AU/mgHYP和(18.1±1I 2)AU/mgHYP,t=7.18,P<0.05],血清中SOD和GSH-PX减少[分别为(138.4±3.8)U/ml和(1283.8±28.8)U/ml、(227.7±13.8)U/ml和(2114.1±135.9)U/ml,t分别为-19.59和-18.79,均P<0.01],MDA增多[分别为(6.7±0.6)mmol/ml与(4.1±1.O)mmol/ml,t=7.18,P<0.05],线粒体mtDNA缺失率增多[(0.1805±0.0718)%和(0.0060±0.0001)%,t=6.98,P<0.01],EGB和ALT-711治疗组与老年对照组比较,心肌内AGEs产物减少(P<0.05).血清内SOD、GSH-PX抗氧化物质增多(P<0.05),血清氧化代谢产物MDA减少(P<0.05),mtDNA缺失率减少(P<0.01).结论 老龄大鼠心肌老化和非酶糖基化及氧化应激相关,EGB和ALT-711同样具有抑制非酶糖基化和抑制氧化应激的作用,通过对心肌内线粒体mtDNA缺失率的抑制,具有抗衰老作用.
目的 探討銀杏葉提取物對老齡大鼠心肌的保護作用.方法 選擇20月齡大鼠,分彆給予銀杏葉提取物(EGB)和非酶糖基化產物(AGEs)交聯結裂解劑(ALT-711)灌胃,經16週治療後,觀察心肌內AGEs、血清內抗氧化活性物質超氧化物歧化酶(SOD)和穀胱甘肽過氧化酶(GSH-Px)及氧化代謝產物丙二醛(MDA)的含量,觀察心肌細胞內線粒體DNA的缺失率及心肌超微結構的改變.結果 老齡對照組大鼠和成年對照組比較.心肌細胞間質增生、腫大,線粒體和內質網膜受損,心肌組織內AGEs含量減少[分彆為(33.5±1.3)AU/mgHYP和(18.1±1I 2)AU/mgHYP,t=7.18,P<0.05],血清中SOD和GSH-PX減少[分彆為(138.4±3.8)U/ml和(1283.8±28.8)U/ml、(227.7±13.8)U/ml和(2114.1±135.9)U/ml,t分彆為-19.59和-18.79,均P<0.01],MDA增多[分彆為(6.7±0.6)mmol/ml與(4.1±1.O)mmol/ml,t=7.18,P<0.05],線粒體mtDNA缺失率增多[(0.1805±0.0718)%和(0.0060±0.0001)%,t=6.98,P<0.01],EGB和ALT-711治療組與老年對照組比較,心肌內AGEs產物減少(P<0.05).血清內SOD、GSH-PX抗氧化物質增多(P<0.05),血清氧化代謝產物MDA減少(P<0.05),mtDNA缺失率減少(P<0.01).結論 老齡大鼠心肌老化和非酶糖基化及氧化應激相關,EGB和ALT-711同樣具有抑製非酶糖基化和抑製氧化應激的作用,通過對心肌內線粒體mtDNA缺失率的抑製,具有抗衰老作用.
목적 탐토은행협제취물대노령대서심기적보호작용.방법 선택20월령대서,분별급여은행협제취물(EGB)화비매당기화산물(AGEs)교련결렬해제(ALT-711)관위,경16주치료후,관찰심기내AGEs、혈청내항양화활성물질초양화물기화매(SOD)화곡광감태과양화매(GSH-Px)급양화대사산물병이철(MDA)적함량,관찰심기세포내선립체DNA적결실솔급심기초미결구적개변.결과 노령대조조대서화성년대조조비교.심기세포간질증생、종대,선립체화내질망막수손,심기조직내AGEs함량감소[분별위(33.5±1.3)AU/mgHYP화(18.1±1I 2)AU/mgHYP,t=7.18,P<0.05],혈청중SOD화GSH-PX감소[분별위(138.4±3.8)U/ml화(1283.8±28.8)U/ml、(227.7±13.8)U/ml화(2114.1±135.9)U/ml,t분별위-19.59화-18.79,균P<0.01],MDA증다[분별위(6.7±0.6)mmol/ml여(4.1±1.O)mmol/ml,t=7.18,P<0.05],선립체mtDNA결실솔증다[(0.1805±0.0718)%화(0.0060±0.0001)%,t=6.98,P<0.01],EGB화ALT-711치료조여노년대조조비교,심기내AGEs산물감소(P<0.05).혈청내SOD、GSH-PX항양화물질증다(P<0.05),혈청양화대사산물MDA감소(P<0.05),mtDNA결실솔감소(P<0.01).결론 노령대서심기노화화비매당기화급양화응격상관,EGB화ALT-711동양구유억제비매당기화화억제양화응격적작용,통과대심기내선립체mtDNA결실솔적억제,구유항쇠로작용.
Objective To investigate the protective effect of the extract of ginkgo biloba on myocardial tissue in aged rat.Methods The rats aged 20 months were given the extract of ginkgo biloba (EGB) and ALT-711 respectively by garage for 16 weeks.The aged controls and adult rats were infused with the same volume saline.The superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), malonyt diadehyde (MDA) in blood samples and advanced glycation end products (AGEs) in the myocardial tissue were measured .The myocardial histopathological changes under electron microscope and the mitochondrial DNA (mtDNA) deletion rate in myocardial cells were observed.Results Compared with the adult rats, the content of AGEs in myocardial cells in aged rats was significantly increased [(33.5±1.3)AU/mgHYP us.(18.1±1.2)AU/mgHYP, t= 7.18,P<0.05] and the levels of SOD and GSH-PX in blood samples were decreased [(138.4±3.8) U/mlvs.(227.7±13.8)U/ml, (1283.8±28.8) U/ml vs.(2114.1 ±135.9)U/ml, t=-19.59, -18.79;both P<0.01].The MDA level in the serum and mtDNA deletion rate in aged rats were higher than in adult rats[(6.7±0.6) mmol/ml vs.(4.1±1.0) mmol/ml, (0.18054±0.0718) % vs.( 0.0060±0.0001)%, t=7.18,6.98;both P<0.05].Compared with the aged controls, the content of AGEs in myocardial cells, the level of MDA and mtDNA deletion rate were significantly decreased in EGB and ALT-711 treatment adults (all P<0.05).The SOD and GSH-PX in blood samples were increased in EGB and ALT-711 treatment adults (all P<0.05).Conclusions Nonenzymatic glycation may play an important role in myocardial aging, which may be amplified by oxidative stress.EGB and ALT-711 may have the same anti-aging effects by inhibiting nonenzymatic glycation and oxidative stress.
