中华行为医学与脑科学杂志
中華行為醫學與腦科學雜誌
중화행위의학여뇌과학잡지
CHINESE JOURNAL OF BEHAVIORAL MEDICINE AND BRAIN SCIENCE
2014年
2期
118-121
,共4页
齐拉西酮%海马神经干细胞%保护作用%脂多糖
齊拉西酮%海馬神經榦細胞%保護作用%脂多糖
제랍서동%해마신경간세포%보호작용%지다당
Ziprasidone%Neural stem cells%Protective effect%Lipopolysaccharide
目的 探讨齐拉西酮对脂多糖(lipopolysaccharide,LPS)损伤后海马神经干细胞(neural stem cells,NSCs)活性的作用及其凋亡的影响.方法 建立体外大鼠海马NSCs的LPS损伤细胞模型,分为对照组(sham组)、LPS组、LPS+齐拉西酮组(包括1μmol/L、5μmol/L、10 μmol/L和20 μmol/L等4个不同剂量组),药物作用48 h或72 h后,采用WST-1试剂检测细胞活性,乳酸脱氢酶(lactate dehydrogenase,LDH)试剂盒检测乳酸脱氢酶释放情况,并采用流式细胞术检测细胞凋亡情况.结果 (1)细胞活力:作用48 h后,与对照组(吸光度值0.380±0.029)相比,LPS组(吸光度值0.265±0.047)细胞活力显著下降(P＜0.01),而LPS+齐拉西酮5μmol/L组(吸光度值0.316±0.008)组与LPS+齐拉西酮10 μmol/L组(吸光度值0.321±0.006)则显著提升其活力(与LPS相比较,均P＜0.05).作用72 h后的细胞活力结果与48 h相似,LPS组细胞活力显著低于对照组(P＜0.01),而LPS+齐拉西酮5μmol/L组与LPS+齐拉西酮10μmol/L组则缓解了LPS对其活力的抑制.(2)LDH检测结果显示,作用48 h或72 h后,LPS组LDH的释放水平显著高于sham组(均P＜0.01),而LPS+齐拉西酮5μmol/L组与LPS+齐拉西酮10 μmol/L组的LDH释放水平均显著低于LPS组(均P＜0.01).(3)流式细胞术检测凋亡的结果显示,作用48 h后,与对照组[(9.15±1.54)％]相比,LPS组[(22.67±2.15)％]凋亡百分率显著上升(P＜0.01),而LPS+齐拉西酮5μmol/L组[(18.45±3.84)％]组与LPS+齐拉西酮10 μmol/L组[(17.87±2.29)％]则显著抑制其凋亡(与LPS相比较,均P＜0.05).作用72 h后,LPS组的凋亡百分率[(15.70±2.97)％]仍然显著高于对照组[(8.45±1.04)％],而LPS+齐拉西酮10 μmol/L组[(10.52±1.42)％]则显著低于LPS组(P＜0.05).结论 适当浓度的齐拉西酮能抑制LPS导致的海马NSCs损伤,这一作用可能是其发挥神经保护效应的细胞学基础之一.
目的 探討齊拉西酮對脂多糖(lipopolysaccharide,LPS)損傷後海馬神經榦細胞(neural stem cells,NSCs)活性的作用及其凋亡的影響.方法 建立體外大鼠海馬NSCs的LPS損傷細胞模型,分為對照組(sham組)、LPS組、LPS+齊拉西酮組(包括1μmol/L、5μmol/L、10 μmol/L和20 μmol/L等4箇不同劑量組),藥物作用48 h或72 h後,採用WST-1試劑檢測細胞活性,乳痠脫氫酶(lactate dehydrogenase,LDH)試劑盒檢測乳痠脫氫酶釋放情況,併採用流式細胞術檢測細胞凋亡情況.結果 (1)細胞活力:作用48 h後,與對照組(吸光度值0.380±0.029)相比,LPS組(吸光度值0.265±0.047)細胞活力顯著下降(P＜0.01),而LPS+齊拉西酮5μmol/L組(吸光度值0.316±0.008)組與LPS+齊拉西酮10 μmol/L組(吸光度值0.321±0.006)則顯著提升其活力(與LPS相比較,均P＜0.05).作用72 h後的細胞活力結果與48 h相似,LPS組細胞活力顯著低于對照組(P＜0.01),而LPS+齊拉西酮5μmol/L組與LPS+齊拉西酮10μmol/L組則緩解瞭LPS對其活力的抑製.(2)LDH檢測結果顯示,作用48 h或72 h後,LPS組LDH的釋放水平顯著高于sham組(均P＜0.01),而LPS+齊拉西酮5μmol/L組與LPS+齊拉西酮10 μmol/L組的LDH釋放水平均顯著低于LPS組(均P＜0.01).(3)流式細胞術檢測凋亡的結果顯示,作用48 h後,與對照組[(9.15±1.54)％]相比,LPS組[(22.67±2.15)％]凋亡百分率顯著上升(P＜0.01),而LPS+齊拉西酮5μmol/L組[(18.45±3.84)％]組與LPS+齊拉西酮10 μmol/L組[(17.87±2.29)％]則顯著抑製其凋亡(與LPS相比較,均P＜0.05).作用72 h後,LPS組的凋亡百分率[(15.70±2.97)％]仍然顯著高于對照組[(8.45±1.04)％],而LPS+齊拉西酮10 μmol/L組[(10.52±1.42)％]則顯著低于LPS組(P＜0.05).結論 適噹濃度的齊拉西酮能抑製LPS導緻的海馬NSCs損傷,這一作用可能是其髮揮神經保護效應的細胞學基礎之一.
목적 탐토제랍서동대지다당(lipopolysaccharide,LPS)손상후해마신경간세포(neural stem cells,NSCs)활성적작용급기조망적영향.방법 건입체외대서해마NSCs적LPS손상세포모형,분위대조조(sham조)、LPS조、LPS+제랍서동조(포괄1μmol/L、5μmol/L、10 μmol/L화20 μmol/L등4개불동제량조),약물작용48 h혹72 h후,채용WST-1시제검측세포활성,유산탈경매(lactate dehydrogenase,LDH)시제합검측유산탈경매석방정황,병채용류식세포술검측세포조망정황.결과 (1)세포활력:작용48 h후,여대조조(흡광도치0.380±0.029)상비,LPS조(흡광도치0.265±0.047)세포활력현저하강(P＜0.01),이LPS+제랍서동5μmol/L조(흡광도치0.316±0.008)조여LPS+제랍서동10 μmol/L조(흡광도치0.321±0.006)칙현저제승기활력(여LPS상비교,균P＜0.05).작용72 h후적세포활력결과여48 h상사,LPS조세포활력현저저우대조조(P＜0.01),이LPS+제랍서동5μmol/L조여LPS+제랍서동10μmol/L조칙완해료LPS대기활력적억제.(2)LDH검측결과현시,작용48 h혹72 h후,LPS조LDH적석방수평현저고우sham조(균P＜0.01),이LPS+제랍서동5μmol/L조여LPS+제랍서동10 μmol/L조적LDH석방수평균현저저우LPS조(균P＜0.01).(3)류식세포술검측조망적결과현시,작용48 h후,여대조조[(9.15±1.54)％]상비,LPS조[(22.67±2.15)％]조망백분솔현저상승(P＜0.01),이LPS+제랍서동5μmol/L조[(18.45±3.84)％]조여LPS+제랍서동10 μmol/L조[(17.87±2.29)％]칙현저억제기조망(여LPS상비교,균P＜0.05).작용72 h후,LPS조적조망백분솔[(15.70±2.97)％]잉연현저고우대조조[(8.45±1.04)％],이LPS+제랍서동10 μmol/L조[(10.52±1.42)％]칙현저저우LPS조(P＜0.05).결론 괄당농도적제랍서동능억제LPS도치적해마NSCs손상,저일작용가능시기발휘신경보호효응적세포학기출지일.
Objective To investigate the effects of ziprasidone on the hippocampal-derived neural stem cells (NSCs) viability and apoptosis injured.by LPS.Methods The NSCs were derived from the hippocampus of fetal rats,after the primary neurospheres passaged,the cells were treated with LPS (200 μg/L) and different concentrations of ziprasidone for 48 h or 72 h.The cell viability and the level of LDH were measured by the kit of WST-8 and LDH detected kit,respectively.Furthermore,the apoptosis rate of each dosage group was measured by using Annexin-V-FLUOS Staining Kit.Results (1) Cell viability test showed that the cell viability of LPS group (OD value,0.265± 0.047) was significantly reduced than that of sham (OD value,0.380± 0.029),LPS + 5 μM (OD value,0.316±0.008) and LPS+10 μM (OD value,0.321±0.006) group after ziprasidone treatment for 48 h.There were also significant difference of cell viability between sham,LPS+5 μM,LPS+ 10 μM and LPS group after ziprasidone treatment for 72 h.(2) LDH test showed that the LDH level of LPS group was significantly decreased than that of sham,LPS+5 μM and LPS+10 μM after 48 hour's ziprasidone treatment (P＜0.01).The LDH level of LPS group was also significantly reduced than that of sham,LPS+5 μM and LPS+10 μM after 72 hour's ziprasidone treatment (P＜ 0.01).(3) The apoptosis of LPS + 10 μM ((17.87 ± 2.29) ％),LPS + 5 μM ((18.45 ± 3.84) ％) treated group or sham group ((9.15 ± 1.54) ％) was significantly lower than LPS group ((22.67 ± 2.15)％) by using flow cytometry after 48 h treatment.Furthermore,the apoptosis of LPS+ 10 μM ((10.52± 1.42)％) treated group or sham group((8.45±1.04)％) was significantly lower than LPS group((15.70± 2.97) ％) after 72 h treatment.Conclusion The cellular damage of NSCs injured by LPS can be restrained by ziprasidone,and this effect might be one of the cellular mechanism of neural protective effect of ziprasidone.
