中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2010年
1期
72-75
,共4页
王绍欣%谢云%周雪%沙伟伟%汪玮琳%韩丽萍%王家驰%于德民
王紹訢%謝雲%週雪%沙偉偉%汪瑋琳%韓麗萍%王傢馳%于德民
왕소흔%사운%주설%사위위%왕위림%한려평%왕가치%우덕민
肌细胞%心脏%胰高血糖素样肽1%细胞凋亡%缺氧复氧
肌細胞%心髒%胰高血糖素樣肽1%細胞凋亡%缺氧複氧
기세포%심장%이고혈당소양태1%세포조망%결양복양
Myocytes,cardiac%Glucngon-like peptide 1%Apoptosis%Hypoxia reoxygenation
目的 研究胰高血糖素样肽1(GLP-1)对缺氧复氧诱导的乳鼠心肌细胞损伤的影响及其可能机制.方法 通过给原代培养的乳鼠心室肌细胞缺氧16 h、复氧4 h,建立缺氧复氧(H/R)心室肌细胞损伤模型.于缺氧前随机分为正常对照组,H/R组,GLP-1+H/R组,GLP-1+H/R+U0126组,GLP-1+H/R+LY294002组,H/R+U0126组和H/R+LY294002组.H/R损伤后测定上清液中乳酸脱氢酶(LDH)活性、细胞凋亡率和半胱天冬酶-3(Caspase-3)活性.结果 H/R组LDH活性、细胞凋亡率和Caspase-3活性均明显高于正常对照组(P均<0.01).而GLP-1+H/R组LDH活性[(128.47±7.96)U/L比(223.96±22.10)U/L,P<0.01]、细胞凋亡率[(2.84±2.56)%比(12.58±6.69)%,P<0.01]和Caspase-3活性[(36 809±4750)RLU比(57 602±9161)RLU,P<0.01]则明显低于H/R组,但上述指标变化可分别被LY294002(PI3K抑制剂)和UO126(MAPK抑制剂)抑制.结论 GLP-1可以直接作用于心肌细胞,对H/R诱导的心肌细胞损伤产生一定的保护作用,保护作用可能主要是通过抑制心肌细胞的凋亡实现的,并且GLP-1对凋亡的抑制作用可能与PI3K/Akt和MAPK所介导的抗细胞凋亡作用有关.
目的 研究胰高血糖素樣肽1(GLP-1)對缺氧複氧誘導的乳鼠心肌細胞損傷的影響及其可能機製.方法 通過給原代培養的乳鼠心室肌細胞缺氧16 h、複氧4 h,建立缺氧複氧(H/R)心室肌細胞損傷模型.于缺氧前隨機分為正常對照組,H/R組,GLP-1+H/R組,GLP-1+H/R+U0126組,GLP-1+H/R+LY294002組,H/R+U0126組和H/R+LY294002組.H/R損傷後測定上清液中乳痠脫氫酶(LDH)活性、細胞凋亡率和半胱天鼕酶-3(Caspase-3)活性.結果 H/R組LDH活性、細胞凋亡率和Caspase-3活性均明顯高于正常對照組(P均<0.01).而GLP-1+H/R組LDH活性[(128.47±7.96)U/L比(223.96±22.10)U/L,P<0.01]、細胞凋亡率[(2.84±2.56)%比(12.58±6.69)%,P<0.01]和Caspase-3活性[(36 809±4750)RLU比(57 602±9161)RLU,P<0.01]則明顯低于H/R組,但上述指標變化可分彆被LY294002(PI3K抑製劑)和UO126(MAPK抑製劑)抑製.結論 GLP-1可以直接作用于心肌細胞,對H/R誘導的心肌細胞損傷產生一定的保護作用,保護作用可能主要是通過抑製心肌細胞的凋亡實現的,併且GLP-1對凋亡的抑製作用可能與PI3K/Akt和MAPK所介導的抗細胞凋亡作用有關.
목적 연구이고혈당소양태1(GLP-1)대결양복양유도적유서심기세포손상적영향급기가능궤제.방법 통과급원대배양적유서심실기세포결양16 h、복양4 h,건립결양복양(H/R)심실기세포손상모형.우결양전수궤분위정상대조조,H/R조,GLP-1+H/R조,GLP-1+H/R+U0126조,GLP-1+H/R+LY294002조,H/R+U0126조화H/R+LY294002조.H/R손상후측정상청액중유산탈경매(LDH)활성、세포조망솔화반광천동매-3(Caspase-3)활성.결과 H/R조LDH활성、세포조망솔화Caspase-3활성균명현고우정상대조조(P균<0.01).이GLP-1+H/R조LDH활성[(128.47±7.96)U/L비(223.96±22.10)U/L,P<0.01]、세포조망솔[(2.84±2.56)%비(12.58±6.69)%,P<0.01]화Caspase-3활성[(36 809±4750)RLU비(57 602±9161)RLU,P<0.01]칙명현저우H/R조,단상술지표변화가분별피LY294002(PI3K억제제)화UO126(MAPK억제제)억제.결론 GLP-1가이직접작용우심기세포,대H/R유도적심기세포손상산생일정적보호작용,보호작용가능주요시통과억제심기세포적조망실현적,병차GLP-1대조망적억제작용가능여PI3K/Akt화MAPK소개도적항세포조망작용유관.
Objective To observe the effect of glucagon-like peptide-1 (GLP-1) on hypoxia-reoxygenation (H/R) induced injury in neonatal rat cardiomyocytes. Methods Cultured neonatal rat cardiomyocytes were randomly divided into seven groups: normal control group, H/R group, GLP-1 + H/R group, GLP-1 + H/R + UO126 group, GLP-1 + H/R + LY294002 group, H/R + U0126 group, H/R +LY294002 group. LDH activity, apoptosis rate of cardiomyocytes, Caspase-3 activity were detected. Results Compared with normal control group, the activity of LDH, cardiomyocyte apoptosis rate, Caspsse-3 activity were all significantly increased in H/R group (all P <0.01). However, compared with H/R group, these changes were significantly attenuated in GLP-1 + H/R group [the activity of LDH (128.47±7.96) U/L vs. (223.96±22.10) U/L, P < 0.01, and cardiomyocyte apoptosis rate (2.84±2.56)% vs. (12.58±6.69) %, P < 0.01, and Caspsse-3 activity (36 809±4750) RLU vs. (57 602±9161) RLU, P < 0.01], while LY294002 (PBK inhibitor) and U0126 (MAPK inhibitor) could block the effects of GLP-1 in cardiomyocytes underwent H/R injury. Conclusions GLP-1 could protect H/R injury mainly by inhibiting cardiomyocytes apoptosis via activating PI3K/Akt and MAPK signaling pathway.
