中华生物医学工程杂志
中華生物醫學工程雜誌
중화생물의학공정잡지
CHINESE JOURNAL OF BIOMEDICAL ENGINEERING
2012年
6期
431-436
,共6页
侯传举%齐岩梅%张端珍%王琦光%崔春生%匡丽%陈兵
侯傳舉%齊巖梅%張耑珍%王琦光%崔春生%劻麗%陳兵
후전거%제암매%장단진%왕기광%최춘생%광려%진병
肌细胞,心脏%趋化因子CXCL12%白细胞介素类
肌細胞,心髒%趨化因子CXCL12%白細胞介素類
기세포,심장%추화인자CXCL12%백세포개소류
Myocytes,cardiac%Chemokine CXCL12%Interleukins
目的 探索物理损伤与基质细胞衍生因子1α(stromal cell-derived factor-1α,SDF-1α)对大鼠心肌细胞增殖和细胞因子表达的影响.方法 培养大鼠心肌细胞,采用刮伤法建立物理损伤模型,添加80 μg/L SDF-1α进行联合培养；BrdU法检测各组心肌细胞的增殖能力；碘化丙啶(PI)染色联合流式细胞仪检测各组心肌细胞周期变化；免疫细胞化学法和Western印迹方法检测心肌细胞白细胞介素1α(IL-1α)、白细胞介素6(IL-6)和转化生长因子β1 (TGF-β1)的表达情况.结果 SDF-1α可提高物理损伤下心肌细胞的增殖能力,同时增加细胞周期中S期所占比例；物理损伤可增加心肌细胞IL-1α(1比2.53±0.54)、IL-6(1比1.47±0.12)和TGF-β1(1比1.36±0.09)的表达,物理损伤联合SDF-1α培养组心肌细胞IL-1α和IL-6的蛋白表达量有所增加(1比1.47±0.13,1比1.54±0.17)、TGF-β1的表达却略有下降(1比0.66±0.13).结论 SDF-1α可能通过上调细胞周期中S期所占比例,促进心肌细胞增殖,并可增加物理损伤引起的促炎作用.
目的 探索物理損傷與基質細胞衍生因子1α(stromal cell-derived factor-1α,SDF-1α)對大鼠心肌細胞增殖和細胞因子錶達的影響.方法 培養大鼠心肌細胞,採用颳傷法建立物理損傷模型,添加80 μg/L SDF-1α進行聯閤培養；BrdU法檢測各組心肌細胞的增殖能力；碘化丙啶(PI)染色聯閤流式細胞儀檢測各組心肌細胞週期變化；免疫細胞化學法和Western印跡方法檢測心肌細胞白細胞介素1α(IL-1α)、白細胞介素6(IL-6)和轉化生長因子β1 (TGF-β1)的錶達情況.結果 SDF-1α可提高物理損傷下心肌細胞的增殖能力,同時增加細胞週期中S期所佔比例；物理損傷可增加心肌細胞IL-1α(1比2.53±0.54)、IL-6(1比1.47±0.12)和TGF-β1(1比1.36±0.09)的錶達,物理損傷聯閤SDF-1α培養組心肌細胞IL-1α和IL-6的蛋白錶達量有所增加(1比1.47±0.13,1比1.54±0.17)、TGF-β1的錶達卻略有下降(1比0.66±0.13).結論 SDF-1α可能通過上調細胞週期中S期所佔比例,促進心肌細胞增殖,併可增加物理損傷引起的促炎作用.
목적 탐색물리손상여기질세포연생인자1α(stromal cell-derived factor-1α,SDF-1α)대대서심기세포증식화세포인자표체적영향.방법 배양대서심기세포,채용괄상법건립물리손상모형,첨가80 μg/L SDF-1α진행연합배양；BrdU법검측각조심기세포적증식능력；전화병정(PI)염색연합류식세포의검측각조심기세포주기변화；면역세포화학법화Western인적방법검측심기세포백세포개소1α(IL-1α)、백세포개소6(IL-6)화전화생장인자β1 (TGF-β1)적표체정황.결과 SDF-1α가제고물리손상하심기세포적증식능력,동시증가세포주기중S기소점비례；물리손상가증가심기세포IL-1α(1비2.53±0.54)、IL-6(1비1.47±0.12)화TGF-β1(1비1.36±0.09)적표체,물리손상연합SDF-1α배양조심기세포IL-1α화IL-6적단백표체량유소증가(1비1.47±0.13,1비1.54±0.17)、TGF-β1적표체각략유하강(1비0.66±0.13).결론 SDF-1α가능통과상조세포주기중S기소점비례,촉진심기세포증식,병가증가물리손상인기적촉염작용.
Objective To investigate the effects of mechanical injury and stromal cell-derived factor-(SDF-1α) on rat cardiomyocytes proliferation and cytokine expression.Methods Rat cardiomyocytes were cultured followed by mechanical injury by scratching and were treated with 80 μg/L SDF-1α during incubation.The proliferative capacity of cardiomyocytes was assessed by BrdU assay and changes in cell cycles were examined by PI staining and flow cytometry.Immunocytochemistry and Western blot were employed to determine the expression of interleukin (IL)-1α,IL-6 and transforming growth factor (TGF)-β1.Results SDF-1α significantly stimulated the growth of mechanically injured cardiomyocytes and increased the proportion of cells in phase S.Mechanical injury promoted the expression of IL-1α (1 vs 2.53±0.54),IL-6 (1 vs 1.47±0.12) and TGF-β1 (1 vs 1.36±0.09) in cardiomyocytes.The combination of mechanical injury and SDF-1α resulted in up-regulated lL-1α and lL-6 (1 vs 1.47±0.13,1 vs 1.54±0.17) expression yet slightly suppressed TCF-β1 expression(1 vs 0.66±0.13).Conclusion SDF-1α may promote proliferation by increasing the proportion of cells in phase S and augment mechanical injury-induced proinflammatory responses in cardiomyocytes.
