中国组织工程研究与临床康复
中國組織工程研究與臨床康複
중국조직공정연구여림상강복
JOURNAL OF CLINICAL REHABILITATIVE TISSUE ENGINEERING RESEARCH
2011年
20期
3789-3792
,共4页
仇静%张广耘%田臻%张月%于江波%袁晓
仇靜%張廣耘%田臻%張月%于江波%袁曉
구정%장엄운%전진%장월%우강파%원효
丝裂原活化蛋白激酶%周期性张应力%凋亡%成纤维细胞
絲裂原活化蛋白激酶%週期性張應力%凋亡%成纖維細胞
사렬원활화단백격매%주기성장응력%조망%성섬유세포
背景:当牙齿受异常咬合力时会导致牙体吸收、牙周组织的大量破坏.目的:研究牙周膜成纤维细胞在受到周期性张应力刺激后是否发生凋亡及p38MAPK信号通路是否参与该凋亡过程.方法:取4~7代成纤维细胞,同步化后随机分为对照组、加力组和SB203580组.加力组和SB203580组细胞加载力值为12%表面应变率,加力频率为6个循环/min,即5 s拉伸,5 s松弛.SB203580组细胞在加力前1 h加入终浓度为20 mmol/L的p38MAPK抑制剂SB203580.分别在加力6,12,24 h,取各组细胞,流式细胞仪检测细胞凋亡,RT-PCR检测细胞凋亡基因bax mRNA的表达.结果与结论:与对照组比较,加力后成纤维细胞凋亡率及bax mRNA表达增加(P < 0.05),且随着加力时间的延长而增强,12 h达高峰,之后逐渐下降.与加力组比较,SB203580组对应时间点细胞凋亡减少(P < 0.05),bax mRNA表达降低.说明细胞受到力学刺激会发生凋亡,而丝裂原活化蛋白激酶p38MAPK信号通路参与了该凋亡过程.
揹景:噹牙齒受異常咬閤力時會導緻牙體吸收、牙週組織的大量破壞.目的:研究牙週膜成纖維細胞在受到週期性張應力刺激後是否髮生凋亡及p38MAPK信號通路是否參與該凋亡過程.方法:取4~7代成纖維細胞,同步化後隨機分為對照組、加力組和SB203580組.加力組和SB203580組細胞加載力值為12%錶麵應變率,加力頻率為6箇循環/min,即5 s拉伸,5 s鬆弛.SB203580組細胞在加力前1 h加入終濃度為20 mmol/L的p38MAPK抑製劑SB203580.分彆在加力6,12,24 h,取各組細胞,流式細胞儀檢測細胞凋亡,RT-PCR檢測細胞凋亡基因bax mRNA的錶達.結果與結論:與對照組比較,加力後成纖維細胞凋亡率及bax mRNA錶達增加(P < 0.05),且隨著加力時間的延長而增彊,12 h達高峰,之後逐漸下降.與加力組比較,SB203580組對應時間點細胞凋亡減少(P < 0.05),bax mRNA錶達降低.說明細胞受到力學刺激會髮生凋亡,而絲裂原活化蛋白激酶p38MAPK信號通路參與瞭該凋亡過程.
배경:당아치수이상교합력시회도치아체흡수、아주조직적대량파배.목적:연구아주막성섬유세포재수도주기성장응력자격후시부발생조망급p38MAPK신호통로시부삼여해조망과정.방법:취4~7대성섬유세포,동보화후수궤분위대조조、가력조화SB203580조.가력조화SB203580조세포가재력치위12%표면응변솔,가력빈솔위6개순배/min,즉5 s랍신,5 s송이.SB203580조세포재가력전1 h가입종농도위20 mmol/L적p38MAPK억제제SB203580.분별재가력6,12,24 h,취각조세포,류식세포의검측세포조망,RT-PCR검측세포조망기인bax mRNA적표체.결과여결론:여대조조비교,가력후성섬유세포조망솔급bax mRNA표체증가(P < 0.05),차수착가력시간적연장이증강,12 h체고봉,지후축점하강.여가력조비교,SB203580조대응시간점세포조망감소(P < 0.05),bax mRNA표체강저.설명세포수도역학자격회발생조망,이사렬원활화단백격매p38MAPK신호통로삼여료해조망과정.
BACKGROUND: When the teeth affected abnormal biting force, tooth absorption and periodontium would be greatly damaged. OBJECTIVE: To study whether periodontal membrane fibroblast affected apoptosis following cyclic tensile stress stimulation and whether p38MAPK signaling pathway participated in apoptosis. METHODS: Fibroblasts at passages from 4 to 7 were randomly assigned to control, loading and SB203580 groups after synchronization. In the loading and SB203580 groups, 12% strain was applied at a loading frequency of 6 cycles per minute, i.e. 5 seconds for tension and 5 seconds for relaxation. In the SB203580 group, cells were treated with 20 mmol/L p38MAPK inhibitor SB203580 at 1 hour before loading. At 6, 12 and 24 hours after loading, cells from each group were harvested, and cell apoptosis was detected using a flow cytometry. Expression of bax mRNA was determined using reverse transcription-polymerase chain reaction. RESULTS AND CONCLUSION: Compared with the control group, apoptotic rate of fibroblasts and bax mRNA expression were increased after loading (P < 0.05), and enhanced over time, and peaked at 12 hour following loading, and then decreased gradually. Compared with the loading group, cell apoptosis was reduced at corresponding time points in the SB203580 group (P < 0.05), and bax mRNA expression was diminished. These results indicated that cells affected apoptosis after mechanics stimulation, and mitogen activated protein kinase p38MAPK signaling pathway participates in the process of apoptosis.