中国医药科学
中國醫藥科學
중국의약과학
CHINA MEDICINE AND PHARMACY
2013年
20期
9-12
,共4页
跨膜型肿瘤坏死因子-α%分泌型肿瘤坏死因子-α%肿瘤坏死因子受体%压力负荷性心肌肥厚
跨膜型腫瘤壞死因子-α%分泌型腫瘤壞死因子-α%腫瘤壞死因子受體%壓力負荷性心肌肥厚
과막형종류배사인자-α%분비형종류배사인자-α%종류배사인자수체%압력부하성심기비후
Transmembrane TNF-α%Secreted TNF-α%TNF-αreceptor%Pressure-overload hypertrophy
目的:检测压力负荷所致心肌肥厚小鼠模型心肌组织中两型TNF及其受体的表达。方法使用野生型BALB/c小鼠,将其分为假手术组(n=10只)和手术组(n=8只),通过胸主动脉缩窄术诱导压力负荷性心肌肥厚模型。术后2周处死小鼠,并对小鼠进行心脏形态学、血流动力学检测;使用Western Blot方法对心肌组织中两型TNF-α及其受体表达进行检测。结果(1)在BALB/c小鼠中成功建立胸主动脉缩窄诱导心肌肥厚模型;(2)术后2周手术组小鼠心脏组织中可见分泌型TNF-α和跨膜型TNF-α表达量均有增加,且分泌型TNF-α表达量明显高于跨膜型TNF-α,差异有统计学意义(P<0.05);(3)术后2周小鼠心脏组织中TNFR1和TNFR2表达量均有增加,但TNFR1表达量高于TNFR2(P<0.05)。结论在小鼠压力负荷诱导心肌肥厚模型中,两型TNF-α及其两种受体表达量均有增加。虽然起负性肌力作用的分泌型TNF-α及TNFR1表达起主导作用,其研究相对集中且广泛,但跨膜型TNF-α和TNFR2表达量增加提示其在这一病理过程中具有生物学作用。其作用和机制仍需进一步研究。
目的:檢測壓力負荷所緻心肌肥厚小鼠模型心肌組織中兩型TNF及其受體的錶達。方法使用野生型BALB/c小鼠,將其分為假手術組(n=10隻)和手術組(n=8隻),通過胸主動脈縮窄術誘導壓力負荷性心肌肥厚模型。術後2週處死小鼠,併對小鼠進行心髒形態學、血流動力學檢測;使用Western Blot方法對心肌組織中兩型TNF-α及其受體錶達進行檢測。結果(1)在BALB/c小鼠中成功建立胸主動脈縮窄誘導心肌肥厚模型;(2)術後2週手術組小鼠心髒組織中可見分泌型TNF-α和跨膜型TNF-α錶達量均有增加,且分泌型TNF-α錶達量明顯高于跨膜型TNF-α,差異有統計學意義(P<0.05);(3)術後2週小鼠心髒組織中TNFR1和TNFR2錶達量均有增加,但TNFR1錶達量高于TNFR2(P<0.05)。結論在小鼠壓力負荷誘導心肌肥厚模型中,兩型TNF-α及其兩種受體錶達量均有增加。雖然起負性肌力作用的分泌型TNF-α及TNFR1錶達起主導作用,其研究相對集中且廣汎,但跨膜型TNF-α和TNFR2錶達量增加提示其在這一病理過程中具有生物學作用。其作用和機製仍需進一步研究。
목적:검측압력부하소치심기비후소서모형심기조직중량형TNF급기수체적표체。방법사용야생형BALB/c소서,장기분위가수술조(n=10지)화수술조(n=8지),통과흉주동맥축착술유도압력부하성심기비후모형。술후2주처사소서,병대소서진행심장형태학、혈류동역학검측;사용Western Blot방법대심기조직중량형TNF-α급기수체표체진행검측。결과(1)재BALB/c소서중성공건립흉주동맥축착유도심기비후모형;(2)술후2주수술조소서심장조직중가견분비형TNF-α화과막형TNF-α표체량균유증가,차분비형TNF-α표체량명현고우과막형TNF-α,차이유통계학의의(P<0.05);(3)술후2주소서심장조직중TNFR1화TNFR2표체량균유증가,단TNFR1표체량고우TNFR2(P<0.05)。결론재소서압력부하유도심기비후모형중,량형TNF-α급기량충수체표체량균유증가。수연기부성기력작용적분비형TNF-α급TNFR1표체기주도작용,기연구상대집중차엄범,단과막형TNF-α화TNFR2표체량증가제시기재저일병리과정중구유생물학작용。기작용화궤제잉수진일보연구。
Objective The aim of this study is to detect expressions of soluble TNF-α, transmembrane TNF-αand their receptors in pressure-overload cardiac hypertrophy models induced by transverse aortic constriction (TAC). Methods Pressure-overload cardiac hypertrophy model was induced in BABL/c mice by TAC. Sham served as a control. We characterized models by using morphological and hemodynamic analysis 14 days after surgery. Expression of sTNF-α, tmTNF-α, TNFR1 and TNFR2 in heart tissue was examined by Western Blot. Results (1) Pressure-overload cardiac hypertrophy model by TAC was successfully established. (2) Expression of sTNF-α and tmTNF-αwas elevated in pressure-overload cardiac hypertrophy mice compared with the sham group. But the expression of sTNF-α was much higher than tmTNF-α. (3)Expression of TNFR1 and TNFR2 was upregulated in operation group compared with the sham group. But the expression of TNFR1 was much higher than TNFR2. Conclusion Expression of sTNF-α, tmTNF-α, TNFR1 and TNFR2 in heart tissue was elevated in pressure-overload cardiac hypertrophy group compared with the sham group. Although sTNF-α and TNFR1 play a dominant negative inotropic role in pressure overloaded hypertrophy model,which were relatively concentrated and widely researched, increased amount of tmTNF-αand TNFR2 points out a role of tmTNF-αin this pathological process. However, the biological actions of tmTNF-αand TNFR2 and the mechanisms in hypertrophy need to be further studied in the future.