中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2012年
10期
869-873
,共5页
金成吉%王晓梅%段薇%李湘%曲建梅%张弢%刘璟瑶
金成吉%王曉梅%段薇%李湘%麯建梅%張弢%劉璟瑤
금성길%왕효매%단미%리상%곡건매%장도%류경요
肌,平滑,血管%S-腺苷甲硫氨酸%NF-κB%血小板源性生长因子
肌,平滑,血管%S-腺苷甲硫氨痠%NF-κB%血小闆源性生長因子
기,평활,혈관%S-선감갑류안산%NF-κB%혈소판원성생장인자
Muscle,smooth,vascular%S-adenosylmethionine%NF-kappa B%Platelet-derived growth factor
目的 观察S-腺苷甲硫氨酸(S-adenosyl-L-methionine,SAMe)对肿瘤坏死因子α(TNF-α)诱导的血管平滑肌细胞(VSMC)增殖与迁移的影响.方法 根据干预方式将大鼠VSMC分为对照组、TNF-α组、SAMe组和TNFα+ SAMe组4组.刮片法观察VSMC迁移距离,MTT法测定VSMC增殖,凝胶电泳迁移率(EMSA)分析检测核因子κB(NF-κB)的活性,Northern印迹法检测各组细胞血小板源性生长因子(PDGF) mRNA表达水平.将SD大鼠分为正常对照组、颈动脉球囊损伤模型生理盐水注射组(损伤组)和SAMe治疗组(15 mg·kg-1·d-1)3组,苏木素伊红染色观察血管内膜增生和管腔面积变化.结果 (1) TNF-α组VSMC迁移距离、490 nm吸光度值、PDGF mRNA表达水平、NF-κB活性大于对照组(P均＜0.01),TNF-α+ SAMe组上述指标均小于TNF-α组(P均＜0.01), 且与对照组比较差异无统计学意义.(2)损伤组和SAMe治疗组大鼠血管内膜面积均大于正常对照组(P均＜0.01),而管腔面积均小于正常对照组(P均＜0.01) . SAMe治疗组大鼠血管内膜面积小于损伤组(P＜0.01),而管腔面积大于损伤组(P＜0.01) 结论 SAMe可抑制TNF-α诱导的VSMC增殖和迁移,该作用可能与其抑制NF-κB活性和PDGF基因表达有关.
目的 觀察S-腺苷甲硫氨痠(S-adenosyl-L-methionine,SAMe)對腫瘤壞死因子α(TNF-α)誘導的血管平滑肌細胞(VSMC)增殖與遷移的影響.方法 根據榦預方式將大鼠VSMC分為對照組、TNF-α組、SAMe組和TNFα+ SAMe組4組.颳片法觀察VSMC遷移距離,MTT法測定VSMC增殖,凝膠電泳遷移率(EMSA)分析檢測覈因子κB(NF-κB)的活性,Northern印跡法檢測各組細胞血小闆源性生長因子(PDGF) mRNA錶達水平.將SD大鼠分為正常對照組、頸動脈毬囊損傷模型生理鹽水註射組(損傷組)和SAMe治療組(15 mg·kg-1·d-1)3組,囌木素伊紅染色觀察血管內膜增生和管腔麵積變化.結果 (1) TNF-α組VSMC遷移距離、490 nm吸光度值、PDGF mRNA錶達水平、NF-κB活性大于對照組(P均＜0.01),TNF-α+ SAMe組上述指標均小于TNF-α組(P均＜0.01), 且與對照組比較差異無統計學意義.(2)損傷組和SAMe治療組大鼠血管內膜麵積均大于正常對照組(P均＜0.01),而管腔麵積均小于正常對照組(P均＜0.01) . SAMe治療組大鼠血管內膜麵積小于損傷組(P＜0.01),而管腔麵積大于損傷組(P＜0.01) 結論 SAMe可抑製TNF-α誘導的VSMC增殖和遷移,該作用可能與其抑製NF-κB活性和PDGF基因錶達有關.
목적 관찰S-선감갑류안산(S-adenosyl-L-methionine,SAMe)대종류배사인자α(TNF-α)유도적혈관평활기세포(VSMC)증식여천이적영향.방법 근거간예방식장대서VSMC분위대조조、TNF-α조、SAMe조화TNFα+ SAMe조4조.괄편법관찰VSMC천이거리,MTT법측정VSMC증식,응효전영천이솔(EMSA)분석검측핵인자κB(NF-κB)적활성,Northern인적법검측각조세포혈소판원성생장인자(PDGF) mRNA표체수평.장SD대서분위정상대조조、경동맥구낭손상모형생리염수주사조(손상조)화SAMe치료조(15 mg·kg-1·d-1)3조,소목소이홍염색관찰혈관내막증생화관강면적변화.결과 (1) TNF-α조VSMC천이거리、490 nm흡광도치、PDGF mRNA표체수평、NF-κB활성대우대조조(P균＜0.01),TNF-α+ SAMe조상술지표균소우TNF-α조(P균＜0.01), 차여대조조비교차이무통계학의의.(2)손상조화SAMe치료조대서혈관내막면적균대우정상대조조(P균＜0.01),이관강면적균소우정상대조조(P균＜0.01) . SAMe치료조대서혈관내막면적소우손상조(P＜0.01),이관강면적대우손상조(P＜0.01) 결론 SAMe가억제TNF-α유도적VSMC증식화천이,해작용가능여기억제NF-κB활성화PDGF기인표체유관.
Objective To investigate the effect of S-adenosyl-L-methionine (SAMe) on vascular smooth muscle cells (VSMCs) proliferation and migration and neointima formation in rat carotid artery balloon injury model.Methods Rat VSMCs were divided into control group,TNF-α (10 ng/ml) group,SAMe (0.2 mmol/L) group and TNF-α + SAMe group.VSMC migration distance and proliferation were examined by cell scrape tests and MTT method.NF-κB activity was analyzed by EMSA.PDGF mRNA expression was detected by Northern blot.SD rat were divided into control group,carotid balloon injury group treated with saline or SAMe (15 mg · kg-1 · d-1 for 14 d),then blood vessel proliferation was observed histologically in rat carotid artery.Results (1) In vitro,the VSMCs migration distance,absorbance at 490 nm,PDGF mRNA expression,NF-κB activitv were all increased in TNF-α group compared to the control group (P ＜ 0.01),and decreased in TNF-α + SAMe group compared to the TNF-α group (P ＜ 0.01).(2) In the balloon injury in vivo models,the intima area of saline group and SAMe group was increased compared to the control group,while the lumen area was larger and the intima area was smaller in the SAMe group than in the saline group (all P ＜0.05).Conclusion SAMe could reduce TNF-α induced VSMC proliferation and migration possibly through inhibiting NF-κB activity and downregulating PDGF gene expression.
