心血管康复医学杂志
心血管康複醫學雜誌
심혈관강복의학잡지
JOURNAL OF CARDIOVASCULAR REHABILITATION MEDICINE
2015年
1期
10-15
,共6页
人参皂甙%肌细胞,心脏%蛋白激酶 C
人參皂甙%肌細胞,心髒%蛋白激酶 C
인삼조대%기세포,심장%단백격매 C
Ginsenoside%Myocyte,cardiac%Protein kinase C
目的：探讨人参皂甙 Rb1（Gs-Rb1）是否可通过蛋白激酶 C （PKC）系统减轻内皮素-1（ET-1）诱导的乳鼠心肌细胞肥大。方法：将乳鼠心肌细胞随机分为空白对照组、Gs-Rb1组、ET-1组、Gs-Rb1＋ ET-1组、ET-1＋CHE 组（PKC 阻断剂白屈菜季氨碱）组和 Gs-Rb1＋ET-1＋CHE 组；干预96 h 后，测定心肌细胞表面积、总蛋白含量、PKC 活性、c-fos 和 p-c-jun 表达。结果：（1）Gs-Rb1＋ ET-1组心肌细胞表面积、心肌细胞总蛋白含量显著少于 ET-1组（P ＜0.05～＜0.001）；而与 Gs-Rb1＋ET-1＋CHE 组没有统计学意义（P ＝0.569）；（2）Gs-Rb1＋ET-1组 PKC 活性较 ET-1组显著下降[（9.3±0.6）pmol·min－1·mg－1比（14.1±0.9）pmol·min－1·mg－1]，但显著强于 Gs-Rb1＋ET-1＋CHE 组[（2.7±0.2）pmol·min－1·mg－1]，P 均＜0.001；（3）ET-1组 c-fos、p-c-jun基因和蛋白的表达显著高于空白对照组（P 均＜0.001）；与 ET-1组比较，Gs-Rb1＋ET-1组 c-fos [mRNA／蛋白：（0.53±0.05／0.39±0.02）比（0.43±0.03／0.31±0.03）]、p-c-jun [mRNA／蛋白：（0.64±0.04／0.44±0.02）比（0.33±0.05／0.37±0.03）]表达和 ET-1＋CHE 组 c-fos [mRNA／蛋白：0.41±0.05／0.31±0.02]、p-c-jun [mR-NA／蛋白：0.31±0.05／0.36±0.03]表达均显著下降（P ＜0.05或＜0.001），Gs-Rb1＋ET-1＋CHE 组 c-fos、p-c-jun 基因和蛋白的表达显著低于 Gs-Rb1＋ET-1组和 ET-1＋CHE 组（P ＜0.05或＜0.001）。结论：Gs-Rb1显著抑制 ET-1所致的心肌细胞肥大，PKC 系统是介导此生物学效应的途径之一。
目的：探討人參皂甙 Rb1（Gs-Rb1）是否可通過蛋白激酶 C （PKC）繫統減輕內皮素-1（ET-1）誘導的乳鼠心肌細胞肥大。方法：將乳鼠心肌細胞隨機分為空白對照組、Gs-Rb1組、ET-1組、Gs-Rb1＋ ET-1組、ET-1＋CHE 組（PKC 阻斷劑白屈菜季氨堿）組和 Gs-Rb1＋ET-1＋CHE 組；榦預96 h 後，測定心肌細胞錶麵積、總蛋白含量、PKC 活性、c-fos 和 p-c-jun 錶達。結果：（1）Gs-Rb1＋ ET-1組心肌細胞錶麵積、心肌細胞總蛋白含量顯著少于 ET-1組（P ＜0.05～＜0.001）；而與 Gs-Rb1＋ET-1＋CHE 組沒有統計學意義（P ＝0.569）；（2）Gs-Rb1＋ET-1組 PKC 活性較 ET-1組顯著下降[（9.3±0.6）pmol·min－1·mg－1比（14.1±0.9）pmol·min－1·mg－1]，但顯著彊于 Gs-Rb1＋ET-1＋CHE 組[（2.7±0.2）pmol·min－1·mg－1]，P 均＜0.001；（3）ET-1組 c-fos、p-c-jun基因和蛋白的錶達顯著高于空白對照組（P 均＜0.001）；與 ET-1組比較，Gs-Rb1＋ET-1組 c-fos [mRNA／蛋白：（0.53±0.05／0.39±0.02）比（0.43±0.03／0.31±0.03）]、p-c-jun [mRNA／蛋白：（0.64±0.04／0.44±0.02）比（0.33±0.05／0.37±0.03）]錶達和 ET-1＋CHE 組 c-fos [mRNA／蛋白：0.41±0.05／0.31±0.02]、p-c-jun [mR-NA／蛋白：0.31±0.05／0.36±0.03]錶達均顯著下降（P ＜0.05或＜0.001），Gs-Rb1＋ET-1＋CHE 組 c-fos、p-c-jun 基因和蛋白的錶達顯著低于 Gs-Rb1＋ET-1組和 ET-1＋CHE 組（P ＜0.05或＜0.001）。結論：Gs-Rb1顯著抑製 ET-1所緻的心肌細胞肥大，PKC 繫統是介導此生物學效應的途徑之一。
목적：탐토인삼조대 Rb1（Gs-Rb1）시부가통과단백격매 C （PKC）계통감경내피소-1（ET-1）유도적유서심기세포비대。방법：장유서심기세포수궤분위공백대조조、Gs-Rb1조、ET-1조、Gs-Rb1＋ ET-1조、ET-1＋CHE 조（PKC 조단제백굴채계안감）조화 Gs-Rb1＋ET-1＋CHE 조；간예96 h 후，측정심기세포표면적、총단백함량、PKC 활성、c-fos 화 p-c-jun 표체。결과：（1）Gs-Rb1＋ ET-1조심기세포표면적、심기세포총단백함량현저소우 ET-1조（P ＜0.05～＜0.001）；이여 Gs-Rb1＋ET-1＋CHE 조몰유통계학의의（P ＝0.569）；（2）Gs-Rb1＋ET-1조 PKC 활성교 ET-1조현저하강[（9.3±0.6）pmol·min－1·mg－1비（14.1±0.9）pmol·min－1·mg－1]，단현저강우 Gs-Rb1＋ET-1＋CHE 조[（2.7±0.2）pmol·min－1·mg－1]，P 균＜0.001；（3）ET-1조 c-fos、p-c-jun기인화단백적표체현저고우공백대조조（P 균＜0.001）；여 ET-1조비교，Gs-Rb1＋ET-1조 c-fos [mRNA／단백：（0.53±0.05／0.39±0.02）비（0.43±0.03／0.31±0.03）]、p-c-jun [mRNA／단백：（0.64±0.04／0.44±0.02）비（0.33±0.05／0.37±0.03）]표체화 ET-1＋CHE 조 c-fos [mRNA／단백：0.41±0.05／0.31±0.02]、p-c-jun [mR-NA／단백：0.31±0.05／0.36±0.03]표체균현저하강（P ＜0.05혹＜0.001），Gs-Rb1＋ET-1＋CHE 조 c-fos、p-c-jun 기인화단백적표체현저저우 Gs-Rb1＋ET-1조화 ET-1＋CHE 조（P ＜0.05혹＜0.001）。결론：Gs-Rb1현저억제 ET-1소치적심기세포비대，PKC 계통시개도차생물학효응적도경지일。
Objective:To explore whether ginsenosides-Rb1 (Gs-Rb1)can relieve cardiomyocyte hypertrophy induced by endothelin-1 (ET-1)via protein kinase C (PKC)system.Methods:Cardiomyocytes of neonatal rat were random-ly divided into blank control group,Gs-Rb1 group,ET-1 group,Gs-Rb1+ET-1 group,ET-1+CHE (chelerythrine, PKC blocker)group and Gs-Rb1 +ET-1 +CHE group.After 96h intervention,cardiomyocyte surface area,total protein content,PKC activity,c-fos and p-c-jun expressions were measured.Results: (1)Cardiomyocyte surface area and total protein content in Gs-Rb1+ET-1 group were significantly lower than those of ET-1 group (P <0.05~<0.001),but not significant different with those of Gs-Rb1+ET-1+CHE group,P =0.569;(2)PKC activity in Gs-Rb1+ET-1 group was significantly lower than that of ET-1 group [(9.3±0.6)pmol·min-1 ·mg-1 vs.(14.1± 0.9)pmol·min-1 ·mg-1 ],but significantly higher than that of Gs-Rb1+ET-1+CHE group [(2.7±0.2)pmol· min-1 ·mg-1 ],P <0.001 all;(3)Expressions of c-fos and p-c-jun gene and protein in ET-1 group were significant-ly higher than those of blank control group (P <0.001 all);compared with ET-1 group,there were significant re-ductions in expressions of c-fos [mRNA/protein:(0.53±0.05/0.39±0.02)vs.(0.43±0.03/0.31±0.03)]and p-c-jun [mRNA/protein:(0.64±0.04/0.44±0.02)vs.(0.33±0.05/0.37±0.03)]in Gs-Rb1+ET-1 group and ex-pressions of c-fos [mRNA/protein:0.41 ± 0.05/0.31 ± 0.02]and p-c-jun [mRNA/protein:0.31 ± 0.05/0.36 ±0.03]in ET-1+CHE group (P <0.05 or <0.001),expressions of c-fos and p-c-jun gene and protein in Gs-Rb1+ET-1+CHE group were significantly lower than those of Gs-Rb1+ET-1 group and ET-1+CHE group (P <0.05 or<0.001).Conclusion:Gs-Rb1 can significantly inhibit cardiomyocyte hypertrophy induced by ET-1 and PKC system is one of pathways mediating this biological effect.
