目的观察头针加体针对脑梗死大鼠骨骼肌α-actin m RNA表达的影响,初步探讨针刺对脑梗死偏瘫骨骼肌的作用机制。方法按时相在规定的骨骼肌部位取材并标记,采用定量法提取骨骼肌RNA、通过荧光定量qRT-PCR检测,观察大鼠患侧骨骼肌中α-act...目的观察头针加体针对脑梗死大鼠骨骼肌α-actin m RNA表达的影响,初步探讨针刺对脑梗死偏瘫骨骼肌的作用机制。方法按时相在规定的骨骼肌部位取材并标记,采用定量法提取骨骼肌RNA、通过荧光定量qRT-PCR检测,观察大鼠患侧骨骼肌中α-actin m RNA的表达变化。结果 A、B、C三组的前肢肌、腓肠肌、腰大肌中α-actin m RNA表达与D、E组相比较均有明显的变化,且C组在0h、24h、48h时与其他组比较,基因表达均有显著差异性(P﹤0.001),B组与A、D、E比较,在0h,24h有显著性差异(P﹤0.05),A组与D、E组在48h有显著性差异(P﹤0.05),且在48h时α-actin在腰大肌中的表达最强,有显著性差异(P﹤0.01)。结论头针加体针可上调脑梗死大鼠早期骨骼肌中α-actin m RNA表达,且在48h时α-actin在腰大肌中的表达最强,这可能是针刺改善脑梗死偏瘫骨骼肌肌力的作用途径之一。展开更多
Cardiotrophin-1 （CT-1） activates a distinct form of cardiac muscle cell hypertrophy in which the sarcomeric units are assembled in series. The aim of the study was to determine the expres- sion pattern of sarcomeric...Cardiotrophin-1 （CT-1） activates a distinct form of cardiac muscle cell hypertrophy in which the sarcomeric units are assembled in series. The aim of the study was to determine the expres- sion pattern of sarcomeric contractile protein α-actin, specialized eytoskeletal protein α-actinin and mitochondrial uncoupling protein-2 （UCP2） in myocardial remodeling induced by chronic exposure to CT-1. Kunming mice were intraperitoneally injected with carboxy-terminal polypeptide （CP） of CT-1 （CT-1-CP, 500 μg·kg-1·day^-1） for 1, 2, 3 and 4 week （s）, respectively （4 groups obtained according to the injection time, n=10 each, with 5 males and 5 females in each group）, Those injected with physiological saline for 4 weeks served as controls （n=10, with 5 males and 5 females）. The heart tissues of mice were harvested at 1, 2, 3 or 4 week （s）. Immunohistochemistry （IHC） and Western blotting （WB） were used to detect the distribution and expression of sarcomeric α-actin, α-aetinin and mitoehondrial UCP2 in myocardial tissues. IHC showed that α-actin was mainly distributed around the nuclei of cardiomyo- cytes, α-actinin concentrated around the striae and UCP2 scattered rather evenly in the plasma. The ex- pression of α-actin was slightly greater than that of α-actinin and UCP2 in the control group （IHC： χ^2=6.125; WB： F=0.249, P〉0.05） and it gradually decreased after exposure to CT-1-CP. There was no significant difference in the expression of α-actin between the control group and the CT-1-CP-treated groups （χ^2=7.386, P〉0.05）. But Western blotting revealed significant difference in the expression of α-actin between the control group and the 4-week CT-1-CP-treated group （F=2.912; q=4.203, P〈0.05）. Moreover, it was found that the expression of α-actinin increased stepwise with the exposure time in CT-1-CP-treated groups and differed significantly between CT-1-CP-treated groups and the control group （ICH： χ^2=21.977; WB： F=50.388; P〈0.01）. The expression of UCP2 was initially increased （WB： control group vs. 1- or 2-week group, q values： 5.603 and 9.995, respectively, P〈0.01） and then de- creased （WB： control group vs. 3-week group, q=4.742, P〈0.01; control group vs. 4-week group, q=0.558, P〉0.05）. It was suggested that long-term exposure to CT-1-CP could lead to the alteration in the expression of sarcomeric α-actin, α-actinin and mitochonclrial UCP2. The different expressions of sarcomeric structure proteins and mitochondrial UCP2 may be involved in myocardial remodeling.展开更多
文摘目的观察头针加体针对脑梗死大鼠骨骼肌α-actin m RNA表达的影响,初步探讨针刺对脑梗死偏瘫骨骼肌的作用机制。方法按时相在规定的骨骼肌部位取材并标记,采用定量法提取骨骼肌RNA、通过荧光定量qRT-PCR检测,观察大鼠患侧骨骼肌中α-actin m RNA的表达变化。结果 A、B、C三组的前肢肌、腓肠肌、腰大肌中α-actin m RNA表达与D、E组相比较均有明显的变化,且C组在0h、24h、48h时与其他组比较,基因表达均有显著差异性(P﹤0.001),B组与A、D、E比较,在0h,24h有显著性差异(P﹤0.05),A组与D、E组在48h有显著性差异(P﹤0.05),且在48h时α-actin在腰大肌中的表达最强,有显著性差异(P﹤0.01)。结论头针加体针可上调脑梗死大鼠早期骨骼肌中α-actin m RNA表达,且在48h时α-actin在腰大肌中的表达最强,这可能是针刺改善脑梗死偏瘫骨骼肌肌力的作用途径之一。
文摘Cardiotrophin-1 （CT-1） activates a distinct form of cardiac muscle cell hypertrophy in which the sarcomeric units are assembled in series. The aim of the study was to determine the expres- sion pattern of sarcomeric contractile protein α-actin, specialized eytoskeletal protein α-actinin and mitochondrial uncoupling protein-2 （UCP2） in myocardial remodeling induced by chronic exposure to CT-1. Kunming mice were intraperitoneally injected with carboxy-terminal polypeptide （CP） of CT-1 （CT-1-CP, 500 μg·kg-1·day^-1） for 1, 2, 3 and 4 week （s）, respectively （4 groups obtained according to the injection time, n=10 each, with 5 males and 5 females in each group）, Those injected with physiological saline for 4 weeks served as controls （n=10, with 5 males and 5 females）. The heart tissues of mice were harvested at 1, 2, 3 or 4 week （s）. Immunohistochemistry （IHC） and Western blotting （WB） were used to detect the distribution and expression of sarcomeric α-actin, α-aetinin and mitoehondrial UCP2 in myocardial tissues. IHC showed that α-actin was mainly distributed around the nuclei of cardiomyo- cytes, α-actinin concentrated around the striae and UCP2 scattered rather evenly in the plasma. The ex- pression of α-actin was slightly greater than that of α-actinin and UCP2 in the control group （IHC： χ^2=6.125; WB： F=0.249, P〉0.05） and it gradually decreased after exposure to CT-1-CP. There was no significant difference in the expression of α-actin between the control group and the CT-1-CP-treated groups （χ^2=7.386, P〉0.05）. But Western blotting revealed significant difference in the expression of α-actin between the control group and the 4-week CT-1-CP-treated group （F=2.912; q=4.203, P〈0.05）. Moreover, it was found that the expression of α-actinin increased stepwise with the exposure time in CT-1-CP-treated groups and differed significantly between CT-1-CP-treated groups and the control group （ICH： χ^2=21.977; WB： F=50.388; P〈0.01）. The expression of UCP2 was initially increased （WB： control group vs. 1- or 2-week group, q values： 5.603 and 9.995, respectively, P〈0.01） and then de- creased （WB： control group vs. 3-week group, q=4.742, P〈0.01; control group vs. 4-week group, q=0.558, P〉0.05）. It was suggested that long-term exposure to CT-1-CP could lead to the alteration in the expression of sarcomeric α-actin, α-actinin and mitochonclrial UCP2. The different expressions of sarcomeric structure proteins and mitochondrial UCP2 may be involved in myocardial remodeling.
