Limits...
Shuangshen Ningxin Capsule, a Traditional Chinese Medicinal Preparation, Alleviates Myocardial Ischemia through Autophagy Regulation.

Wang J, Hou J, Lin C, Fu J, Ren J, Li L, Guo H, Han X, Wang B, Liu J - Evid Based Complement Alternat Med (2015)

Bottom Line: The results showed that CMS treated with SSNX exhibited the correction for the disturbed cardiac hemodynamics, increase of coronary artery diameter, reduction of high plaque burden and plaque volume, and decrease of LDH.The inhibitory effect of SSNX on CMS autophagy was demonstrated by the reduction of autophagosome and the downregulation of beclin-1 and LC3-I/II.SSNX may protect coronary artery and increase the stability of plaque through the suppression of myocardial cellular autophagy, which suggests the potentially therapeutic effect of SSNX on ischemic cardiovascular disease.

View Article: PubMed Central - PubMed

Affiliation: Institute of Basic Medical Sciences of Xiyuan Hospital, Beijing Key Laboratory of Pharmacology of Chinese Materia Medicine, 1 Xiyuan Caochang, Haidian District, Beijing 100091, China ; Institute of Basic Theory, China Academy of Chinese Medical Sciences, 16 Dong Zhi Men Nei Nan Xiao Jie, Beijing 100700, China.

ABSTRACT
Shuangshen Ningxin capsule (SSNX), a modern Chinese formula, has been used to treat cardiovascular diseases in Eastern Asia. Our study focuses on the autophagy regulation of SSNX against coronary artery injuries. Myocardial infarction model was established in Chinese miniswines (CMS) by coronary artery balloon injury. SSNX was administered to the CMS for 8 weeks with 4 mg/kg or 16 mg/kg. Myocardial cells were incubated with 20% SSNX medicated serum for 2 hours. Assays were performed to detect the effects of SSNX on (i) coronary artery diameter by angiography, (ii) hemodynamics by noninvasive hemodynamic monitoring system, (iii) plaque burden and plaque volume by intravenous ultrasound (iv) coronary artery histology by H&E staining, (v) autophagosome by transmission electron microscopy, (vi) lactate dehydrogenase (LDH) leakage, and (vii) Beclin-1 and LC3-I/II expressions by Western blot. The results showed that CMS treated with SSNX exhibited the correction for the disturbed cardiac hemodynamics, increase of coronary artery diameter, reduction of high plaque burden and plaque volume, and decrease of LDH. The inhibitory effect of SSNX on CMS autophagy was demonstrated by the reduction of autophagosome and the downregulation of beclin-1 and LC3-I/II. SSNX may protect coronary artery and increase the stability of plaque through the suppression of myocardial cellular autophagy, which suggests the potentially therapeutic effect of SSNX on ischemic cardiovascular disease.

No MeSH data available.


Related in: MedlinePlus

Ultrastructural features of autophagosomes change in myocardial tissue of swines treated by different condition. SSNX high dose obviously reduces the amount of autophagosomes determined by transmission electron microscopic: (a) control, (b) model, (c) simvastatin (0.5 mg/kg), (d) SSNX low dose (4 mg/kg), and (e) SSNX high dose (16 mg/kg).
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4339791&req=5

fig6: Ultrastructural features of autophagosomes change in myocardial tissue of swines treated by different condition. SSNX high dose obviously reduces the amount of autophagosomes determined by transmission electron microscopic: (a) control, (b) model, (c) simvastatin (0.5 mg/kg), (d) SSNX low dose (4 mg/kg), and (e) SSNX high dose (16 mg/kg).

Mentions: Transmission electron microscopic examination in the group model showed large amounts of autophagosomes with bistratal membrane and surrounded by degenerated mitochondria, characterized by mitochondrial crista disappearance or fusion (Figure 6(b)). Simvastatin (Figure 6(c)) and SSNX with low dose (Figure 6(d)) also displayed an autophagosomes characterized by intermittent bistratal membrane which was not shown in high dose of SSNX group, indicating that SSNX with high dose could significantly reduce the formation of autophagosome.


Shuangshen Ningxin Capsule, a Traditional Chinese Medicinal Preparation, Alleviates Myocardial Ischemia through Autophagy Regulation.

Wang J, Hou J, Lin C, Fu J, Ren J, Li L, Guo H, Han X, Wang B, Liu J - Evid Based Complement Alternat Med (2015)

Ultrastructural features of autophagosomes change in myocardial tissue of swines treated by different condition. SSNX high dose obviously reduces the amount of autophagosomes determined by transmission electron microscopic: (a) control, (b) model, (c) simvastatin (0.5 mg/kg), (d) SSNX low dose (4 mg/kg), and (e) SSNX high dose (16 mg/kg).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4339791&req=5

fig6: Ultrastructural features of autophagosomes change in myocardial tissue of swines treated by different condition. SSNX high dose obviously reduces the amount of autophagosomes determined by transmission electron microscopic: (a) control, (b) model, (c) simvastatin (0.5 mg/kg), (d) SSNX low dose (4 mg/kg), and (e) SSNX high dose (16 mg/kg).
Mentions: Transmission electron microscopic examination in the group model showed large amounts of autophagosomes with bistratal membrane and surrounded by degenerated mitochondria, characterized by mitochondrial crista disappearance or fusion (Figure 6(b)). Simvastatin (Figure 6(c)) and SSNX with low dose (Figure 6(d)) also displayed an autophagosomes characterized by intermittent bistratal membrane which was not shown in high dose of SSNX group, indicating that SSNX with high dose could significantly reduce the formation of autophagosome.

Bottom Line: The results showed that CMS treated with SSNX exhibited the correction for the disturbed cardiac hemodynamics, increase of coronary artery diameter, reduction of high plaque burden and plaque volume, and decrease of LDH.The inhibitory effect of SSNX on CMS autophagy was demonstrated by the reduction of autophagosome and the downregulation of beclin-1 and LC3-I/II.SSNX may protect coronary artery and increase the stability of plaque through the suppression of myocardial cellular autophagy, which suggests the potentially therapeutic effect of SSNX on ischemic cardiovascular disease.

View Article: PubMed Central - PubMed

Affiliation: Institute of Basic Medical Sciences of Xiyuan Hospital, Beijing Key Laboratory of Pharmacology of Chinese Materia Medicine, 1 Xiyuan Caochang, Haidian District, Beijing 100091, China ; Institute of Basic Theory, China Academy of Chinese Medical Sciences, 16 Dong Zhi Men Nei Nan Xiao Jie, Beijing 100700, China.

ABSTRACT
Shuangshen Ningxin capsule (SSNX), a modern Chinese formula, has been used to treat cardiovascular diseases in Eastern Asia. Our study focuses on the autophagy regulation of SSNX against coronary artery injuries. Myocardial infarction model was established in Chinese miniswines (CMS) by coronary artery balloon injury. SSNX was administered to the CMS for 8 weeks with 4 mg/kg or 16 mg/kg. Myocardial cells were incubated with 20% SSNX medicated serum for 2 hours. Assays were performed to detect the effects of SSNX on (i) coronary artery diameter by angiography, (ii) hemodynamics by noninvasive hemodynamic monitoring system, (iii) plaque burden and plaque volume by intravenous ultrasound (iv) coronary artery histology by H&E staining, (v) autophagosome by transmission electron microscopy, (vi) lactate dehydrogenase (LDH) leakage, and (vii) Beclin-1 and LC3-I/II expressions by Western blot. The results showed that CMS treated with SSNX exhibited the correction for the disturbed cardiac hemodynamics, increase of coronary artery diameter, reduction of high plaque burden and plaque volume, and decrease of LDH. The inhibitory effect of SSNX on CMS autophagy was demonstrated by the reduction of autophagosome and the downregulation of beclin-1 and LC3-I/II. SSNX may protect coronary artery and increase the stability of plaque through the suppression of myocardial cellular autophagy, which suggests the potentially therapeutic effect of SSNX on ischemic cardiovascular disease.

No MeSH data available.


Related in: MedlinePlus