Combination of total Astragalus extract and total Panax notoginseng saponins strengthened the protective effects on brain damage through improving energy metabolism and inhibiting apoptosis after cerebral ischemia-reperfusion in mice

Xiao-ping Huang; Hua Tan; Bei-yang Chen; Chang-qing Deng

doi:10.1007/s11655-015-1965-0

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Combination of total Astragalus extract and total Panax notoginseng saponins strengthened the protective effects on brain damage through improving energy metabolism and inhibiting apoptosis after cerebral ischemia-reperfusion in mice

OriginalPaper | Updated：2021-08-27

- Combination of total Astragalus extract and total Panax notoginseng saponins strengthened the protective effects on brain damage through improving energy metabolism and inhibiting apoptosis after cerebral ischemia-reperfusion in mice
- Combination of total Astragalus extract and total Panax notoginseng saponins strengthened the protective effects on brain damage through improving energy metabolism and inhibiting apoptosis after cerebral ischemia-reperfusion in mice
- 中国结合医学杂志（英文版） 2017年23卷第6期页码：445-452
- Affiliations：
  
  1. Key Laboratory of Hunan Universities for Cell Biology and Molecular Techniques, Key Laboratory of Hunan Province for Prevention and Treatment of Integrated Traditional Chinese and Western Medicine on Cardio-Cerebral Diseases, Hunan University of Chinese Medicine,Changsha,China
  2. Department of Histology and Embryology, Hunan University of Chinese Medicine,Changsha,China
- Author bio：
- Funds：
  
  Supported by National Natural Science Foundation of China (No. 81102557), Doctoral Program Foundation of Higher Education of China (No. 20104323110001), Key Project of Hunan Province Education Department (No. 08A050), Aid Project for Innovation Platform Open Fund of Hunan Province University (No. 11K050 and No. 14K068), Key Project of Administration of Traditional Chinese Medicine of Hunan Province (No. 201301), General Project of Science and Technology Department of Hunan Province (No. 2014SK3001), General Project of Education Bureau of Hunan Province (No. 11C0963)
- DOI：10.1007/s11655-015-1965-0
  中图分类号：
- 纸质出版日期：2017，
  
  网络出版日期：2015-3-24，
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Huang, Xp., Tan, H., Chen, By. et al. Combination of total Astragalus extract and total Panax notoginseng saponins strengthened the protective effects on brain damage through improving energy metabolism and inhibiting apoptosis after cerebral ischemia-reperfusion in mice., Chin. J. Integr. Med. 23, 445–452 (2017). https://doi.org/10.1007/s11655-015-1965-0

Xiao-ping Huang, Hua Tan, Bei-yang Chen, et al. Combination of total Astragalus extract and total Panax notoginseng saponins strengthened the protective effects on brain damage through improving energy metabolism and inhibiting apoptosis after cerebral ischemia-reperfusion in mice[J]. Chinese Journal of Integrative Medicine, 2017,23(6):445-452.
Huang, Xp., Tan, H., Chen, By. et al. Combination of total Astragalus extract and total Panax notoginseng saponins strengthened the protective effects on brain damage through improving energy metabolism and inhibiting apoptosis after cerebral ischemia-reperfusion in mice., Chin. J. Integr. Med. 23, 445–452 (2017). https://doi.org/10.1007/s11655-015-1965-0 DOI：

Xiao-ping Huang, Hua Tan, Bei-yang Chen, et al. Combination of total Astragalus extract and total Panax notoginseng saponins strengthened the protective effects on brain damage through improving energy metabolism and inhibiting apoptosis after cerebral ischemia-reperfusion in mice[J]. Chinese Journal of Integrative Medicine, 2017,23(6):445-452. DOI： 10.1007/s11655-015-1965-0.

摘要

To explore the effects and molecular mechanisms of the combination between total Astragalus extract (TAE) and total Panax notoginseng saponins (TPNS) against cerebral ischemia-reperfusion injury. C57BL/6 mice were randomly divided into sham-operated group

model group

TAE (110 mg/kg) group

TPNS (115 mg/kg) group

TAE-TPNS combination group and Edaravone (4 mg/kg) group

treated for 4 days

then

cerebral ischemia-reperfusion injury was established by bilateral common carotid artery (CCA) ligation for 20 min followed by reperfusion for 1 and 24 h. TPNS could increase adenosine triphosphate (ATP) level

TAE and TAE-TPNS combination increased ATP

adenosine diphosphate (ADP) contents and Na+-K+-ATPase activity

and the effects of TAE-TPNS combination were stronger than those of TAE or TPNS alone after reperfusion for 1 h. After reperfusion for 24 h

TAE

TPNS and TAE-TPNS combination significantly increased neurocyte survival rate and decreased the apoptosis rate as well as down-regulated the expression of phosphorylated c-June N-terminal kinase1/2 (p-JNK1/2)

cytochrome C (Cyt C)

cysteine aspartic acid-specific protease (Caspase)-9 and Caspase-3. Furthermore

the effects in TAE-TPNS combination were better than those in TAE or TPNS alone. The combination of TAE 110 mg/kg and TPNS 115 mg/kg could strengthen protective effects on cerebral ischemia injury

the mechanism underlying might be related to improving jointly the early energy metabolism

and relieving the delayed apoptosis via inhibiting the mitochondrial apoptosis pathway of JNK signal transduction.

Abstract

model group

TAE (110 mg/kg) group

TPNS (115 mg/kg) group

TAE-TPNS combination group and Edaravone (4 mg/kg) group

treated for 4 days

then

TAE and TAE-TPNS combination increased ATP

adenosine diphosphate (ADP) contents and Na+-K+-ATPase activity

and the effects of TAE-TPNS combination were stronger than those of TAE or TPNS alone after reperfusion for 1 h. After reperfusion for 24 h

TAE

cytochrome C (Cyt C)

cysteine aspartic acid-specific protease (Caspase)-9 and Caspase-3. Furthermore

the effects in TAE-TPNS combination were better than those in TAE or TPNS alone. The combination of TAE 110 mg/kg and TPNS 115 mg/kg could strengthen protective effects on cerebral ischemia injury

the mechanism underlying might be related to improving jointly the early energy metabolism

and relieving the delayed apoptosis via inhibiting the mitochondrial apoptosis pathway of JNK signal transduction.

关键词

total Astragalus extracttotal Panax notoginseng saponinscombinationcerebral ischemia-reperfusionenergy metabolismC-Jun N-terminal kinase signal transductionmitochondrial apoptosis pathwayChinese Medicine

Keywords

references

Yin YY, Li WP, Gong HL, Zhu FF, Li WZ, Wu GC. Protective effect of astragaloside on focal cerebral ischemia/reperfusion injury in rats. Am J Chin Med 2010;38:517–527.

Luo Y, Qin Z, Hong Z, Zhang X, Ding D, Fu JH, et al. Astragaloside IV protects agaist ischemic brain injure in a murine model of transient focal ischemia. Neurosci Lett 2004;363:218–223.

Qu YZ, Li M, Zhao YL, Zhao ZW, Wei XY, Liu JP, et al. Astragaloside IV attenuates cerebral ischemia-reperfusion induced increase in permeability of the blood-brain barrier in rats. Eur J Pharmacol 2009;606:137–141.

Liu Q, Kou JP, Yu BY. Ginsenoside Rg1 protects against hydrogen peroxide-induced cell death in PC12 cell via inhibiting NF-kB activation. Neurochem Int 2011;58:119–125.

Zhang YF, Fan XJ, Li X, Peng LL, Wang GH, Ke KF, et al. Ginsenoside Rg1 protects neurons from hypoxicischemic injury possibly by inhibiting Ca2+ influx through NMDA receptors and L-type voltage-depedent Ca2+ channels. Eur J Pharmacol 2008;586:90–99.

Yuan QL, Yang CX, Xu P, Gao XQ, Deng L, Chen P, et al. Neuroprotective effects of ginsenoside Rb1 on transient cerebral ischemia in rats. Brain Res 2007;1167:1–12.

Li H, Deng CQ, Chen BY, Zhang SP, Liang Y, Luo XG. Total saponins of Panax notoginseng modulate the expression of caspases and attenuate apoptosis in rats following focal cerebral ischemia-reperfusion. J Ethnopharmacol 2009;121:412–418.

The Ministry of Science and Technology of the People’s Republic of China. Guidance Suggestions for the Care and Use of Laboratory Animals. 2006-9-30.

Chinese Pharmacopoeia Commission. Pharmacopoeia of the People’s Republic of China. Vol 1. Beijing: China Medica Science Press; 2010:369.

Wu L, Zhang W, Tang YH, Li H, Chen BY, Zhang GM, et al. Effect of total saponins of "Panax notoginseng root" on aortic intimal hyperplasia and the expressions of cell cycle protein and extracellular matrix in rats. Phytomedicine 2010;17:233–240.

Yang G, Kitagawa K, Matsushita K, Mabuchi T, Yagita Y, Yanagihara T, et al. C57BL/6 strain is most susceptible to cerebral ischemia following bilateral common carotid occlusion among seven mouse strains: selective neuronal death in the murine transient forebrain ischemia. Brain Res 1997;752:209–218.

Manfredi G, Yang L, Gajewski CD, Mattiazzi M. Measurements of ATP in mammalian cells. Methods 2002;26:317–326.

Kilic E, Kilic U, Matter CM, Lüscher TF, Bassetti CL, Hermann DM. Aggravation of focal cerebral ischemia by tissue plasminogen activator is reversed by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor but does not depend on endothelial NO synthase. Stroke 2005;36:332–336.

Zhan C, Yang J. Protective effects of isoliquiritigenin in transient middle cerebral artery occlusion-induced focal cerebral ischemia in rats. Pharm Res 2006;53:303–309.

Moldovan L, Moldovan NI. Oxygen free radicals and redox biology of organelles. Histochem Cell Biol 2004;122:395–412.

Jürgensmeier JM, Xie Z, Deveraux Q, Ellerby L, Bredesen D, Reed JC. Bax directly induces release of cytoehrome C from isolated mitochondria. Proc Natl Acad Sci USA 1998;95:4997–5002.

Acehan D, Jiang X, Morgan DG, Heuser JE, Wang X, Akey CW. Three-structure of the apoptosome: implications for assembly, procaspase-9 binding and activation. Mol Cell 2002;9:423–432.

Rodriguez J, Lazebnik Y. Caspase-9 and APAF-1 form an active holoenzyme. Genes Dev 1999;13:3179–3184.

Martindale JL, Holbrook NJ. Cellular response to oxidative stress: signaling for suicide and survival. Cell Physiol 2002;192:1–15.

Irving EA, Bamford M. Role of mitogen-and stress-activated kinases in ischemic injury. Cereb Blood Flow Metab 2002;22:631–647.

Johnson GL, Lapadat R. Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases. Science 2002;298:1911–1912.

Davis RJ. Signal transduction by the JNK group of MAP kinases. Cell 2000;103:239–252.

Kharbanda S, Saxena S, Yoshida K, Pandey P, Kaneki M, Wang Q, et al. Translocation of SAPK/JNK to mitochondria and interaction with Bc1-x (L) in response to DNA damage. Biol Chem 2000;275:322–327.

Yoshida H, Yanai H, Namiki Y, Fukatsu-Sasaki K, Furutani N, Tada N. Neuroprotective effects of edaravone: a novel free radical scavenger in cerebrovascular injury. CNS Drug Rev 2006;12:9–20.

Rajesh KG, Sasaguri S, Suzuki R, Maeda H. Antioxidant MCI-186 inhibits mitochondrial permeability transition pore and upregulates Bcl-2 expression. Am J Physiol Heart Circ Physiol 2003;285:H2171–H2178.

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