Effects of Astragaloside IV on sepsis myocardiopathy and peroxisomal proliferate activation receptor alpha in mice induced by lipopolysaccharide

NIE Qu, LI Meng-fei, WANG Hong-xin

Chinese Journal of Clinical Anatomy ›› 2020, Vol. 38 ›› Issue (2) : 189-193.

Chinese Journal of Clinical Anatomy ›› 2020, Vol. 38 ›› Issue (2) : 189-193. DOI: 10.13418/j.issn.1001-165x.2020.02.017

Effects of Astragaloside IV on sepsis myocardiopathy and peroxisomal proliferate activation receptor alpha in mice induced by lipopolysaccharide

  • NIE Qu1,2,  LI Meng-fei2,WANG Hong-xin2
Author information +
History +

Abstract

Objective  To investigate the effects of Astragaloside IV (ASIV) on myocardial myocardiopathy and peroxisomal proliferate activation receptor α (PPARα) in mice induced by lipopolysaccharide (LPS). Methods 50 healthy male C57BL/6J mice were randomly divided into 5 groups, each group of 10 mice, which were divided into a blank control group, a lipopolysaccharide model group and three astragaloside IV (20, 40, 80 mg/kg/d) groups. Astragaloside IV was administered to the ASIV groups for 7 days, and then the model group was given LPS (10 mg/kg) to establish an acute endotoxin damage model. After 8 h, ultrasound was used to observe the mouse heart function index: ejection fraction (EF), shortening fraction (FS), left ventricular diastolic inner diameter (LVIDd), and left ventricular end-systolic diameter (LVIDs); HE staining was used to observe the morphological changes of the heart tissue of mice; Enzyme linked immunosorbent assay (ELISA) was used to detect tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and free fatty acid (FFA); High performance liquid chromatography (HPLC) was used to detect the content of adenosine triphosphate (ATP), adenosine diphosphate(ADP) and adenosine monophosphate (AMP); Western Blot was used to detect the protein expression levels of PPARα and ATP5D in myocardial tissues.  Results Compared with the model group, the increasing of the cardiac function index EF, FS, LVIDd and LVIDs of the ASIV groups improved the infiltration of inflammatory cells and the deformation of myocardial fibers, decreased the content of TNF-α, IL-1β, IL-6, FFA, and increased the ratio of ATP/AMP and ADP/AMP ; increased the protein expressions of PPARα and ATP5D. Conclusions Astragaloside IV may be used to improve the energy metabolism of myocardial injury induced by lipopolysaccharide by PPARα, which can protect the cardiomyopathy of sepsis.

Key words

  / Astragaloside IV /  Lipopolysaccharide /  Sepsis cardiomyopathy /  PPARα /  Energy metabolism 

Cite this article

Download Citations
NIE Qu, LI Meng-fei, WANG Hong-xin. Effects of Astragaloside IV on sepsis myocardiopathy and peroxisomal proliferate activation receptor alpha in mice induced by lipopolysaccharide[J]. Chinese Journal of Clinical Anatomy. 2020, 38(2): 189-193 https://doi.org/10.13418/j.issn.1001-165x.2020.02.017

References

[1] Kimmoun A, Ducrocq N, Levy B, et al. Mechanisms of vascular hyporesponsiveness in septic shock[J]. Curr Vasc Pharmacol, 2013, 11(2): 139-149.
[2]  Merx MW, Weber C. Sepsis and the heart[J]. Circulation, 2007, 116(7): 793-802.
[3] Gilde AJ, van der Lee KA, Willemsen PH, et al. Peroxisome proliferator-activatedreceptor (PPAR) alpha and PPARbeta/delta, but not PPARgamma, modulate the expression of genes involved in cardiac lipid metabolism[J]. Circ Res, 2003, 92(5): 518-524.
[4]  Suzuki M, Nakamura F, Taguchi E, et al. 4',6-Dimethoxyisoflavone-7-O-β-D-glucopyranoside (wistin) is a peroxisome proliferator-activatedreceptor α (PPARα) agonist in mouse hepatocytes[J]. Mol Cell Biochem, 2018, 446(1-2): 35-41.
[5] Kaimoto S, Hoshino A, Arlyoshi M, et al. Activation of PPAR-alpha in the early stage of heart failure maintained myocardial function and energetics in pressure-overload heart failure[J]. Am J Physiol Heart Circ Physiol, 2017, 312(2): H305-H313.
[6] Kodde IF, van der Stok J, Smolenski RT, et al. Metabolic and genetic regulationof cardiac energy substrate preference[J]. Comp Biochem Physiol A Mol Integr Physiol, 2007, 146(1): 26-39.
[7] Mei M, Tang F, Lu M, et al. Astragaloside IV attenuates apoptosis of hypertrophic cardiomyocyte through inhibiting oxidative stress and calpain-1 activation[J]. Environ Toxicol Pharmacol, 2015, 40(3): 764-773.
[8] Li L, Hou X, Xu R, et al. Research review on the pharmacological effects of astragaloside IV[J]. Fundam Clin Pharmacol, 2017, 31(1): 17-36.
[9] Zhang S, Tang F, Yang Y, et al. Astragaloside IV protects against isoproterenol-induced cardiac hypertrophy by regulating NF-κB/PGC-1α signaling mediated energy biosynthesis[J]. PLoS One, 2015, 10(3): e0118759.
[10]Uchihashi M, Hoshino A, Okawa Y, et al. Cardiac-specific Bdh1 overexpression ameliorates oxidative stress and cardiac remodeling in pressure overload induced heart failure[J]. Circ Heart Fail, 2017, 10(12): e004417.
[11]Rowe GC, Jiang A, Arany Z, et al. PGC-1 coactivators in cardiac development and disease[J]. Circ Res, 2010, 107(7): 825-838.
[12]Finck BN. The PPAR regulatory system in cardiac physiology and disease[J]. Cardiovasc Res, 2007, 73(2): 269-277.
[13]Azevedo PS, Minicucci MF, Santos PP, et al. Energy metabolism in cardiac remodeling and heart failure[J]. Cardiol Rev, 2013, 21(3): 135-140.
[14]Pol CJ, Lieu M, Drosatos K, et al. PPARs: protectors or opponents of myocardial function[J]. PPAR Res, 2015, 2015(2): 1-19.
[15]Barger PM, Brandt JM, Leone TC, et al. Deactivation of peroxisome proliferator-activated receptor-α during cardiac hypertrophic growth[J]. J Clin Invest, 2000, 105(12): 1723-1730.
[16]Masamura K, Tanaka N, Yoshida M, et al. Myocardial metabolic regulation through peroxisome proliferator-activated receptor alpha after myocardial infarction[J]. Exp Clin Cardiol, 2003, 8(2): 61-66.

Accesses

Citation

Detail

Sections
Recommended

/