Astragaloside IV attenuates inflammatory cytokines by inhibiting TLR4/NF-кB signaling pathway in isoproterenol-induced myocardial hypertrophy

Yang, Juan; Wang, Hongxin; Zhang, Yingjie; Yang, Yuhong; Lü, Meili; Zhang, Jing; Li, Shengtao; Zhang, Suping; Li, Guang

doi:10.1016/j.jep.2013.10.017

Cited by 102 publications

(82 citation statements)

References 24 publications

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“…Our previous studies confirmed that AsIV can suppressmyocardial hypertrophy and attenuate apoptosis of hypertrophic cardiomyocyte Yang et al 2013;Zhang et al 2015), which may be partially due to its anti-oxidative, anti-inflammatory and anti-apoptotic activities that might be endothelium-protective under pathophysiological conditions. Previous study has been demonstrated that AsIV inhibits H 2 O 2 -induced HUVECs apoptosis by suppressing Nox4 expression (Ma et al 2015).…”

supporting

confidence: 72%

Pretreatment with Astragaloside IV protects human umbilical vein endothelial cells from hydrogen peroxide induced oxidative stress and cell dysfunction via inhibiting eNOS uncoupling and NADPH oxidase – ROS – NF-κB pathway

Che

Tang

Lü

et al. 2016

Can. J. Physiol. Pharmacol.

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Keyword:Astragaloside IV, hydrogen peroxide, eNOS uncoupling, NF-κB, NADPH oxidase https://mc06.manuscriptcentral.com/cjpp-pubs production and decrease in intracellular superoxide anion production. Furthermore, pretreatment with AsIV increased endothelial nitric oxide synthase (eNOS) dimer/monomer ratio and its critical cofactor tetrahydrobiopterin (BH 4 ) content, decreased Nox4 protein expression, the most abundant Nox isoform in HUVECs, inhibited translocation of NF-κB p65 subunit into nuclear fraction while enhanced the protein expression of IκB-α, the inhibitor of NF-κB p65, reduced the levels of IL-1β, IL-6 and TNF-α in HUVECs medium, and decreased iNOS protein expression,. These results suggest that AsIV may protect HUVECs from H 2 O 2 induced oxidative stress via inhibiting NADPH oxidase-ROS-NF-κB pathway and eNOS uncoupling.

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supporting

confidence: 72%

Pretreatment with Astragaloside IV protects human umbilical vein endothelial cells from hydrogen peroxide induced oxidative stress and cell dysfunction via inhibiting eNOS uncoupling and NADPH oxidase – ROS – NF-κB pathway

Che

Tang

Lü

et al. 2016

Can. J. Physiol. Pharmacol.

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“…16 MIRI is a complicated process that is associated with various factors and mechanisms, including oxidative damage, necrosis, apoptosis, inflammation, energy metabolism disruption and calcium overload. [17][18][19][20][21] All of these conditions could lead to the apoptosis of heart cells, mitochondrial injury and elevation of levels of cardiac enzymes and inflammation factors. Since 2013, the number of deaths caused by MIRI has increased remarkably, and therefore, the treatment of MIRI is one of the most significant problems that needs to be solved.…”

Section: Introductionmentioning

confidence: 99%

Development of solid lipid nanoparticles containing total flavonoid extract from<em> Dracocephalum moldavica</em> L. and their therapeutic effect against myocardial ischemia–reperfusion injury in rats

Tan¹,

He²,

Wen³

et al. 2017

IJN

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Total flavonoid extract from Dracocephalum moldavica L. (TFDM) contains effective components of D. moldavica L. that have myocardial protective function. However, the cardioprotection function of TFDM is undesirable due to its poor solubility. In order to improve the solubility and efficacy of TFDM, we developed TFDM-loaded solid lipid nanoparticles (TFDM-SLNs) and optimized the formulation of TFDM-SLNs using central composite design and response surface methodology. The physicochemical properties of TFDM-SLNs were characterized, and the pharmacodynamics was investigated using the myocardial ischemia–reperfusion injury model in rats. The nanoparticles of optimal formulation for TFDM-SLNs were spherical in shape with the average particle size of 104.83 nm and had a uniform size distribution with the polydispersity index value of 0.201. TFDM-SLNs also had a negative zeta potential of −28.7 mV to ensure the stability of the TFDM-SLNs emulsion system. The results of pharmacodynamics demonstrated that both TFDM and TFDM-SLN groups afforded myocardial protection, and the protective effect of TFDM-SLNs was significantly superior to that of TFDM alone, based on the infarct area, histopathological examination, cardiac enzyme levels and inflammatory factors in serum. Due to the optimal quality and the better myocardial protective effect, TFDM-SLNs are expected to become a safe and effective nanocarrier for the oral delivery of TFDM.

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“…A significant increase of HW/BW ratio induced by ISO injection as compared with control rats is considered as a sensitive indicator of cardiac hypertrophy [15,58,60]. Co-administration of SIM significantly reduced HW and HW/BW ratio in ISO-injected rats.…”

Section: Discussionmentioning

confidence: 99%

“…Animals were randomly allocated into four groups of 6 rats each: -Control group: rats received normal saline orally for 30 days and intraperitoneally for the last 7 days; -SIM group: rats received SIM (10 mg/kg/day) dissolved in saline by oral gavage for 30 days [8]; -ISO group: rats received normal saline orally for 30 days and ISO (5 mg/kg/day intraperitoneally) for the last 7 days [57,60]; -ISO/SIM group: rats received SIM (10 mg/kg) dissolved in saline by oral gavage for 30 days and ISO (5 mg/kg/day intraperitoneally) for the last 7 days. At the end of the experiment, all animals were sacrificed by cervical decapitation under anaesthesia and truncal blood samples were collected and centrifuged to separate sera.…”

Section: Experimental Designmentioning

confidence: 99%

Inhibition of inducible nitric oxide synthase (iNOS) by simvastatin attenuates cardiac hypertrophy in rats

Ahmed

2017

Folia Morphol

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Background:The left ventricular hypertrophy (LVH) occurs in response to Results: The results of the present study confirmed the ISO-induced myocardial lesions including significant increase of heart weight (HW), heart weight/body weight (HW/BW) ratio, LVH, interstitial myocardial fibrosis (increased collagen types I and III), inflammatory cellular infiltration, necrosis of cardiomyocytes, and increased expression of inducible nitric oxide synthase (iNOS) and thioredoxin in cardiomyocytes. These changes were accompanied by significant increase in serum levels of troponin-T, creatine phosphokinase-MB (CPK-MB), tumour necrosis factor-alpha (TNF-a) and interleukin-6 (IL-6). Co-administration of SIM to ISO-injected rats significantly reduced all these cardiac changes and serum biochemical markers in addition to marked depletion of iNOS and thioredoxin expression in cardiomyocytes. Conclusions: It is concluded that SIM co-administration attenuated ISO-induced cardiac lesions including LVH by inhibiting iNOS expression in cardiomyocytes. (Folia Morphol 2017; 76, 1: 15-27)

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Astragaloside IV attenuates inflammatory cytokines by inhibiting TLR4/NF-кB signaling pathway in isoproterenol-induced myocardial hypertrophy

Cited by 102 publications

References 24 publications

Pretreatment with Astragaloside IV protects human umbilical vein endothelial cells from hydrogen peroxide induced oxidative stress and cell dysfunction via inhibiting eNOS uncoupling and NADPH oxidase – ROS – NF-κB pathway

Pretreatment with Astragaloside IV protects human umbilical vein endothelial cells from hydrogen peroxide induced oxidative stress and cell dysfunction via inhibiting eNOS uncoupling and NADPH oxidase – ROS – NF-κB pathway

Development of solid lipid nanoparticles containing total flavonoid extract from<em> Dracocephalum moldavica</em> L. and their therapeutic effect against myocardial ischemia–reperfusion injury in rats

Inhibition of inducible nitric oxide synthase (iNOS) by simvastatin attenuates cardiac hypertrophy in rats

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Astragaloside IV attenuates inflammatory cytokines by inhibiting TLR4/NF-кB signaling pathway in isoproterenol-induced myocardial hypertrophy

Cited by 102 publications

References 24 publications

Pretreatment with Astragaloside IV protects human umbilical vein endothelial cells from hydrogen peroxide induced oxidative stress and cell dysfunction via inhibiting eNOS uncoupling and NADPH oxidase – ROS – NF-κB pathway

Pretreatment with Astragaloside IV protects human umbilical vein endothelial cells from hydrogen peroxide induced oxidative stress and cell dysfunction via inhibiting eNOS uncoupling and NADPH oxidase – ROS – NF-κB pathway

Development of solid lipid nanoparticles containing total flavonoid extract from<em> Dracocephalum moldavica</em> L. and their therapeutic effect against myocardial ischemia&ndash;reperfusion injury in rats

Inhibition of inducible nitric oxide synthase (iNOS) by simvastatin attenuates cardiac hypertrophy in rats

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Development of solid lipid nanoparticles containing total flavonoid extract from<em> Dracocephalum moldavica</em> L. and their therapeutic effect against myocardial ischemia–reperfusion injury in rats