Protective Effect of Astragalosides on Myocardial Injury by Isoproterenol in SD Rats

Chen, Xiangjian; Meng, Dan; Feng, Lin; Bian, Yun-Yun; Li, Ping; Yang, Di; Cao, Kejiang; Zhang, Jinan

doi:10.1142/s0192415x0600448x

Cited by 36 publications

(24 citation statements)

References 20 publications

(19 reference statements)

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“…It has been reported that AGS plays a beneficial role without evident toxic or side effects such as the anti-inflammatory, anti-aging, anti-oxidative and anti-myocardial injury [11, 12, 14, 15, 22-24]. In the current study, we demonstrated that AGS significantly inhibits the progression of hepatic fibrosis induced by CCl 4 and the effects of AGS appear to be greater in diabetic animals.…”

Section: Discussionsupporting

confidence: 66%

Astragaloside Alleviates Hepatic Fibrosis Function via PAR2 Signaling Pathway in Diabetic Rats

Wang

Xiang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Astragaloside (AGS) extracted from radix astragalin (Huangqi) has been considered to be beneficial to liver diseases. In this study, we examined the role played by AGS in alleviating hepatic fibrosis function via protease-activated receptor-2 (PAR2) mechanisms. We hypothesized that AGS affects PAR2 signaling pathway thereby improving hepatic function in rats with hepatic fibrosis induced by carbon tetrachloride (CCl₄). We further hypothesized that AGS attenuates impaired hepatic function evoked by CCl₄ to a greater degree in diabetic animals. Methods: ELISA and Western Blot analysis were used to examine PAR2 signaling pathway in diabetic CCl₄-rats and non-diabetic CCl₄-rats. Results: AGS inhibited the protein expression of PAR2 and its downstream pathway PKA and PKCɛ in CCl₄-rats. Notably, the effects of AGS were greater in CCl₄-rats with diabetes. AGS also significantly attenuated the CCl₄-induced upregulations of pro-inflammatory cytokines, namely interleukin-1β, interleukin-6 and tumor necrosis factor-α accompanied with decreases of collagenic parameters such as hexadecenoic acid, laminin and hydroxyproline. Additionally, AGS improved the CCl₄-induced exaggerations of liver index and functions including alanine aminotransferase, aspartate aminotransferase. Moreover, TGF-β1, a marker of hepatic fibrosis, was increased in CCl₄-rats and AGS inhibited increases in TGF-β1 induced by CCl₄. Conclusions: AGS alleviates hepatic fibrosis by inhibiting PAR2 signaling expression and its effects are largely enhanced in diabetic animals. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of hepatic fibrosis; and results of our study are likely to shed light on strategies for application of AGS because it has potentially greater therapeutic effectiveness for hepatic fibrosis in diabetes.

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Section: Discussionsupporting

confidence: 66%

Astragaloside Alleviates Hepatic Fibrosis Function via PAR2 Signaling Pathway in Diabetic Rats

Wang

Xiang

et al. 2017

Cell Physiol Biochem

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“…This forms a catastrophic cycle of mitochondrial functional declination, leading to ATP depletion and ROS excess, which could induce Bax translocation from cytosol to mitochondria, resulting in the activation of MAP. 17,19) Based on the serious cytotoxicity observed and the notions mentioned above, we investigated the effects of AS-IV on DOX-induced mitochondrial toxicity. As a result, AS-IV substantially reduced the elevated mitochondrial ROS level, and LDH and CK-MB activities in mitochondrial supernatant in DOX-treated cardiomyocytes, which are three important cardiac injury markers, suggesting that AS-IV attenuates the mitochondrial damage caused by DOX.…”

Section: Discussionmentioning

confidence: 99%

“…19,20) In addition to these mitochondrial protective effects, AS-IV has also been shown to protect against cardiomyocyte apoptosis. 21,22) Taken together, these lines of evidence suggest that AS-IV may possess a mitochondria-targeted anti-apoptotic effect.…”

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confidence: 99%

Astragaloside IV Inhibits Doxorubicin-Induced Cardiomyocyte Apoptosis Mediated by Mitochondrial Apoptotic Pathway <i>via</i> Activating the PI3K/Akt Pathway

Jia

Zuo

et al. 2014

Chem. Pharm. Bull.

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“…To evaluate the SR Ca 2+ loading state, caffeine-induced Ca 2+ transients were measured [17,18] . Caffeine (10 mmol/l) was perfused directly onto the cell for 10 s using a puffer pipette.…”

Section: Measurement Of [Ca 2+ ] I and Caffeine-induced Calcium Transmentioning

confidence: 99%

Astragaloside IV Improved Intracellular Calcium Handling in Hypoxia-Reoxygenated Cardiomyocytes via the Sarcoplasmic Reticulum Ca<sup>2+</sup>-ATPase

Chen

et al. 2008

Pharmacology

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Although astragaloside IV, a saponin isolated from Astragalus membranaceus, has been shown to protect the myocardium against ischemia/reperfusion injury, its effect on the status of sarcoplasmic reticulum (SR) Ca²⁺ transport in the injured myocardium remains largely unknown. In this study, we investigated whether in cultured cardiomyocytes subjected to hypoxia and reoxygenation (H/R) administration of astragaloside IV during H/R attenuates the myocardial cell injury and prevents changes in Ca²⁺ handling activities and gene expression of SR Ca²⁺ pump. Cultured cardiomyocytes from neonatal rats were exposed to 6 h of hypoxia followed by 3 h of reoxygenation. Myocyte injury was determined by the release of cardiac troponin I in supernatant. Astragaloside IV significantly inhibited cardiac troponin I release after H/R in a dose-dependent manner. The diastolic [Ca²⁺]_i measured with Fura-2/AM was significantly increased after reoxygenation. Astragaloside IV prevented the rise of diastolic [Ca²⁺]_i and the depression of caffeine-induced Ca²⁺ transients caused by H/R. Furthermore, the observed depressions in SR Ca²⁺-ATPase activity as well as the mRNA and protein expression of SR Ca²⁺-ATPase in hypoxic-reoxygenated cardiomyocytes were attenuated by astragaloside IV treatment. These results suggest that the beneficial effect of astragaloside IV in H/R-induced injury may be related to normalization of SR Ca²⁺ pump expression and, thus, may prevent the depression in SR Ca²⁺ handling.

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Protective Effect of Astragalosides on Myocardial Injury by Isoproterenol in SD Rats

Cited by 36 publications

References 20 publications

Astragaloside Alleviates Hepatic Fibrosis Function via PAR2 Signaling Pathway in Diabetic Rats

Astragaloside Alleviates Hepatic Fibrosis Function via PAR2 Signaling Pathway in Diabetic Rats

Astragaloside IV Inhibits Doxorubicin-Induced Cardiomyocyte Apoptosis Mediated by Mitochondrial Apoptotic Pathway <i>via</i> Activating the PI3K/Akt Pathway

Astragaloside IV Improved Intracellular Calcium Handling in Hypoxia-Reoxygenated Cardiomyocytes via the Sarcoplasmic Reticulum Ca<sup>2+</sup>-ATPase

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