Dioscin Attenuates Myocardial Ischemic/Reperfusion-Induced Cardiac Dysfunction through Suppression of Reactive Oxygen Species

Lyu, Dayin; Tian, Qing; Qian, Huitao; Shen, Tianyu; Xi, Jinxing; Xiao, Pingxi; Lu, Qiulun

doi:10.1155/2021/3766919

Cited by 5 publications

(5 citation statements)

References 37 publications

(30 reference statements)

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“…27 Dioscin, a natural steroid saponin isolated from the root bark of wild dioscorea nipponica, is currently widely employed for cardiovascular disease treatment. 28 It was implied by Kong that Dioscin alleviated hypoxic-caused cardiac dysfunction in myocardial infarction via elevating the level of lncRNA MANTIS. 29 Dioscin improved myocardial infarction damage through adjusting BMP4/NOX1-mediated inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…It has been widely recognized that estradiol decreases the risk for cardiovascular disease, but estrogen replacement therapy is limited for its side effects 27 . Dioscin, a natural steroid saponin isolated from the root bark of wild dioscorea nipponica, is currently widely employed for cardiovascular disease treatment 28 . It was implied by Kong that Dioscin alleviated hypoxic‐caused cardiac dysfunction in myocardial infarction via elevating the level of lncRNA MANTIS 29 .…”

Section: Discussionmentioning

confidence: 99%

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Dioscin ameliorates doxorubicin‐induced heart failure via inhibiting autophagy and apoptosis by controlling the PDK1‐mediated Akt/mTOR signaling pathway

Yuan,

Ji,

Yan

et al. 2023

The Kaohsiung J of Med Scie

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Heart failure (HF) is a disease with high mortality and morbidity rate. Autophagy is critically implicated in HF progression. The current research was designed to investigate the function of Dioscin on oxidative stress, autophagy, and apoptosis in HF. In this study, doxorubicin (Dox) was employed to induce HF model and HL‐1 cell damage model. Echocardiography implied that Dioscin could dramatically relieve heart function in vivo. Western blotting determined that Dioscin treatment reversed the promotive effect of autophagy caused by Dox through modulating levels of key autophagy‐associated molecules, including Atg5 and Beclin1. Dioscin also impaired apoptosis by regulating apoptosis‐related protein, including Bcl‐2 and cleaved caspase‐3 following Dox treatment in vivo and in vitro. Furthermore, the impacts of Dioscin were mediated by upregulation of PDK1‐mediated Akt/mTOR signaling. The mTOR inhibitor (rapamycin) could counteract the therapeutic impact of Dioscin in vitro. Taken together, Dioscin could relieve cardiac function through blocking apoptosis and autophagy by activating the PDK1‐elicited Akt/mTOR pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Dioscin ameliorates doxorubicin‐induced heart failure via inhibiting autophagy and apoptosis by controlling the PDK1‐mediated Akt/mTOR signaling pathway

Yuan,

Ji,

Yan

et al. 2023

The Kaohsiung J of Med Scie

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show abstract

“…Dihydroethidium (DHE) staining was applied to detect the ROS level(Lyu et al. 2021 ). The sections were stained with 10 μM DHE for 30 min at 37 °C, and then stained with 4′,6-diamidino-2-phenylindole (DAPI) for 5 min.…”

Section: Methodsmentioning

confidence: 99%

Salvianolic acid B inhibits myocardial I/R-induced ROS generation and cell apoptosis by regulating the TRIM8/GPX1 pathway

Lü

Gui

et al. 2022

Pharmaceutical Biology

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Context Salvianolic acid B (SalB) can attenuate myocardial ischemia/reperfusion (I/R) injury, but the mechanisms are not entirely known. Objective Our study investigates if SalB protects cardiomyocytes against I/R injury by regulating Tripartite motif (TRIM) protein. Materials and methods AC16 cardiomyocytes were treated with I/R, and then with SalB (10, 25 and 50 μM) for 24 h, while control cells were cultured under normal conditions. Female Sprague-Dawley rats were subjected to I/R injury, and then intravenously injected with 20, 40, or 60 mg/kg SalB or saline, as a control, rats received sham operation and saline injection. Results Upon treatment, apoptotic rate, reactive oxygen species (ROS), and malondialdehyde (MDA) were increased 10-, 3.8-, and 1.3-fold, respectively, while superoxide dismutase (SOD) activity was reduced by 62.1% compared to control cells. I/R treatment elevated the mRNA and protein expression of TRIM8. SalB treatment remarkably abolished the above-mentioned effects of I/R treatment. TRIM8 knock-down could partially alleviate I/R-induced myocardial injury. TRIM8 overexpression promoted cardiomyocyte injury, which was alleviated by SalB. Moreover, TRIM8 negatively regulated protein expression of antioxidant enzyme glutathione peroxidase 1 (GPX1). TRIM8 protein interacted with GPX1 and TRIM8 overexpression promoted GPX1 ubiquitnation. GPX1 knock-down abolished the protective effects of SalB on I/R-injured cardiomyocytes. Our in vivo experiments confirmed the effects of SalB on I/R-induced myocardial injury. Discussion and conclusions SalB protected cardiomyocytes from I/R-induced apoptosis and oxidative stress in vitro and in vivo , which was partly mediated by the TRIM8/GPX1 axis. This suggests that down-regulation of TRIM8 expression may ameliorate I/R-induced myocardial injury.

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“…The content of ROS was detected as previously described (21). The frozen lung sections were treated with dihydroethidium (DHE) dye (Beyotime, China) at 37 • C for 30 min, then using PBS washed for 5 min for three times.…”

Section: Determination Of Reactive Oxygen Species (Ros)mentioning

confidence: 99%

Berberine Ameliorates Inflammation in Acute Lung Injury via NF-κB/Nlrp3 Signaling Pathway

et al. 2022

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The inflammatory response is the key pathophysiological character of acute lung injury (ALI). Berberine (BBR), a natural quaternary ammonium alkaloid, plays a functional role in anti-inflammation both in vitro and in vivo. However, the underlying mechanism between BBR and ALI has not been expounded. Here, we found that BBR improved the permeability of pulmonary and repressed the inflammatory factors in the lipopolysaccharides (LPSs)-induced ALI model. We demonstrated that BBR could suppress the expression of phosphorylated nuclear factor-kappa B (NF-κB) and further restrain the downstream gene nucleotide-binding domain and leucine-rich repeat protein-3 (Nlrp3). Moreover, we also revealed that BBR could directly interact with Nlrp3 protein. After knocked down of Nlrp3 by using siRNA, the protective role of BBR was abrogated in vitro. The expression of IL-1β and IL-18 was downregulated by BBR via the two signaling pathways. Notably, in Nlrp3 deficient mice, the protective effect of BBR was abolished. These findings demonstrate that BBR has a depressant effect on inflammatory response caused by LPS via regulating NF-κB/Nlrp3 signaling pathway, providing a potential therapeutic strategy in ALI.

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Dioscin Attenuates Myocardial Ischemic/Reperfusion-Induced Cardiac Dysfunction through Suppression of Reactive Oxygen Species

Cited by 5 publications

References 37 publications

Dioscin ameliorates doxorubicin‐induced heart failure via inhibiting autophagy and apoptosis by controlling the PDK1‐mediated Akt/mTOR signaling pathway

Dioscin ameliorates doxorubicin‐induced heart failure via inhibiting autophagy and apoptosis by controlling the PDK1‐mediated Akt/mTOR signaling pathway

Salvianolic acid B inhibits myocardial I/R-induced ROS generation and cell apoptosis by regulating the TRIM8/GPX1 pathway

Berberine Ameliorates Inflammation in Acute Lung Injury via NF-κB/Nlrp3 Signaling Pathway

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