Oral administration of Ginsenoside Rg1 prevents cardiac toxicity induced by doxorubicin in mice through anti-apoptosis

Zhu, Cairong; Wang, Yi; Liu, Hua; Mu, Haiman; Lu, Yue; Zhang, Jiayi; Huang, Jianhua

doi:10.18632/oncotarget.19698

Cited by 29 publications

(37 citation statements)

References 40 publications

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“…The Sham group was administered equivalent volumes of DMSO (daily for a week) and DDW subcutaneously and intraperitoneally respectively. Then, 7 and 28 days were selected as time‐points for early and late heart injury due to doxorubicin respectively . Echocardiography was performed to evaluate cardiac function immediately before doxorubicin treatment and at 7 and 28 days thereafter.…”

Section: Methodsmentioning

confidence: 99%

“…The CKMB measurement was done as previously reported . In brief, five mice in each group were killed on day 7 after doxorubicin treatment, and the blood samples were withdrawn immediately through the right atrium.…”

Section: Methodsmentioning

confidence: 99%

“…Then, 7 and 28 days were selected as time-points for early and late heart injury due to doxorubicin respectively. 6 Echocardiography was performed to evaluate cardiac function immediately before doxorubicin treatment and at 7 and 28 days thereafter. To assess the effects of ursolic acid on early injury to the heart, 10 mice in each group were killed at 7 days, obtaining heart specimens.…”

Section: Experimental Settingsmentioning

confidence: 99%

“…The CKMB measurement was done as previously reported. 6 In brief, five mice in each group were killed on day 7 after doxorubicin treatment, and the blood samples were withdrawn immediately through the right atrium. After standing at room temperature for 30 minutes, the samples were centrifuged (634 g, 10 minute), and serum samples were collected.…”

Section: Creatine Kinase Mb (Ckmb) Measurementmentioning

confidence: 99%

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Ursolic acid prevents doxorubicin‐induced cardiac toxicity in mice through eNOS activation and inhibition of eNOS uncoupling

Mu¹,

Liu²,

Zhang³

et al. 2019

J Cellular Molecular Medi

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In addition to the known antitumour effects of ursolic acid (UA), increasing evidence indicates that this molecule plays a role in cardiac protection. In this study, the effects of ursolic acid on the heart in mice treated with doxorubicin (DOX) were assessed. The results showed that ursolic acid improved left ventrical fractional shortening (LVFS) and left ventrical ejection fraction (LVEF) of the heart, increased nitrogen oxide (NO) levels, inhibited reactive oxygen species (ROS) production and decreased cardiac apoptosis in mice treated with doxorubicin. Mechanistically, ursolic acid increased AKT and endothelial nitric‐oxide synthase (eNOS) phosphorylation levels, and enhanced eNOS expression, while inhibiting doxorubicin induced eNOS uncoupling through NADPH oxidase 4 (NOX4) down‐regulation. These effects of ursolic acid resulted in heart protection from doxorubicin‐induced injury. Therefore, ursolic acid may be considered a potential therapeutic agent for doxorubicin‐associated cardiac toxicity in clinical practice.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Experimental Settingsmentioning

confidence: 99%

Section: Creatine Kinase Mb (Ckmb) Measurementmentioning

confidence: 99%

See 2 more Smart Citations

Ursolic acid prevents doxorubicin‐induced cardiac toxicity in mice through eNOS activation and inhibition of eNOS uncoupling

Mu¹,

Liu²,

Zhang³

et al. 2019

J Cellular Molecular Medi

Self Cite

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“…These conditions and the animal care procedures were established according to the protocols issued by the Tabriz University of Medical Sciences and ratified by the Animal Ethics Council of the university. The animals were allocated into five groups of 7 each; 1—healthy control receiving the DOX and B‐LAP vehicles (normal saline and 0.05% DMSO, respectively); 2—B‐LAP (5 mg/kg); 3—DOX control (15 mg/kg); 4—DOX + low‐dose B‐LAP (15 mg/kg and 2.5 mg/kg, respectively); and 5—DOX + high‐dose B‐LAP (15 mg/kg and 5 mg/kg, respectively). After a 3‐day period of B‐LAP administration via intra‐gastric gavage, a single intraperitoneal injection of DOX (15 mg/kg) was received, and then, B‐LAP was administered for 11 extra days.…”

Section: Methodsmentioning

confidence: 99%

β‐LAPachone ameliorates doxorubicin‐induced cardiotoxicity via regulating autophagy and Nrf2 signalling pathways in mice

Ahmad

Sanajou

Kalantary‐Charvadeh

et al. 2019

Basic Clin Pharma Tox

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β‐LAPachone (B‐LAP) is a naphthoquinone that possesses antioxidant properties. In the present investigation, the protective effect of B‐LAP against doxorubicin (DOX)‐induced cardiotoxicity was examined in mice. Thirty‐five mice were divided into 5 groups: control group, B‐LAP (5 mg/kg) group, DOX (15 mg/kg) group, DOX+B‐LAP (2.5 mg/kg) group and DOX+B‐LAP (5 mg/kg) group. B‐LAP was administered orally for 14 days of experimental period. A single dose of DOX (15 mg/kg) was injected intraperitoneally on day 3. Cardiac function, histoarchitecture, indices of oxidative stress and circulating markers of cardiac injury were examined. B‐LAP (5 mg/kg) decreased serum levels of lactate dehydrogenase (LDH), creatine kinase MB (CK‐MB) and cardiac troponin I (cTnI), and ameliorated cardiac histopathological alterations. In addition to increasing cellular NAD+/NADH ratio, B‐LAP up‐regulated the cardiac levels of SIRT1, beclin‐1, p‐LKB1 and p‐AMPK, and reduced the cardiac levels of p‐mTOR, interleukin (IL)‐1β, TNF (tumour necrosis factor)‐α and caspase‐3. B‐LAP also elevated the nuclear accumulation of Nrf2 and simultaneously up‐regulated the protein levels of haem oxygenase (HO‐1) and glutathione S‐transferase (GST) in the hearts of DOX mice. While B‐LAP reduced malondialdehyde concentrations in heart of DOX‐treated mice, it further promoted the activities of cardiac superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT).In accordance with increased cell survival, B‐LAP significantly improved the cardiac function of DOX mice. Collectively, these findings underline the protective potential of B‐LAP against DOX‐induced cardiotoxicity by regulating autophagy and AMPK/Nrf2 signalling pathway in mice.

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Ginsenoside RG1 augments doxorubicin‐induced apoptotic cell death in MDA‐MB‐231 breast cancer cell lines

Liu

Huang

Gao

et al. 2021

J Biochem & Molecular Tox

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This study determined the chemosensitizing potential of ginsenoside Rg1 in triplenegative MDA-MB-231 breast cancer cell lines. Ginsenoside Rg1 (10 µM) treated breast cancer cells were exposed to 8 nM of doxorubicin, and the chemosensitizing potential was measured by cell-based assays. Ginsenoside Rg1 (10 µM) treatment lowered the doxorubicin IC 50 value to 0.01 nM. Furthermore, the ginsenoside pretreatment augments doxorubicin-mediated reactive oxygen species (ROS) generation and subsequent alterations of mitochondrial membrane potential in MDA-MB-231 cell lines. The alkaline comet assay results illustrated an increased % tail DNA during ginsenoside Rg1 plus doxorubicin treatment than doxorubicin alone treatment. In addition, the number of apoptotic cells was also increased in ginsenoside Rg1 plus doxorubicin-treated cells. Furthermore, the polymerase chain reaction array results illustrate activation of mitogen-activated protein kinase (MAPK) gene expression (AKT, ERK, and MAPK) during doxorubicin alone treatment and it has been attenuated by ginsenoside Rg1 pretreatment. Moreover, ginsenoside Rg1 treatment before doxorubicin activates the DNA damage response elements (ATM, H2AX, RAD51, and XRCC1) and subsequent apoptosis-related gene expression (p21, TP53. APAF1, Bax, CASP3, and CASP9) patterns in MDA-MB-231 cell lines. The ginsenoside Rg1 plus doxorubicin combination shows less cytotoxicity and ROS generation in MDA10A normal breast cancer cell lines. Therefore, the present results support the chemosensitizing property of ginsenoside Rg1 in triple-negative breast cancer cell lines.

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Oral administration of Ginsenoside Rg1 prevents cardiac toxicity induced by doxorubicin in mice through anti-apoptosis

Cited by 29 publications

References 40 publications

Ursolic acid prevents doxorubicin‐induced cardiac toxicity in mice through eNOS activation and inhibition of eNOS uncoupling

Ursolic acid prevents doxorubicin‐induced cardiac toxicity in mice through eNOS activation and inhibition of eNOS uncoupling

β‐LAPachone ameliorates doxorubicin‐induced cardiotoxicity via regulating autophagy and Nrf2 signalling pathways in mice

Ginsenoside RG1 augments doxorubicin‐induced apoptotic cell death in MDA‐MB‐231 breast cancer cell lines

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