Protection against Doxorubicin-Induced Cytotoxicity by Geniposide Involves AMPK<i>α</i> Signaling Pathway

Meng, Yanyan; Yao, Yuan; Zhang, Xin; Kong, Chun-Yan; Song, Peng; Ma, Zhen‐Guo; Tang, Qi‐Zhu

doi:10.1155/2019/7901735

Cited by 13 publications

(8 citation statements)

References 37 publications

(49 reference statements)

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“…These data clearly show that there is overt oxidative stress. The findings of the present study data are linked with previous investigations [ 32 , 33 ]. The deficiency of GSH and the increase in MDA level produced by DOX may be attributed to the depletion of GSH in the interactions of DOX-induced free radicals with biomembrane and following lipid peroxidation.…”

Section: Discussionsupporting

confidence: 92%

Chia Seed Oil Ameliorates Doxorubicin-Induced Cardiotoxicity in Female Wistar Rats: An Electrocardiographic, Biochemical and Histopathological Approach

et al. 2021

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Doxorubicin (DOX) is a potent anti-cancer antibiotic that was widely used for treatment of various cancers. It produces free radicals which result in extreme dose-limiting cardiotoxicity. This study investigated the cardioprotective potential of chia seed oil, an active polyphenolic nutraceutical against doxorubicin-induced cardiotoxicity in Wistar rats. Twenty-four female Wistar rats were divided into four groups (n = 6) which consist of normal control, DOX control, test-A and test-B group. Animals were prophylactically treated with two different doses of test drug, i.e. chia seed oil 2.5 ml/kg/day and 5 ml/kg/day in test-A and test-B groups orally for 7 days. Doxorubicin (25 mg/kg; single dose) was administered intraperitoneally to DOX control, Test-A and Test-B animals on the seventh day to induce cardiotoxicity. ECG analysis was done before and after treatment. Besides ECG, CK, CK-MB, LDH, AST, MDA and GSH were analyzed. DOX had significantly altered ECG, CK, CK-MB, LDH, AST, MDA and GSH. Pre-treatment with chia seed oil significantly alleviated DOX-induced ECG changes and also guarded against DOX-induced rise of serum CK, CK-MB and AST levels. Chia seed oil alleviated histopathological alteration in DOX-treated rats. It also significantly inhibited DOX-induced GSH depletion and elevation of MDA. The present study revealed that chia seed oil exerts cardioprotection against doxorubicin-induced cardiotoxicity in female Wistar rats. Our study opens the perspective to clinical studies to precisely consider chia seed oil as a potential chemoprotectant nutraceutical in the combination chemotherapy with doxorubicin to limit its cardiotoxicity.

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Section: Discussionsupporting

confidence: 92%

Chia Seed Oil Ameliorates Doxorubicin-Induced Cardiotoxicity in Female Wistar Rats: An Electrocardiographic, Biochemical and Histopathological Approach

et al. 2021

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“…The hepatic levels of GSH and CAT were reduced in rats treated with DOX , while CSO/DOX group exhibited an elevation significantly in hepatic GSH and CAT levels related to DOX-treated group .An elevation in MDA levels was noticed in hepatic tissues in DOX group, while CSO/DOX rat groups showed a significance decrease in hepatic MDA levels. These findings agreed with previous studies demonstrated the reduction of hepatotoxicity induced by DOX (Meng Y et al, 2019).…”

Section: Discussionsupporting

confidence: 94%

Chia Seeds Oil Inhibits Hepatic Resistance to Doxorubicin Via Suppressing Cyp3-A4 and Mrp-1 in Male Albino Rats

A.Tawfik¹,

Awad²,

Bakr³

et al. 2023

AAVS

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Background:The oil-seed of chia (Salvia hispanica L.), CSO, had been reported for many biological activities. Doxorubicin (DOX) is one of the active chemotherapies for hepatocellular carcinoma. DOX-resistance is the cause of its limited use. Objectives: This study aimed to explore the influence of CSO on DOX-induced resistance and antioxidant status. Methods: 40 male albino rats weighing 150-200g were divided equally into four groups 10/ each. CSO (5% w/w) were administrated oral daily for 30 consecutive days. DOX treated groups were injected IP at a dose of 2.5 mg/kg trice weekly to be totally 15 mg/kg for two weeks. G1 Control, G2 CSO, G3 Doxorubicin, G4 CSO/DOX. Antioxidant activity, histopathological examination, immunohistochemical analysis of CYP3A4, MRP-1, and c-MYC proteins and expression of miRNAs were assayed. Results: Findings indicated that CSO treatment led to a suppression in hepatotoxicity, nephrotoxicity and cardiotoxicity induced by DOX in male albino rats evidenced by a significant enhancement in the activity of ALT, GGT, LDH, AST, also creatinine and uric acid. CSO induced antioxidant activity GSH, CAT and inhibited MDA. Histopathological examination in sections of liver, kidney and heart tissues were confirmed these findings. In liver tissues, DOX resulted in an observable induction in CYP3A4 and MRP-1, while CSO/DOX showed an inhibition in both proteins. c-MYC was dramatically decreased in DOX group, while CSO/DOX group restored cellular c-MYC. CSO/DOX group resulted in a remarkable inhibition in the tumor suppressor miRNA (let-7a) compared to DOX-induced expression. Moreover, miR-122, as negative regulator of DOX resistance, showed a dramatic induction in CSO/DOX group compared to DOX group. Conclusion, CSO is capable of effectively inhibit DOX resistance, induced hepatic, nephro and cardiac antioxidant status, inhibit lipid peroxidation, and restore hepatic function.

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“…24 CGA also protected cardiomyocytes from oxidative emergency damage caused by doxorubicin. 25 In addition, CGA was found to prevent ISO-induced hypertrophy in neonatal rat myocytes by reducing the expression level of cardiac hypertrophic markers. 14 The present study elucidated the protective mechanism of CGA in cardiac hypertrophy.…”

Section: Discussionmentioning

confidence: 97%

Chlorogenic acid attenuates cardiac hypertrophy via up‐regulating Sphingosine‐1‐phosphate receptor1 to inhibit endoplasmic reticulum stress

Ping,

Yang,

Ning

et al. 2024

ESC Heart Failure

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AimsCardiac hypertrophy, an adaptive response of the heart to stress overload, is closely associated with heart failure and sudden cardiac death. This study aimed to investigate the therapeutic effects of chlorogenic acid (CGA) on cardiac hypertrophy and elucidate the underlying mechanisms.Methods and resultsTo simulate cardiac hypertrophy, myocardial cells were exposed to isoproterenol (ISO, 10 μM). A rat model of ISO‐induced cardiac hypertrophy was also established. The expression levels of cardiac hypertrophy markers, endoplasmic reticulum stress (ERS) markers, and apoptosis markers were measured using quantitative reverse transcription PCR and western blotting. The apoptosis level, size of myocardial cells, and heart tissue pathological changes were determined by terminal deoxynucleotidyl transferase dUTP nick‐end labelling staining, immunofluorescence staining, haematoxylin and eosin staining, and Masson's staining. We found that CGA treatment decreased the size of ISO‐treated H9c2 cells. Moreover, CGA inhibited ISO‐induced up‐regulation of cardiac hypertrophy markers (atrial natriuretic peptide, brain natriuretic peptide, and β‐myosin heavy chain), ERS markers (C/EBP homologous protein, glucose regulatory protein 78, and protein kinase R‐like endoplasmic reticulum kinase), and apoptosis markers (bax and cleaved caspase‐12/9/3) but increased the expression of anti‐apoptosis marker bcl‐2 in a dose‐dependent way (0, 10, 50, and 100 μM). Knockdown of sphingosine‐1‐phosphate receptor 1 (S1pr1) reversed the protective effect of CGA on cardiac hypertrophy, ERS, and apoptosis in vitro (P < 0.05). CGA also restored ISO‐induced inhibition on the AMP‐activated protein kinase (AMPK)/sirtuin 1 (SIRT1) signalling in H9c2 cells, while S1pr1 knockdown abolished these CGA‐induced effects (P < 0.05). CGA (90 mg/kg/day, for six consecutive days) protected rats against cardiac hypertrophy in vivo (P < 0.05).ConclusionsCGA treatment attenuated ISO‐induced ERS and cardiac hypertrophy by activating the AMPK/SIRT1 pathway via modulation of S1pr1.

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Protection against Doxorubicin-Induced Cytotoxicity by Geniposide Involves AMPKα Signaling Pathway

Cited by 13 publications

References 37 publications

Chia Seed Oil Ameliorates Doxorubicin-Induced Cardiotoxicity in Female Wistar Rats: An Electrocardiographic, Biochemical and Histopathological Approach

Chia Seed Oil Ameliorates Doxorubicin-Induced Cardiotoxicity in Female Wistar Rats: An Electrocardiographic, Biochemical and Histopathological Approach

Chia Seeds Oil Inhibits Hepatic Resistance to Doxorubicin Via Suppressing Cyp3-A4 and Mrp-1 in Male Albino Rats

Chlorogenic acid attenuates cardiac hypertrophy via up‐regulating Sphingosine‐1‐phosphate receptor1 to inhibit endoplasmic reticulum stress

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