Ganoderma atrum polysaccharide improves doxorubicin-induced cardiotoxicity in mice by regulation of apoptotic pathway in mitochondria

Li, Wenjuan; Zhang, Xian-Yi; Wu, Ruizhu; Song, Yong; Xie, Mingyong

doi:10.1016/j.carbpol.2018.08.144

Cited by 23 publications

(9 citation statements)

References 38 publications

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“…Histological examination using light and electron microscopes in DOX treated group went in accordance with previous studies [37][38][39][40] as it has revealed extensive myocardial lesions in the form of myofiber degeneration, disintegration and focal loss together with degenerative changes of the sarcoplasmic organelles and even the sarcolemma. Moreover, biochemical markers of cardiac tissue injury CK-MB and LDH were significantly raised in mice sera after DOX exposure.…”

Section: Discussionsupporting

confidence: 85%

The possible protective effect of aldehyde dehydrogenase 2 agonist (Alda-1) on doxorubicin induced toxicity of the left ventricular cardiomyocytes of adult male mice.

Nabil

Ahmed

Sabeh

et al. 2021

Egyptian Journal of Histology

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Background: Doxorubicin (DOX) is an effective antineoplastic drug. However, its cardiotoxicity is a major obstacle that limits its use. Therefore, a novel protective agent is urgently needed. Enzyme activation recently gained much interest as a new therapeutic strategy. In this context, Alda-1 is a newly emerged molecule in the field of cardioprotection through its activation of aldehyde dehydrogenase 2 enzyme. Aim of the Study:To evaluate the possible protective effect of aldehyde dehydrogenase agonist Alda-1 on doxorubicin induced cardiotoxicity. Material and methods: Twenty-four adult male C57BL/6 mice were divided equally into 4 groups. Group I received intraperitoneal injection of saline. Group II received intraperitoneal injection of Alda-1 (10 mg/kg) daily for 5 days. Group III received a single intraperitoneal injection of DOX (20 mg/kg). Group IV received both DOX and Alda-1 in the same regimen as in groups II and III, Alda-1 was administered 1 day before DOX. All mice were euthanized on the 5th day following DOX administration. Blood samples were collected, hearts were excised and further processed for anatomical, histological and biochemical analysis. Results: DOX administration caused extensive cardiotoxicity as evident by the marked decrease in the heart weight and the extensive myocardial lesions shown by the light and electron microscopic examination. Moreover, biochemical serum markers of cardiac injury (CK-MB &LDH) were markedly elevated. Increased oxidative stress was also encountered as shown by the decreased serum TAC and increased tissue MDA. Furthermore, mitochondrial morphometry showed increased mitochondrial size. However, concomitant administration of Alda-1 with DOX has markedly alleviated the heart injury as shown by the restoration of the heart weight and cardiac architecture together with preservation of the mitochondrial structure. Moreover, Alda-1 has ameliorated the biochemical markers of cardiac injury and the oxidative stress. Conclusion:Alda-1 provides a valuable protective effect against doxorubicin triggered cardiotoxicity.

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Section: Discussionsupporting

confidence: 85%

The possible protective effect of aldehyde dehydrogenase 2 agonist (Alda-1) on doxorubicin induced toxicity of the left ventricular cardiomyocytes of adult male mice.

Nabil

Ahmed

Sabeh

et al. 2021

Egyptian Journal of Histology

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“…In vitro, γ-ray pre-irradiation increased manganese superoxide dismutase (Mn-SOD) levels in neonatal rat ventricular myocytes (NRCMs), which up-regulated MMP, Bcl-2 expressions, and decreased the Bax expression and cytochrome C release (Childs et al, 2002;Chae et al, 2005). Nevertheless, polysaccharide elevated MMP and restrained mitochondrial permeability transition (MPT) by activating manganese superoxide dismutase (Mn-SOD) and suppressing the subsequent caspases cascade reactions (Li W. J. et al, 2018).…”

Section: Doxorubicin (Dox) Apoptosismentioning

confidence: 99%

Molecular Mechanisms of Cardiomyocyte Death in Drug-Induced Cardiotoxicity

Wei

Zhang

et al. 2020

Front. Cell Dev. Biol.

109

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Homeostatic regulation of cardiomyocytes plays a crucial role in maintaining the normal physiological activity of cardiac tissue. Severe cardiotoxicity results in cardiac diseases including but not limited to arrhythmia, myocardial infarction and myocardial hypertrophy. Drug-induced cardiotoxicity limits or forbids further use of the implicated drugs. Such drugs that are currently available in the clinic include anti-tumor drugs (doxorubicin, cisplatin, trastuzumab, etc.), antidiabetic drugs (rosiglitazone and pioglitazone), and an antiviral drug (zidovudine). This review focused on cardiomyocyte death forms and related mechanisms underlying clinical drug-induced cardiotoxicity, including apoptosis, autophagy, necrosis, necroptosis, pryoptosis, and ferroptosis. The key proteins involved in cardiomyocyte death signaling were discussed and evaluated, aiming to provide a theoretical basis and target for the prevention and treatment of drug-induced cardiotoxicity in the clinical practice.

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“…The destruction of the immune system, lead to autoimmune diseases and inflammatory diseases, always accompanied the organic damage ( 40 ). As an vital extrinsic diagnostic technology, HE image is easily available to assess the immunosuppressive status of organism ( 41 , 42 ).…”

Section: Resultsmentioning

confidence: 99%

Extraction and immunomodulatory activity of the polysaccharide obtained from Craterellus cornucopioides

Zhang

Shi

et al. 2022

Front. Nutr.

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In this study, we investigated the structural features of the polysaccharide obtained from Craterellus cornucopioides (CCP2) by high-performance liquid chromatography, Fourier transform infrared spectroscopy and ion chromatography. The results showed that CCP2 was a catenarian pyranose that principally comprised of mannose, galactose, glucose, and xylose in the ratio of 1.86: 1.57: 1.00: 1.14, with a molecular weight of 8.28 × 104 Da. Moreover, the immunoregulation effect of CCP2 was evaluated both in vitro and in vivo. It displayed a remarkable immunological activity and activation in RAW264.7 cells by enhancing the phagocytosis of macrophages in a dose-dependent manner without showing cytotoxicity at the concentrations of 10–200 μg/mL in vitro. Additionally, Histopathological analysis indicated the protective function of CCP2 against immunosuppression induced by cyclophosphamide (Cy). Meanwhile, the intake of CCP2 had better immunoregulatory activity for immunosuppression BALB/c mice model. After prevention by CCP2, the spleen and thymus weight indexes of BALB/c mice model were significantly increased. The RT-qPCR and Western Blot results provided comprehensive evidence that the CCP2 could activate macrophages by enhancing the production of cytokines (IL-2, IL-6, and IL-8) and upregulating the protein expression of cell membrane receptor TLR4 and its downstream protein kinase (TRAF6, TRIF, and NF-κB p65) production of immunosuppressive mice through TLR4-NFκB p65 pathway. The results demonstrated that CCP2 could be a potential prebiotic and might provide meaningful information for further research on the immune mechanism.

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Ganoderma atrum polysaccharide improves doxorubicin-induced cardiotoxicity in mice by regulation of apoptotic pathway in mitochondria

Cited by 23 publications

References 38 publications

The possible protective effect of aldehyde dehydrogenase 2 agonist (Alda-1) on doxorubicin induced toxicity of the left ventricular cardiomyocytes of adult male mice.

The possible protective effect of aldehyde dehydrogenase 2 agonist (Alda-1) on doxorubicin induced toxicity of the left ventricular cardiomyocytes of adult male mice.

Molecular Mechanisms of Cardiomyocyte Death in Drug-Induced Cardiotoxicity

Extraction and immunomodulatory activity of the polysaccharide obtained from Craterellus cornucopioides

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