Delivery of astragalus polysaccharide by ultrasound microbubbles attenuate doxorubicin-induced cardiomyopathy in rodent animals

Liu, Yanjie; Chen, Li; Wu, Hao; Zhang, Hebin

doi:10.1080/21655979.2022.2050481

Cited by 7 publications

(5 citation statements)

References 40 publications

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“…It was found that DOX can cause mitochondrial dysfunction by acting on PPAR, activating oxidative stress and inflammation and ultimately inducing apoptosis. On the one hand, DOX can reduce the expression of PPAR by regulating Sirt1 or AMPK and further upregulate NF-κB expression, promote inflammatory factor release and aggravate the inflammatory response [120]. On the other hand, DOX can decrease Nrf2 expression by inhibiting PPAR, reduce the level of antioxidant enzymes and reduce the body's antioxidant capacity, resulting in oxidative stress [121].…”

Section: Sirt1/ppar/pgc-1α Signaling Pathwaymentioning

confidence: 99%

Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy

et al. 2023

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Doxorubicin (DOX) is a powerful and commonly used chemotherapeutic drug, used alone or in combination in a variety of cancers, while it has been found to cause serious cardiac side effects in clinical application. More and more researchers are trying to explore the molecular mechanisms of DOX-induced cardiomyopathy (DIC), in which oxidative stress and inflammation are considered to play a significant role. This review summarizes signaling pathways related to oxidative stress and inflammation in DIC and compounds that exert cardioprotective effects by acting on relevant signaling pathways, including the role of Nrf2/Keap1/ARE, Sirt1/p66Shc, Sirt1/PPAR/PGC-1α signaling pathways and NOS, NOX, Fe2+ signaling in oxidative stress, as well as the role of NLRP3/caspase-1/GSDMD, HMGB1/TLR4/MAPKs/NF-κB, mTOR/TFEB/NF-κB pathways in DOX-induced inflammation. Hence, we attempt to explain the mechanisms of DIC in terms of oxidative stress and inflammation, and to provide a theoretical basis or new idea for further drug research on reducing DIC.

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Section: Sirt1/ppar/pgc-1α Signaling Pathwaymentioning

confidence: 99%

Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy

et al. 2023

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“…Liu et al . have reported that diabetes can lead to oxidative stress mediated myocardial fibrosis, and eventually cardiac dysfunction in the diabetic rat model, which plays an important role in the occurrence of diabetes cardiomyopathy [ 24 ]. Moreover, it has been reported in the literature that inhibiting inflammatory response and improving the immune microenvironment of myocardial tissue can alleviate cardiac dysfunction caused by diabetes [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Glucose fluctuation promotes cardiomyocyte apoptosis by triggering endoplasmic reticulum (ER) stress signaling pathway in vivo and in vitro

Liu

et al. 2022

Bioengineered

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Glucose fluctuation is more harmful than sustained hyperglycemia, but the effect on cardiomyocyte apoptosis have not yet been clarified. In this study, we aim to identify the effect of glucose fluctuation on cardiomyocyte apoptosis and explore the underlying mechanism. Sprague-Dawley rats were intraperitoneally injected with streptozotocin (STZ) and divided into three groups: controlled diabetic group (C-STZ); uncontrolled diabetic group (U-STZ) and glucose fluctuated diabetic group (GF-STZ). After twelve weeks, echocardiography, Hematoxylin-eosin (HE) staining, and Masson staining were adopted to assess the cardiac function and pathological changes. TUNEL staining was used to detect apoptotic cells. Expressions of apoptosis-related proteins and key molecules in the endoplasmic reticulum (ER) stress pathway were determined via western blots. Further, primary cardiomyocytes incubated in different glucose conditions were treated with the inhibitor of ER stress to explore the causative role of ER stress in glucose fluctuation-induced cardiomyocyte apoptosis. In vivo , we demonstrated that glucose fluctuation promoted cardiomyocyte apoptosis, and were more harmful to cardiomyocytes than sustained hyperglycemia. Moreover, glucose fluctuation significantly triggered ER stress signaling pathway. In vitro , primary cardiomyocyte apoptosis induced by glucose fluctuation and the activation of ER stress were significantly attenuated by 4-PBA, which is an ER stress inhibitor. Above all, glucose fluctuation can promote cardiomyocyte apoptosis through triggering the ER stress signaling pathway in diabetic rats and in primary cardiomyocytes.

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“…135 APSs can protect diabetic cardiomyopathy (DCM) rats from myocardial injury and aging by activating the AMPK signaling pathway, reducing myocardial tissue inflammation and oxidative stress. 136 Both raw and honey-processed PSPs inhibited pulmonary inflammation through the NF-κB pathway and reduced the occurrence of pulmonary oxidative stress through the AMPK−Nrf2 pathway. 137 4.7. p53 Signaling Pathway.…”

Section: Insulin/insulin-like Growth Factor-1 (Insulin/igf-1) Signali...mentioning

confidence: 99%

“…ArMPs reduce brain cell apoptosis and neurological deficits by activating the PI3K/AKT/mTOR signaling pathway and its downstream apoptotic protein family . APSs can protect diabetic cardiomyopathy (DCM) rats from myocardial injury and aging by activating the AMPK signaling pathway, reducing myocardial tissue inflammation and oxidative stress . Both raw and honey-processed PSPs inhibited pulmonary inflammation through the NF-κB pathway and reduced the occurrence of pulmonary oxidative stress through the AMPK–Nrf2 pathway …”

Section: Antiaging Targets and Signal Pathways Of Polysaccharidesmentioning

confidence: 99%

Advances in Plant Polysaccharides as Antiaging Agents: Effects and Signaling Mechanisms

Deng

Wang

et al. 2023

J. Agric. Food Chem.

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Aging refers to the gradual physiological changes that occur in an organism after reaching adulthood, resulting in senescence and a decline in biological functions, ultimately leading to death. Epidemiological evidence shows that aging is a driving factor in the developing of various diseases, including cardiovascular diseases, neurodegenerative diseases, immune system disorders, cancer, and chronic low-grade inflammation. Natural plant polysaccharides have emerged as crucial food components in delaying the aging process. Therefore, it is essential to continuously investigate plant polysaccharides as potential sources of new pharmaceuticals for aging. Modern pharmacological research indicates that plant polysaccharides can exert antiaging effects by scavenging free radicals, increasing telomerase activity, regulating apoptosis, enhancing immunity, inhibiting glycosylation, improving mitochondrial dysfunction regulating gene expression, activating autophagy, and modulating gut microbiota. Moreover, the antiaging activity of plant polysaccharides is mediated by one or more signaling pathways, including IIS, mTOR, Nrf2, NF-κB, Sirtuin, p53, MAPK, and UPR signaling pathways. This review summarizes the antiaging properties of plant polysaccharides and signaling pathways participating in the polysaccharide-regulating aging process. Finally, we discuss the structure–activity relationships of antiaging polysaccharides.

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Delivery of astragalus polysaccharide by ultrasound microbubbles attenuate doxorubicin-induced cardiomyopathy in rodent animals

Cited by 7 publications

References 40 publications

Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy

Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy

Glucose fluctuation promotes cardiomyocyte apoptosis by triggering endoplasmic reticulum (ER) stress signaling pathway in vivo and in vitro

Advances in Plant Polysaccharides as Antiaging Agents: Effects and Signaling Mechanisms

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