Hesperetin post-treatment prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating PI3K/Akt signaling pathway

He, Shangfei; Wang, Xianbao; Zhong, Yanyan; Tang, Lu; Zhang, Ya; Ling, Yuanna; Tan, Zhipeng; Yang, Pingzhen; Chen, Aihua

doi:10.1016/j.biopha.2017.05.003

Cited by 32 publications

(18 citation statements)

References 26 publications

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“…Several previous studies have indicated that apoptosis serves a key role in liver I/R (5,30,44) and that inhibiting apoptosis attenuates liver injury (30). Additionally, it is reported that HDN ameliorates apoptosis in many situations (22,(45)(46)(47). The results of the present study demonstrated that HDN suppressed apoptosis in liver i/R injury, as indicated by increased Bcl-2 and decreased cleaved-caspase 3 protein expression levels.…”

Section: Discussionsupporting

confidence: 70%

Hesperidin ameliorates liver ischemia/reperfusion injury via activation of the Akt pathway

Qin

Luo

et al. 2020

Mol Med Rep

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Section: Discussionsupporting

confidence: 70%

Hesperidin ameliorates liver ischemia/reperfusion injury via activation of the Akt pathway

Qin

Luo

et al. 2020

Mol Med Rep

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“…I/R-induced cardiac injury is a complicated pathophysiological process, with the involvement of multiple layers of the body, organs, cells, and molecules, as well as multiple pathways of genes, proteins, and signaling pathways [ 21 ]. It has been confirmed that excessive inflammatory response and oxidative induction during reperfusion are the key factors that lead to cardiac cell death [ 22 , 23 ]. More researches have suggested that nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome has participated in the pathophysiological process of MIRI, and inflammasome is a key factor that regulates IL-1 β and activate caspase-1; inhibition of NLRP3 could shrink the area of myocardial infarction and the reconstruction of left ventricle following infarction [ 24 , 25 ].…”

Section: Discussionmentioning

confidence: 99%

6‐Gingerol Protects Heart by Suppressing Myocardial Ischemia/Reperfusion Induced Inflammation via the PI3K/Akt‐Dependent Mechanism in Rats

Qin

Jiang

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Our previous study has demonstrated that 6-Gingerol (6-G) could alleviate myocardial ischemia/reperfusion injury (MIRI). However, the molecular mechanism underlying the process of myocardial ischemia/reperfusion (I/R) injury alleviation by 6-G remains unelucidated. The objective of the present study is to further investigate the potential mechanism for 6-G to alleviate MIRI in rats. Thirty-two Sprague-Dawley rats were randomly divided into four groups: the Sham group, the I/R group, the 6-G + I/R group, and the LY294002 (LY) + 6-G + I/R group. For the rats in each of the groups, data were collected for cardiogram, cardiac function, area of myocardial infarction, myocardial pathology, myocardial enzyme, marker of inflammatory response, and PI3K/Akt signaling pathway. We found that the pretreatment of 6-G with 6 mg/kg could shrink the ST section of cardiogram, improve the cardiac function, reduce the area of myocardial infarction and the degree of cardiac pathological injury, lower the level of myocardial enzyme, and inhibit the inflammatory response. In addition, our results also indicated that 6-G could upregulate the expression of PI3K and p-Akt and that LY294002, a blocking agent of PI3K/Akt signaling pathway, could nullify the protecting role of 6-G. Our experimental results showed that 6-G could inhibit I/R-induced inflammatory response through the activation of the PI3K/Akt signaling pathway.

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“…The post treatment of rat cardiomyocytes submitted to H/R injury with hesperitin inhibited apoptosis by elevating Bcl-2 expression and decreasing Bax and and cleaved caspase-3 expression levels. It was observed that this protective effect was mediated through the activation of PI3K/Akt signalling pathway [93]. Another evidence of hesperetin anti-apoptotic effect was observed in lipopolysaccharide (LPS)-induced H9C2 cells via the JNK/Bax signalling pathway.…”

Section: Flavanonesmentioning

confidence: 94%

Pure Polyphenols Applications for Cardiac Health and Disease

Santos

Gomes

Oudot

et al. 2018

CPD

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Polyphenols are natural compounds present in fruits and vegetables that can exert beneficial effects on human health and notably, on the cardiovascular system. Some of these compounds showed significant protective activities toward atherosclerosis, hypertension, myocardial infarction, anthracyclin-induced cardiomyopathy, angiogenesis as well as heart failure. Polyphenols can act through systemic effects as well as through modulation of signaling pathways such as redox signaling, inflammation, autophagy and cell death in the heart and vessels. These effects can be mediated by changes in expression level and by post-translational modifications of proteins (e.g. Stat1, CaMKII, Sirtuins, BCL-2 family members, PDEs, TRF2, eNOS and SOD). This non-comprehensive short review aims to summarize recent knowledge on the main pharmacological effects and mechanisms of cardioprotection of pure polyphenols, using different approaches such as cell culture, animal models and human studies.

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Hesperetin post-treatment prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating PI3K/Akt signaling pathway

Cited by 32 publications

References 26 publications

Hesperidin ameliorates liver ischemia/reperfusion injury via activation of the Akt pathway

Hesperidin ameliorates liver ischemia/reperfusion injury via activation of the Akt pathway

6‐Gingerol Protects Heart by Suppressing Myocardial Ischemia/Reperfusion Induced Inflammation via the PI3K/Akt‐Dependent Mechanism in Rats

Pure Polyphenols Applications for Cardiac Health and Disease

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